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Surgery_Schwartz_5702 | Surgery_Schwartz | quality of life and functional status after surgical ventricular restoration. Ann Thorac Surg. 2007;83(4):1381-1387. 204. Isomura T. Surgical left ventricular reconstruction. Gen Tho-rac Cardiovasc Surg. 2011;59(5):315-325. 205. Maxey TS, Reece TB, Ellman PI, et al. Coronary artery bypass with ventricular restoration is superior to coronary artery bypass alone in patients with ischemic cardiomyopathy. J Thorac Cardiovasc Surg. 2004;127(2):428-434. 206. Mickleborough LL, Merchant N, Ivanov J, Rao V, Carson S. Left ventricular reconstruction: early and late results. J Thorac Cardiovasc Surg. 2004;128(1):27-37. 207. Athanasuleas CL, Buckberg GD, Stanley AW, et al. Surgi-cal ventricular restoration: the RESTORE Group experience. Heart Fail Rev. 2004;9(4):287-297. 208. Dor V, Sabatier M, Montiglio F, Rossi P, Toso A, Di Donato M. Results of nonguided subtotal endocardiectomy asso-ciated with left ventricular reconstruction in patients with ischemic ventricular arrhythmias. J Thorac | Surgery_Schwartz. quality of life and functional status after surgical ventricular restoration. Ann Thorac Surg. 2007;83(4):1381-1387. 204. Isomura T. Surgical left ventricular reconstruction. Gen Tho-rac Cardiovasc Surg. 2011;59(5):315-325. 205. Maxey TS, Reece TB, Ellman PI, et al. Coronary artery bypass with ventricular restoration is superior to coronary artery bypass alone in patients with ischemic cardiomyopathy. J Thorac Cardiovasc Surg. 2004;127(2):428-434. 206. Mickleborough LL, Merchant N, Ivanov J, Rao V, Carson S. Left ventricular reconstruction: early and late results. J Thorac Cardiovasc Surg. 2004;128(1):27-37. 207. Athanasuleas CL, Buckberg GD, Stanley AW, et al. Surgi-cal ventricular restoration: the RESTORE Group experience. Heart Fail Rev. 2004;9(4):287-297. 208. Dor V, Sabatier M, Montiglio F, Rossi P, Toso A, Di Donato M. Results of nonguided subtotal endocardiectomy asso-ciated with left ventricular reconstruction in patients with ischemic ventricular arrhythmias. J Thorac |
Surgery_Schwartz_5703 | Surgery_Schwartz | Montiglio F, Rossi P, Toso A, Di Donato M. Results of nonguided subtotal endocardiectomy asso-ciated with left ventricular reconstruction in patients with ischemic ventricular arrhythmias. J Thorac Cardiovasc Surg. 1994;107(5):1301-1307; discussion 1307-1308. 209. Sartipy U, Albåge A, Strååt E, Insulander P, Lindblom D. Sur-gery for ventricular tachycardia in patients undergoing left ventricular reconstruction by the Dor procedure. Ann Thorac Surg. 2006;81(1):65-71. 210. Matthias Bechtel JF, Tölg R, Graf B, et al. High incidence of sudden death late after anterior LV-aneurysm repair. Eur J Cardiothorac Surg. 2004;25(5):807-811. 211. O’Neill JO, Starling RC, Khaykin Y, et al. Residual high inci-dence of ventricular arrhythmias after left ventricular recon-structive surgery. J Thorac Cardiovasc Surg. 2005;130(5): 1250-1256.Brunicardi_Ch21_p0801-p0852.indd 84901/03/19 5:32 PM 850SPECIFIC CONSIDERATIONSPART II 212. Buckberg GD, Athanasuleas CL. The STICH trial: misguided conclusions. | Surgery_Schwartz. Montiglio F, Rossi P, Toso A, Di Donato M. Results of nonguided subtotal endocardiectomy asso-ciated with left ventricular reconstruction in patients with ischemic ventricular arrhythmias. J Thorac Cardiovasc Surg. 1994;107(5):1301-1307; discussion 1307-1308. 209. Sartipy U, Albåge A, Strååt E, Insulander P, Lindblom D. Sur-gery for ventricular tachycardia in patients undergoing left ventricular reconstruction by the Dor procedure. Ann Thorac Surg. 2006;81(1):65-71. 210. Matthias Bechtel JF, Tölg R, Graf B, et al. High incidence of sudden death late after anterior LV-aneurysm repair. Eur J Cardiothorac Surg. 2004;25(5):807-811. 211. O’Neill JO, Starling RC, Khaykin Y, et al. Residual high inci-dence of ventricular arrhythmias after left ventricular recon-structive surgery. J Thorac Cardiovasc Surg. 2005;130(5): 1250-1256.Brunicardi_Ch21_p0801-p0852.indd 84901/03/19 5:32 PM 850SPECIFIC CONSIDERATIONSPART II 212. Buckberg GD, Athanasuleas CL. The STICH trial: misguided conclusions. |
Surgery_Schwartz_5704 | Surgery_Schwartz | Surg. 2005;130(5): 1250-1256.Brunicardi_Ch21_p0801-p0852.indd 84901/03/19 5:32 PM 850SPECIFIC CONSIDERATIONSPART II 212. Buckberg GD, Athanasuleas CL. The STICH trial: misguided conclusions. J Thorac Cardiovasc Surg. 2009;138(5): 1060-1064 e2. 213. Dor V, Civaia F, Alexandrescu C, Sabatier M, Montiglio F. Favorable effects of left ventricular reconstruction in patients excluded from the Surgical Treatments for Isch-emic Heart Failure (STICH) trial. J Thorac Cardiovasc Surg. 2011;141(4):905-916, 916 e1-e4. 214. Kang N, Edwards M, Larbalestier R. Preoperative intraaor-tic balloon pumps in high-risk patients undergoing open heart surgery. Ann Thorac Surg. 2001;72(1):54-57. 215. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012;367(14):1287-1296. 216. Meharwal ZS, Trehan N. Vascular complications of intra-aortic balloon insertion in patients undergoing coronary reavs-cularization: analysis of 911 | Surgery_Schwartz. Surg. 2005;130(5): 1250-1256.Brunicardi_Ch21_p0801-p0852.indd 84901/03/19 5:32 PM 850SPECIFIC CONSIDERATIONSPART II 212. Buckberg GD, Athanasuleas CL. The STICH trial: misguided conclusions. J Thorac Cardiovasc Surg. 2009;138(5): 1060-1064 e2. 213. Dor V, Civaia F, Alexandrescu C, Sabatier M, Montiglio F. Favorable effects of left ventricular reconstruction in patients excluded from the Surgical Treatments for Isch-emic Heart Failure (STICH) trial. J Thorac Cardiovasc Surg. 2011;141(4):905-916, 916 e1-e4. 214. Kang N, Edwards M, Larbalestier R. Preoperative intraaor-tic balloon pumps in high-risk patients undergoing open heart surgery. Ann Thorac Surg. 2001;72(1):54-57. 215. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012;367(14):1287-1296. 216. Meharwal ZS, Trehan N. Vascular complications of intra-aortic balloon insertion in patients undergoing coronary reavs-cularization: analysis of 911 |
Surgery_Schwartz_5705 | Surgery_Schwartz | shock. N Engl J Med. 2012;367(14):1287-1296. 216. Meharwal ZS, Trehan N. Vascular complications of intra-aortic balloon insertion in patients undergoing coronary reavs-cularization: analysis of 911 cases. Eur J Cardiovasc Surg. 2002;21(4):741-747. 217. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017; 36(10): 1080-1086. 218. Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med. 2001;345(20):1435-1443. 219. Maybaum S, Mancini D, Xydas S, et al. Cardiac improve-ment during mechanical circulatory support: a prospective multicenter study of the LVAD Working Group. Circulation. 2007;115(19):2497-2505. 220. Lamarche Y, Kearns M, Josan K, et al. Successful weaning and explantation of the Heartmate II left ventricular assist device. Can J Cardiol. 2011;27(3):358-362. 221. Birks EJ, George RS, Hedger M, et | Surgery_Schwartz. shock. N Engl J Med. 2012;367(14):1287-1296. 216. Meharwal ZS, Trehan N. Vascular complications of intra-aortic balloon insertion in patients undergoing coronary reavs-cularization: analysis of 911 cases. Eur J Cardiovasc Surg. 2002;21(4):741-747. 217. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017; 36(10): 1080-1086. 218. Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med. 2001;345(20):1435-1443. 219. Maybaum S, Mancini D, Xydas S, et al. Cardiac improve-ment during mechanical circulatory support: a prospective multicenter study of the LVAD Working Group. Circulation. 2007;115(19):2497-2505. 220. Lamarche Y, Kearns M, Josan K, et al. Successful weaning and explantation of the Heartmate II left ventricular assist device. Can J Cardiol. 2011;27(3):358-362. 221. Birks EJ, George RS, Hedger M, et |
Surgery_Schwartz_5706 | Surgery_Schwartz | Y, Kearns M, Josan K, et al. Successful weaning and explantation of the Heartmate II left ventricular assist device. Can J Cardiol. 2011;27(3):358-362. 221. Birks EJ, George RS, Hedger M, et al. Reversal of severe heart failure with a continuous-flow left ventricular assist device and pharmacological therapy: a prospective study. Circulation. 2011;123(4):381-390. 222. Birks EJ, Tansley PD, Hardy J, et al. Left ventricular assist device and drug therapy for the reversal of heart failure. N Engl J Med. 2006;355(18):1873-1884. 223. Chugh AR, Beache GM, Loughran JH, et al. Administra-tion of cardiac stem cells in patients with ischemic cardio-myopathy: the SCIPIO trial: surgical aspects and interim analysis of myocardial function and viability by magnetic resonance. Circulation. 2012;126(11 suppl 1):S54-S64. 224. Hare JM, Fishman JE, Gerstenblith G, et al. Comparison of allogeneic vs autologous bone marrow-derived mesenchymal stem cells delivered by transendocardial injection in patients | Surgery_Schwartz. Y, Kearns M, Josan K, et al. Successful weaning and explantation of the Heartmate II left ventricular assist device. Can J Cardiol. 2011;27(3):358-362. 221. Birks EJ, George RS, Hedger M, et al. Reversal of severe heart failure with a continuous-flow left ventricular assist device and pharmacological therapy: a prospective study. Circulation. 2011;123(4):381-390. 222. Birks EJ, Tansley PD, Hardy J, et al. Left ventricular assist device and drug therapy for the reversal of heart failure. N Engl J Med. 2006;355(18):1873-1884. 223. Chugh AR, Beache GM, Loughran JH, et al. Administra-tion of cardiac stem cells in patients with ischemic cardio-myopathy: the SCIPIO trial: surgical aspects and interim analysis of myocardial function and viability by magnetic resonance. Circulation. 2012;126(11 suppl 1):S54-S64. 224. Hare JM, Fishman JE, Gerstenblith G, et al. Comparison of allogeneic vs autologous bone marrow-derived mesenchymal stem cells delivered by transendocardial injection in patients |
Surgery_Schwartz_5707 | Surgery_Schwartz | 1):S54-S64. 224. Hare JM, Fishman JE, Gerstenblith G, et al. Comparison of allogeneic vs autologous bone marrow-derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial. JAMA. 2012;308(22):2369-2379. 225. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart transplantation. N Engl J Med. 2007;357(9):885-896. 226. Frazier OH, Rose EA, Oz MC, et al. Multicenter clinical eval-uation of the HeartMate vented electric left ventricular assist system in patients awaiting heart transplantation. J Thorac Cardiovasc Surg. 2001;122(6):1186-1195. 227. Aaronson KD, Slaughter MS, Miller LW, et al. Use of an intrapericardial, continuous-flow, centrifugal pump in patients awaiting heart transplantation. Circulation. 2012;125(25): 3191-3200. 228. John R, Pagani FD, Naka Y, et al. Post-cardiac transplant survival after support with a continuous-flow left ventricu-lar | Surgery_Schwartz. 1):S54-S64. 224. Hare JM, Fishman JE, Gerstenblith G, et al. Comparison of allogeneic vs autologous bone marrow-derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial. JAMA. 2012;308(22):2369-2379. 225. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart transplantation. N Engl J Med. 2007;357(9):885-896. 226. Frazier OH, Rose EA, Oz MC, et al. Multicenter clinical eval-uation of the HeartMate vented electric left ventricular assist system in patients awaiting heart transplantation. J Thorac Cardiovasc Surg. 2001;122(6):1186-1195. 227. Aaronson KD, Slaughter MS, Miller LW, et al. Use of an intrapericardial, continuous-flow, centrifugal pump in patients awaiting heart transplantation. Circulation. 2012;125(25): 3191-3200. 228. John R, Pagani FD, Naka Y, et al. Post-cardiac transplant survival after support with a continuous-flow left ventricu-lar |
Surgery_Schwartz_5708 | Surgery_Schwartz | awaiting heart transplantation. Circulation. 2012;125(25): 3191-3200. 228. John R, Pagani FD, Naka Y, et al. Post-cardiac transplant survival after support with a continuous-flow left ventricu-lar assist device: impact of duration of left ventricular assist device support and other variables. J Thorac Cardiovasc Surg. 2010;140(1):174-181. 229. Pal JD, Piacentino V, Cuevas AD, et al. Impact of left ven-tricular assist device bridging on posttransplant outcomes. Ann Thorac Surg. 2009;88(5):1457-1461; discussion 1461. 230. Mehra MR, Naka Y, Uriel N, et al. A fully magnetically levi-tated circulatory pump for advanced heart failure. N Engl J Med. 2017;376(5):440-450. 231. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251. 232. Kirklin JK, Naftel DC, Pagani FD, et al. Long-term mechani-cal circulatory support (destination therapy): on track to com-pete with heart | Surgery_Schwartz. awaiting heart transplantation. Circulation. 2012;125(25): 3191-3200. 228. John R, Pagani FD, Naka Y, et al. Post-cardiac transplant survival after support with a continuous-flow left ventricu-lar assist device: impact of duration of left ventricular assist device support and other variables. J Thorac Cardiovasc Surg. 2010;140(1):174-181. 229. Pal JD, Piacentino V, Cuevas AD, et al. Impact of left ven-tricular assist device bridging on posttransplant outcomes. Ann Thorac Surg. 2009;88(5):1457-1461; discussion 1461. 230. Mehra MR, Naka Y, Uriel N, et al. A fully magnetically levi-tated circulatory pump for advanced heart failure. N Engl J Med. 2017;376(5):440-450. 231. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251. 232. Kirklin JK, Naftel DC, Pagani FD, et al. Long-term mechani-cal circulatory support (destination therapy): on track to com-pete with heart |
Surgery_Schwartz_5709 | Surgery_Schwartz | assist device. N Engl J Med. 2009;361(23):2241-2251. 232. Kirklin JK, Naftel DC, Pagani FD, et al. Long-term mechani-cal circulatory support (destination therapy): on track to com-pete with heart transplantation? J Thorac Cardiovasc Surg. 2012;144(3):584-603; discussion 597-598. 233. Slaughter MS, Pagani FD, McGee EC, et al. HeartWare ven-tricular assist system for bridge to transplant: combined results of the bridge to transplant and continued access protocol trial. J Heart Lung Transplant. 2013;32(7):675-683. 234. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. J Am Coll Cardiol. 2013;62(16):e147-e239. 235. John R, Liao K, Kamdar F, Eckman P, Boyle A, Colvin-Adams M. Effects on preand posttransplant pulmonary hemody-namics in patients with continuous-flow left ventricular assist devices. J Thorac Cardiovasc Surg. | Surgery_Schwartz. assist device. N Engl J Med. 2009;361(23):2241-2251. 232. Kirklin JK, Naftel DC, Pagani FD, et al. Long-term mechani-cal circulatory support (destination therapy): on track to com-pete with heart transplantation? J Thorac Cardiovasc Surg. 2012;144(3):584-603; discussion 597-598. 233. Slaughter MS, Pagani FD, McGee EC, et al. HeartWare ven-tricular assist system for bridge to transplant: combined results of the bridge to transplant and continued access protocol trial. J Heart Lung Transplant. 2013;32(7):675-683. 234. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. J Am Coll Cardiol. 2013;62(16):e147-e239. 235. John R, Liao K, Kamdar F, Eckman P, Boyle A, Colvin-Adams M. Effects on preand posttransplant pulmonary hemody-namics in patients with continuous-flow left ventricular assist devices. J Thorac Cardiovasc Surg. |
Surgery_Schwartz_5710 | Surgery_Schwartz | K, Kamdar F, Eckman P, Boyle A, Colvin-Adams M. Effects on preand posttransplant pulmonary hemody-namics in patients with continuous-flow left ventricular assist devices. J Thorac Cardiovasc Surg. 2010;140(2):447-452. 236. Kormos RL, Teuteberg JJ, Pagani FD, et al. Right ventricu-lar failure in patients with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes. J Thorac Cardiovasc Surg. 2010;139(5): 1316-1324. 237. Neragi-Miandoab S. A ventricular assist device as a bridge to recovery, decision making, or transplantation in patients with advanced cardiac failure. Surg Today. 2012;42(10):917-926. 238. Copeland JG, Smith RG, Arabia FA, et al. Cardiac replace-ment with a total artificial heart as a bridge to transplantation. N Engl J Med. 2004;351(9):859-867. 239. El-Hamamsy I, Jacques F, Perrault LP, et al. Results follow-ing implantation of mechanical circulatory support systems: the Montreal Heart Institute experience. Can J | Surgery_Schwartz. K, Kamdar F, Eckman P, Boyle A, Colvin-Adams M. Effects on preand posttransplant pulmonary hemody-namics in patients with continuous-flow left ventricular assist devices. J Thorac Cardiovasc Surg. 2010;140(2):447-452. 236. Kormos RL, Teuteberg JJ, Pagani FD, et al. Right ventricu-lar failure in patients with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes. J Thorac Cardiovasc Surg. 2010;139(5): 1316-1324. 237. Neragi-Miandoab S. A ventricular assist device as a bridge to recovery, decision making, or transplantation in patients with advanced cardiac failure. Surg Today. 2012;42(10):917-926. 238. Copeland JG, Smith RG, Arabia FA, et al. Cardiac replace-ment with a total artificial heart as a bridge to transplantation. N Engl J Med. 2004;351(9):859-867. 239. El-Hamamsy I, Jacques F, Perrault LP, et al. Results follow-ing implantation of mechanical circulatory support systems: the Montreal Heart Institute experience. Can J |
Surgery_Schwartz_5711 | Surgery_Schwartz | J Med. 2004;351(9):859-867. 239. El-Hamamsy I, Jacques F, Perrault LP, et al. Results follow-ing implantation of mechanical circulatory support systems: the Montreal Heart Institute experience. Can J Cardiol. 2009;25(2):107-110. 240. Meyer A, Slaughter M. The total artificial heart. Panminerva Med. 2011;53(3):141-154. 241. Gammie JS, Haddad M, Milford Beland S, et al. Atrial fibril-lation correction surgery: lessons from the Society of Tho-racic Surgeons national cardiac database. Ann Thorac Surg. 2008;85(3):909-914. 242. Ad N, Suri RM, Gammie JS, Sheng S, O’Brien SM, Henry L. Surgical ablation of atrial fibrillation trends and outcomes in North America. J Thorac Cardiovasc Surg. 2012;144(5): 1051-1060. 243. Calkins H, Kuck KH, Cappato R, et al. 2012 HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial | Surgery_Schwartz. J Med. 2004;351(9):859-867. 239. El-Hamamsy I, Jacques F, Perrault LP, et al. Results follow-ing implantation of mechanical circulatory support systems: the Montreal Heart Institute experience. Can J Cardiol. 2009;25(2):107-110. 240. Meyer A, Slaughter M. The total artificial heart. Panminerva Med. 2011;53(3):141-154. 241. Gammie JS, Haddad M, Milford Beland S, et al. Atrial fibril-lation correction surgery: lessons from the Society of Tho-racic Surgeons national cardiac database. Ann Thorac Surg. 2008;85(3):909-914. 242. Ad N, Suri RM, Gammie JS, Sheng S, O’Brien SM, Henry L. Surgical ablation of atrial fibrillation trends and outcomes in North America. J Thorac Cardiovasc Surg. 2012;144(5): 1051-1060. 243. Calkins H, Kuck KH, Cappato R, et al. 2012 HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial |
Surgery_Schwartz_5712 | Surgery_Schwartz | on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design: a report of the Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Ablation of Atrial Fibrillation. Devel-oped in partnership with the European Heart Rhythm Associa-tion (EHRA), a registered branch of the European Society of Cardiology (ESC) and the European Cardiac Arrhythmia Soci-ety (ECAS); and in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), the Asia Pacific Heart Rhythm Society (APHRS), and the Society of Thoracic Surgeons (STS). Endorsed by the governing bod-ies of the American College of Cardiology Foundation, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, the Asia Pacific Heart Rhythm Soci-ety, and the Heart Rhythm | Surgery_Schwartz. on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design: a report of the Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Ablation of Atrial Fibrillation. Devel-oped in partnership with the European Heart Rhythm Associa-tion (EHRA), a registered branch of the European Society of Cardiology (ESC) and the European Cardiac Arrhythmia Soci-ety (ECAS); and in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), the Asia Pacific Heart Rhythm Society (APHRS), and the Society of Thoracic Surgeons (STS). Endorsed by the governing bod-ies of the American College of Cardiology Foundation, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, the Asia Pacific Heart Rhythm Soci-ety, and the Heart Rhythm |
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Surgery_Schwartz_5724 | Surgery_Schwartz | KF, Ohe T. Cardiac tumors that cause arrhythmias. Cardiac Electrophysiol Rev. 2002;6(1-2):174-177. 294. Lee VH, Connolly HM, Brown RD, Jr. Central nervous system manifestations of cardiac myxoma. Arch Neurol. 2007;64(8): 1115-1120. 295. Jean WC, Walski-Easton SM, Nussbaum ES. Multiple intra-cranial aneurysms as delayed complications of an atrial myxoma: case report. Neurosurgery. 2001;49(1):200-202; discussion 202-203. 296. Jain D, Maleszewski JJ, Halushka MK. Benign cardiac tumors and tumorlike conditions. Ann Diagn Pathol. 2010;14(3):215-230. 297. Pucci A, Gagliardotto P, Zanini C, Pansini S, di Summa M, Mollo F. Histopathologic and clinical characterization of car-diac myxoma: review of 53 cases from a single institution. Am Heart J. 2000;140(1):134-138. 298. Bakaeen FG, Reardon MJ, Coselli JS, et al. Surgical out-come in 85 patients with primary cardiac tumors. Am J Surg. 2003;186(6):641-647; discussion 647. 299. Gammie JS, Abrishamchian AR, Griffith BP. Cardiac | Surgery_Schwartz. KF, Ohe T. Cardiac tumors that cause arrhythmias. Cardiac Electrophysiol Rev. 2002;6(1-2):174-177. 294. Lee VH, Connolly HM, Brown RD, Jr. Central nervous system manifestations of cardiac myxoma. Arch Neurol. 2007;64(8): 1115-1120. 295. Jean WC, Walski-Easton SM, Nussbaum ES. Multiple intra-cranial aneurysms as delayed complications of an atrial myxoma: case report. Neurosurgery. 2001;49(1):200-202; discussion 202-203. 296. Jain D, Maleszewski JJ, Halushka MK. Benign cardiac tumors and tumorlike conditions. Ann Diagn Pathol. 2010;14(3):215-230. 297. Pucci A, Gagliardotto P, Zanini C, Pansini S, di Summa M, Mollo F. Histopathologic and clinical characterization of car-diac myxoma: review of 53 cases from a single institution. Am Heart J. 2000;140(1):134-138. 298. Bakaeen FG, Reardon MJ, Coselli JS, et al. Surgical out-come in 85 patients with primary cardiac tumors. Am J Surg. 2003;186(6):641-647; discussion 647. 299. Gammie JS, Abrishamchian AR, Griffith BP. Cardiac |
Surgery_Schwartz_5725 | Surgery_Schwartz | FG, Reardon MJ, Coselli JS, et al. Surgical out-come in 85 patients with primary cardiac tumors. Am J Surg. 2003;186(6):641-647; discussion 647. 299. Gammie JS, Abrishamchian AR, Griffith BP. Cardiac autotransplantation and radical bi-atrial resection for recurrent atrial myxoma. Ann Thorac Surg. 2007;83(4): 1545-1547. 300. Goldstein DJ, Oz MC, Michler RE. Radical excisional therapy and total cardiac transplantation for recurrent atrial myxoma. Ann Thorac Surg. 1995;60(4):1105-1107. 301. Shah IK, Dearani JA, Daly RC, et al. Cardiac myxomas: a 50-year experience with resection and analysis of risk factors for recurrence. Ann Thorac Surg. 2015;100(2):495-500. 302. Putnam JB, Jr, Sweeney MS, Colon R, Lanza LA, Frazier OH, Cooley DA. Primary cardiac sarcomas. Ann Thorac Surg. 1991;51(6):906-910. 303. Neuville A, Collin F, Bruneval P, et al. Intimal sarcoma is the most frequent primary cardiac sarcoma: clinicopathologic and molecular retrospective analysis of 100 primary cardiac sarco-mas. | Surgery_Schwartz. FG, Reardon MJ, Coselli JS, et al. Surgical out-come in 85 patients with primary cardiac tumors. Am J Surg. 2003;186(6):641-647; discussion 647. 299. Gammie JS, Abrishamchian AR, Griffith BP. Cardiac autotransplantation and radical bi-atrial resection for recurrent atrial myxoma. Ann Thorac Surg. 2007;83(4): 1545-1547. 300. Goldstein DJ, Oz MC, Michler RE. Radical excisional therapy and total cardiac transplantation for recurrent atrial myxoma. Ann Thorac Surg. 1995;60(4):1105-1107. 301. Shah IK, Dearani JA, Daly RC, et al. Cardiac myxomas: a 50-year experience with resection and analysis of risk factors for recurrence. Ann Thorac Surg. 2015;100(2):495-500. 302. Putnam JB, Jr, Sweeney MS, Colon R, Lanza LA, Frazier OH, Cooley DA. Primary cardiac sarcomas. Ann Thorac Surg. 1991;51(6):906-910. 303. Neuville A, Collin F, Bruneval P, et al. Intimal sarcoma is the most frequent primary cardiac sarcoma: clinicopathologic and molecular retrospective analysis of 100 primary cardiac sarco-mas. |
Surgery_Schwartz_5726 | Surgery_Schwartz | A, Collin F, Bruneval P, et al. Intimal sarcoma is the most frequent primary cardiac sarcoma: clinicopathologic and molecular retrospective analysis of 100 primary cardiac sarco-mas. Am J Surg Pathol. 2014;38(4):461-469. 304. Neragi-Miandoab S, Kim J, Vlahakes GJ. Malignant tumours of the heart: a review of tumour type, diagnosis and therapy. Clin Oncol (R Coll Radiol). 2007;19(10):748-756.Brunicardi_Ch21_p0801-p0852.indd 85201/03/19 5:32 PM | Surgery_Schwartz. A, Collin F, Bruneval P, et al. Intimal sarcoma is the most frequent primary cardiac sarcoma: clinicopathologic and molecular retrospective analysis of 100 primary cardiac sarco-mas. Am J Surg Pathol. 2014;38(4):461-469. 304. Neragi-Miandoab S, Kim J, Vlahakes GJ. Malignant tumours of the heart: a review of tumour type, diagnosis and therapy. Clin Oncol (R Coll Radiol). 2007;19(10):748-756.Brunicardi_Ch21_p0801-p0852.indd 85201/03/19 5:32 PM |
Surgery_Schwartz_5727 | Surgery_Schwartz | Thoracic Aneurysms and Aortic DissectionScott A. LeMaire, Ourania Preventza, and Joseph S. Coselli 22chapterANATOMY OF THE AORTAThe aorta consists of two major segments—the proximal aorta and the distal aorta—whose anatomic characteristics affect both the clinical manifestations of disease in these segments and the selection of treatment strategies for such disease (Fig. 22-1). The proximal aortic segment includes the ascending aorta and the transverse aortic arch. The ascending aorta begins at the aortic valve and ends at the origin of the innominate artery. The first portion of the ascending aorta is the aortic root, which includes the aortic valve annulus and the three sinuses of Valsalva; the coronary arteries originate from two of these sinuses. The aortic root joins the tubular portion of the ascending aorta at the sinotubular ridge. The transverse aortic arch is the area from which the brachio-cephalic branches arise. The distal aortic segment includes the descending thoracic | Surgery_Schwartz. Thoracic Aneurysms and Aortic DissectionScott A. LeMaire, Ourania Preventza, and Joseph S. Coselli 22chapterANATOMY OF THE AORTAThe aorta consists of two major segments—the proximal aorta and the distal aorta—whose anatomic characteristics affect both the clinical manifestations of disease in these segments and the selection of treatment strategies for such disease (Fig. 22-1). The proximal aortic segment includes the ascending aorta and the transverse aortic arch. The ascending aorta begins at the aortic valve and ends at the origin of the innominate artery. The first portion of the ascending aorta is the aortic root, which includes the aortic valve annulus and the three sinuses of Valsalva; the coronary arteries originate from two of these sinuses. The aortic root joins the tubular portion of the ascending aorta at the sinotubular ridge. The transverse aortic arch is the area from which the brachio-cephalic branches arise. The distal aortic segment includes the descending thoracic |
Surgery_Schwartz_5728 | Surgery_Schwartz | of the ascending aorta at the sinotubular ridge. The transverse aortic arch is the area from which the brachio-cephalic branches arise. The distal aortic segment includes the descending thoracic aorta and the abdominal aorta. The descending thoracic aorta begins distal to the origin of the left subclavian artery and extends to the diaphragmatic hia-tus, where it joins the abdominal aorta. The descending tho-racic aorta gives rise to multiple bronchial and esophageal branches, as well as to the segmental intercostal arteries, which provide circulation to the spinal cord.The volume of blood that flows through the thoracic aorta at high pressure is far greater than that found in any other vascular structure. For this reason, any condition that disrupts the integrity of the thoracic aorta, such as aortic dissection, aneurysm rupture, or traumatic injury, can have catastrophic consequences.Historically, open surgical repair of such conditions has been an intimidating undertaking associated | Surgery_Schwartz. of the ascending aorta at the sinotubular ridge. The transverse aortic arch is the area from which the brachio-cephalic branches arise. The distal aortic segment includes the descending thoracic aorta and the abdominal aorta. The descending thoracic aorta begins distal to the origin of the left subclavian artery and extends to the diaphragmatic hia-tus, where it joins the abdominal aorta. The descending tho-racic aorta gives rise to multiple bronchial and esophageal branches, as well as to the segmental intercostal arteries, which provide circulation to the spinal cord.The volume of blood that flows through the thoracic aorta at high pressure is far greater than that found in any other vascular structure. For this reason, any condition that disrupts the integrity of the thoracic aorta, such as aortic dissection, aneurysm rupture, or traumatic injury, can have catastrophic consequences.Historically, open surgical repair of such conditions has been an intimidating undertaking associated |
Surgery_Schwartz_5729 | Surgery_Schwartz | as aortic dissection, aneurysm rupture, or traumatic injury, can have catastrophic consequences.Historically, open surgical repair of such conditions has been an intimidating undertaking associated with significant morbidity and mortality. Strategies for protecting the brain and spinal cord during such repairs have become critical in preventing devastating complications. Endovascular therapy for such conditions in selected patients has become accepted practice, producing fewer adverse outcomes than traditional approaches.THORACIC AORTIC ANEURYSMSAortic aneurysm is defined as a permanent, localized dilatation of the aorta to a diameter that is at least 50% greater than is normal at that anatomic level.1 The annual incidence of thoracic aortic aneurysms is estimated to be 5.9 per 100,000 persons.2 The clinical manifestations, methods of treatment, and treatment results in patients with aortic aneurysms vary according to the cause and the aortic segment involved. Causes of thoracic | Surgery_Schwartz. as aortic dissection, aneurysm rupture, or traumatic injury, can have catastrophic consequences.Historically, open surgical repair of such conditions has been an intimidating undertaking associated with significant morbidity and mortality. Strategies for protecting the brain and spinal cord during such repairs have become critical in preventing devastating complications. Endovascular therapy for such conditions in selected patients has become accepted practice, producing fewer adverse outcomes than traditional approaches.THORACIC AORTIC ANEURYSMSAortic aneurysm is defined as a permanent, localized dilatation of the aorta to a diameter that is at least 50% greater than is normal at that anatomic level.1 The annual incidence of thoracic aortic aneurysms is estimated to be 5.9 per 100,000 persons.2 The clinical manifestations, methods of treatment, and treatment results in patients with aortic aneurysms vary according to the cause and the aortic segment involved. Causes of thoracic |
Surgery_Schwartz_5730 | Surgery_Schwartz | persons.2 The clinical manifestations, methods of treatment, and treatment results in patients with aortic aneurysms vary according to the cause and the aortic segment involved. Causes of thoracic aortic aneurysms include degenerative disease of the aortic wall, aor-tic dissection, aortitis, infection, and trauma. Aneurysms can be localized to a single aortic segment, or they can involve multiple segments. Thoracoabdominal aortic aneurysms, for example, involve both the descending thoracic aorta and the abdominal aorta. In the most extreme cases, the entire aorta is aneurysmal; this condition is often called mega-aorta.Aortic aneurysms can be either “true” or “false.” True aneurysms can take two forms: fusiform and saccular. Fusiform aneurysms are more common and can be described as sym-metrical dilatations of the aorta. Saccular aneurysms are local-ized outpouchings of the aorta. False aneurysms, also called pseudoaneurysms, are leaks in the aortic wall that are contained by the | Surgery_Schwartz. persons.2 The clinical manifestations, methods of treatment, and treatment results in patients with aortic aneurysms vary according to the cause and the aortic segment involved. Causes of thoracic aortic aneurysms include degenerative disease of the aortic wall, aor-tic dissection, aortitis, infection, and trauma. Aneurysms can be localized to a single aortic segment, or they can involve multiple segments. Thoracoabdominal aortic aneurysms, for example, involve both the descending thoracic aorta and the abdominal aorta. In the most extreme cases, the entire aorta is aneurysmal; this condition is often called mega-aorta.Aortic aneurysms can be either “true” or “false.” True aneurysms can take two forms: fusiform and saccular. Fusiform aneurysms are more common and can be described as sym-metrical dilatations of the aorta. Saccular aneurysms are local-ized outpouchings of the aorta. False aneurysms, also called pseudoaneurysms, are leaks in the aortic wall that are contained by the |
Surgery_Schwartz_5731 | Surgery_Schwartz | dilatations of the aorta. Saccular aneurysms are local-ized outpouchings of the aorta. False aneurysms, also called pseudoaneurysms, are leaks in the aortic wall that are contained by the outer layer of the aorta and/or the periaortic tissue; they are caused by disruption of the aortic wall and lead blood to collect in pouches of fibrotic tissue.Aneurysms of the thoracic aorta consistently increase in size and eventually progress to cause serious complications. These include rupture, which usually is a fatal event. Therefore, aggressive treatment is indicated in all but the poorest surgical candidates. Small, asymptomatic thoracic aortic aneurysms can be followed, especially in high-surgical-risk patients, and can be treated surgically later if symptoms or complications develop, or if progressive enlargement occurs. Meticulous control of hyper-tension is the primary medical treatment for patients with small, asymptomatic aneurysms.Elective resection with graft replacement is indicated | Surgery_Schwartz. dilatations of the aorta. Saccular aneurysms are local-ized outpouchings of the aorta. False aneurysms, also called pseudoaneurysms, are leaks in the aortic wall that are contained by the outer layer of the aorta and/or the periaortic tissue; they are caused by disruption of the aortic wall and lead blood to collect in pouches of fibrotic tissue.Aneurysms of the thoracic aorta consistently increase in size and eventually progress to cause serious complications. These include rupture, which usually is a fatal event. Therefore, aggressive treatment is indicated in all but the poorest surgical candidates. Small, asymptomatic thoracic aortic aneurysms can be followed, especially in high-surgical-risk patients, and can be treated surgically later if symptoms or complications develop, or if progressive enlargement occurs. Meticulous control of hyper-tension is the primary medical treatment for patients with small, asymptomatic aneurysms.Elective resection with graft replacement is indicated |
Surgery_Schwartz_5732 | Surgery_Schwartz | enlargement occurs. Meticulous control of hyper-tension is the primary medical treatment for patients with small, asymptomatic aneurysms.Elective resection with graft replacement is indicated in asymptomatic patients with an aortic diameter of at least twice Anatomy of the Aorta853Thoracic Aortic Aneurysms853Causes and Pathogenesis / 854Clinical History / 857Clinical Manifestations / 857Diagnostic Evaluation / 858Treatment / 860Aortic Dissection876Pathology and Classification / 876Causes and Clinical History / 879Clinical Manifestations / 879Diagnostic Evaluation / 880Treatment / 881Outcomes885Repair of Proximal Aortic Aneurysms / 885Treatment of Acute Ascending Aortic Dissection / 888Repair of Distal Aortic Aneurysms / 888Treatment of Descending Thoracic Aortic Dissection / 888Conclusions889Acknowledgments889Brunicardi_Ch22_p0853-p0896.indd 85301/03/19 5:40 PM 854Figure 22-1. Illustration of normal thoracic aortic anatomy. The brachiocephalic vessels arise from the transverse | Surgery_Schwartz. enlargement occurs. Meticulous control of hyper-tension is the primary medical treatment for patients with small, asymptomatic aneurysms.Elective resection with graft replacement is indicated in asymptomatic patients with an aortic diameter of at least twice Anatomy of the Aorta853Thoracic Aortic Aneurysms853Causes and Pathogenesis / 854Clinical History / 857Clinical Manifestations / 857Diagnostic Evaluation / 858Treatment / 860Aortic Dissection876Pathology and Classification / 876Causes and Clinical History / 879Clinical Manifestations / 879Diagnostic Evaluation / 880Treatment / 881Outcomes885Repair of Proximal Aortic Aneurysms / 885Treatment of Acute Ascending Aortic Dissection / 888Repair of Distal Aortic Aneurysms / 888Treatment of Descending Thoracic Aortic Dissection / 888Conclusions889Acknowledgments889Brunicardi_Ch22_p0853-p0896.indd 85301/03/19 5:40 PM 854Figure 22-1. Illustration of normal thoracic aortic anatomy. The brachiocephalic vessels arise from the transverse |
Surgery_Schwartz_5733 | Surgery_Schwartz | 85301/03/19 5:40 PM 854Figure 22-1. Illustration of normal thoracic aortic anatomy. The brachiocephalic vessels arise from the transverse aortic arch and are used as anatomic landmarks to define the aortic regions. The ascending aorta is proximal to the innominate artery, whereas the descending aorta is distal to the left subclavian artery.normal in the involved segment (5 to 6 cm in most thoracic segments). Elective repair is contraindicated by extreme opera-tive risk due to severe coexisting cardiac or pulmonary dis-ease and by other conditions that limit life expectancy, such as malignancy. An emergency operation is performed for any patient in whom a ruptured aneurysm is suspected.Patients with thoracic aortic aneurysm often have coexisting aneurysms of other aortic segments. A common cause of death after repair of a thoracic aortic aneurysm is rupture of a different aortic aneurysm. Therefore, staged repair of multiple aortic seg-ments often is necessary. As with any major | Surgery_Schwartz. 85301/03/19 5:40 PM 854Figure 22-1. Illustration of normal thoracic aortic anatomy. The brachiocephalic vessels arise from the transverse aortic arch and are used as anatomic landmarks to define the aortic regions. The ascending aorta is proximal to the innominate artery, whereas the descending aorta is distal to the left subclavian artery.normal in the involved segment (5 to 6 cm in most thoracic segments). Elective repair is contraindicated by extreme opera-tive risk due to severe coexisting cardiac or pulmonary dis-ease and by other conditions that limit life expectancy, such as malignancy. An emergency operation is performed for any patient in whom a ruptured aneurysm is suspected.Patients with thoracic aortic aneurysm often have coexisting aneurysms of other aortic segments. A common cause of death after repair of a thoracic aortic aneurysm is rupture of a different aortic aneurysm. Therefore, staged repair of multiple aortic seg-ments often is necessary. As with any major |
Surgery_Schwartz_5734 | Surgery_Schwartz | common cause of death after repair of a thoracic aortic aneurysm is rupture of a different aortic aneurysm. Therefore, staged repair of multiple aortic seg-ments often is necessary. As with any major operation, careful pre-operative evaluation for coexisting disease and subsequent medical optimization are important for successful surgical treatment.An alternative to traditional open repair of a descending thoracic aortic aneurysm is endovascular stent grafting. Certain anatomic criteria for use—such as a landing zone that includes at least 2 cm of landing zone of healthy aortic tissue proximal and distal to the targeted aneurysm—are preferable, but not absolutely necessary. Although few data on long-term outcomes have recently been published, endovascular repair of descending thoracic aortic aneurysm has become an accepted practice that produces excellent midterm results.Causes and PathogenesisGeneral Considerations. The normal aorta derives its elastic-ity and tensile strength from | Surgery_Schwartz. common cause of death after repair of a thoracic aortic aneurysm is rupture of a different aortic aneurysm. Therefore, staged repair of multiple aortic seg-ments often is necessary. As with any major operation, careful pre-operative evaluation for coexisting disease and subsequent medical optimization are important for successful surgical treatment.An alternative to traditional open repair of a descending thoracic aortic aneurysm is endovascular stent grafting. Certain anatomic criteria for use—such as a landing zone that includes at least 2 cm of landing zone of healthy aortic tissue proximal and distal to the targeted aneurysm—are preferable, but not absolutely necessary. Although few data on long-term outcomes have recently been published, endovascular repair of descending thoracic aortic aneurysm has become an accepted practice that produces excellent midterm results.Causes and PathogenesisGeneral Considerations. The normal aorta derives its elastic-ity and tensile strength from |
Surgery_Schwartz_5735 | Surgery_Schwartz | aneurysm has become an accepted practice that produces excellent midterm results.Causes and PathogenesisGeneral Considerations. The normal aorta derives its elastic-ity and tensile strength from the medial layer, which contains approximately 45 to 55 lamellae of elastin, collagen, smooth muscle cells, and ground substance. Elastin content is highest within the ascending aorta, as would be expected because of its compliant nature, and decreases distally into the descending and abdominal aorta. Maintenance of the aortic matrix involves complex interactions among smooth muscle cells, macrophages, proteases, and protease inhibitors. Any alteration in this delicate balance can lead to aortic disease.Thoracic aortic aneurysms have a variety of causes (Table 22-1). Although these disparate pathologic processes differ in biochemical and histologic terms, they share the final common pathway of progressive aortic expansion and eventual rupture.Hemodynamic factors clearly contribute to the | Surgery_Schwartz. aneurysm has become an accepted practice that produces excellent midterm results.Causes and PathogenesisGeneral Considerations. The normal aorta derives its elastic-ity and tensile strength from the medial layer, which contains approximately 45 to 55 lamellae of elastin, collagen, smooth muscle cells, and ground substance. Elastin content is highest within the ascending aorta, as would be expected because of its compliant nature, and decreases distally into the descending and abdominal aorta. Maintenance of the aortic matrix involves complex interactions among smooth muscle cells, macrophages, proteases, and protease inhibitors. Any alteration in this delicate balance can lead to aortic disease.Thoracic aortic aneurysms have a variety of causes (Table 22-1). Although these disparate pathologic processes differ in biochemical and histologic terms, they share the final common pathway of progressive aortic expansion and eventual rupture.Hemodynamic factors clearly contribute to the |
Surgery_Schwartz_5736 | Surgery_Schwartz | pathologic processes differ in biochemical and histologic terms, they share the final common pathway of progressive aortic expansion and eventual rupture.Hemodynamic factors clearly contribute to the process of aortic dilatation. The vicious cycle of increasing diameter and increasing wall tension, as characterized by Laplace’s law (tension = pressure × radius), is well established. Turbulent Key Points1 Assessing urgency of repair is essential to developing the appropriate management plan. Although emergent repair carries greater operative risk than does elective repair, any inappropriate delay of repair risks death.2 The clinical progression of an aortic aneurysm is continued expansion and eventual dissection or rupture. Hence, regular noninvasive imaging studies, as part of a lifelong surveil-lance plan, are necessary to ensure long-term patient health. Even small asymptomatic aneurysms should be routinely imaged to assess overall size and yearly rate of expansion.3 Endovascular | Surgery_Schwartz. pathologic processes differ in biochemical and histologic terms, they share the final common pathway of progressive aortic expansion and eventual rupture.Hemodynamic factors clearly contribute to the process of aortic dilatation. The vicious cycle of increasing diameter and increasing wall tension, as characterized by Laplace’s law (tension = pressure × radius), is well established. Turbulent Key Points1 Assessing urgency of repair is essential to developing the appropriate management plan. Although emergent repair carries greater operative risk than does elective repair, any inappropriate delay of repair risks death.2 The clinical progression of an aortic aneurysm is continued expansion and eventual dissection or rupture. Hence, regular noninvasive imaging studies, as part of a lifelong surveil-lance plan, are necessary to ensure long-term patient health. Even small asymptomatic aneurysms should be routinely imaged to assess overall size and yearly rate of expansion.3 Endovascular |
Surgery_Schwartz_5737 | Surgery_Schwartz | surveil-lance plan, are necessary to ensure long-term patient health. Even small asymptomatic aneurysms should be routinely imaged to assess overall size and yearly rate of expansion.3 Endovascular repair devices are approved for the treatment of descending thoracic aortic aneurysms, descending thoracic aortic dissections, aortic trauma, and penetrating aortic ulcer.4 Practice guidelines have been published to help standardize the decision-making process and select an appropriate surgi-cal intervention, as well as to standardize the use of imaging studies for patients with thoracic aortic disease.5 Ascending aortic aneurysms that are symptomatic or ≥5.5 cm in diameter should be repaired regardless of whether the patient has a bicuspid or tricuspid aortic valve. This threshold is lowered for patients with certain heritable disor-ders affecting the aorta and for patients with additional risk factors, such as rapid aortic expansion (≥0.5 cm per year) or a family history of | Surgery_Schwartz. surveil-lance plan, are necessary to ensure long-term patient health. Even small asymptomatic aneurysms should be routinely imaged to assess overall size and yearly rate of expansion.3 Endovascular repair devices are approved for the treatment of descending thoracic aortic aneurysms, descending thoracic aortic dissections, aortic trauma, and penetrating aortic ulcer.4 Practice guidelines have been published to help standardize the decision-making process and select an appropriate surgi-cal intervention, as well as to standardize the use of imaging studies for patients with thoracic aortic disease.5 Ascending aortic aneurysms that are symptomatic or ≥5.5 cm in diameter should be repaired regardless of whether the patient has a bicuspid or tricuspid aortic valve. This threshold is lowered for patients with certain heritable disor-ders affecting the aorta and for patients with additional risk factors, such as rapid aortic expansion (≥0.5 cm per year) or a family history of |
Surgery_Schwartz_5738 | Surgery_Schwartz | is lowered for patients with certain heritable disor-ders affecting the aorta and for patients with additional risk factors, such as rapid aortic expansion (≥0.5 cm per year) or a family history of dissection.6 Surgical repair involves the development of a patienttailored plan based on careful preoperative medical evalua-tion. When appropriate, optimizing a patient’s health status—to mitigate existing comorbidities—is important before surgical intervention.7 The development and use of surgical adjuncts like antegrade selective cerebral perfusion and cerebrospinal fluid drainage have significantly reduced the morbidity rates traditionally associated with complex aortic repair.8 Proximal aortic dissection is a life-threatening condition, and immediate operative repair is generally indicated, although definitive aortic repair may be delayed until after severe mal-perfusion has been treated.Brunicardi_Ch22_p0853-p0896.indd 85401/03/19 5:40 PM 855THORACIC ANEURYSMS AND AORTIC | Surgery_Schwartz. is lowered for patients with certain heritable disor-ders affecting the aorta and for patients with additional risk factors, such as rapid aortic expansion (≥0.5 cm per year) or a family history of dissection.6 Surgical repair involves the development of a patienttailored plan based on careful preoperative medical evalua-tion. When appropriate, optimizing a patient’s health status—to mitigate existing comorbidities—is important before surgical intervention.7 The development and use of surgical adjuncts like antegrade selective cerebral perfusion and cerebrospinal fluid drainage have significantly reduced the morbidity rates traditionally associated with complex aortic repair.8 Proximal aortic dissection is a life-threatening condition, and immediate operative repair is generally indicated, although definitive aortic repair may be delayed until after severe mal-perfusion has been treated.Brunicardi_Ch22_p0853-p0896.indd 85401/03/19 5:40 PM 855THORACIC ANEURYSMS AND AORTIC |
Surgery_Schwartz_5739 | Surgery_Schwartz | indicated, although definitive aortic repair may be delayed until after severe mal-perfusion has been treated.Brunicardi_Ch22_p0853-p0896.indd 85401/03/19 5:40 PM 855THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22Table 22-1Causes of thoracic aortic aneurysmNonspecific medial degenerationAortic dissectionHeritable conditions Marfan syndrome Loeys-Dietz syndrome Ehlers-Danlos syndrome Turner syndrome Familial thoracic aortic aneurysm Aneurysms-osteoarthritis syndrome Congenital bicuspid aortic valve Bovine aortic archPoststenotic dilatationInfectionAortitis Takayasu arteritis Giant cell arteritis Rheumatoid aortitisTrauma (pseudoaneurysm)blood flow also is recognized as a factor. Poststenotic aortic dilatation, for example, occurs in some patients with aortic valve stenosis or coarctation of the descending thoracic aorta. Hemodynamic derangements, however, are only one piece of a complex puzzle.Atherosclerosis is commonly cited as a cause of thoracic aortic aneurysms. However, | Surgery_Schwartz. indicated, although definitive aortic repair may be delayed until after severe mal-perfusion has been treated.Brunicardi_Ch22_p0853-p0896.indd 85401/03/19 5:40 PM 855THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22Table 22-1Causes of thoracic aortic aneurysmNonspecific medial degenerationAortic dissectionHeritable conditions Marfan syndrome Loeys-Dietz syndrome Ehlers-Danlos syndrome Turner syndrome Familial thoracic aortic aneurysm Aneurysms-osteoarthritis syndrome Congenital bicuspid aortic valve Bovine aortic archPoststenotic dilatationInfectionAortitis Takayasu arteritis Giant cell arteritis Rheumatoid aortitisTrauma (pseudoaneurysm)blood flow also is recognized as a factor. Poststenotic aortic dilatation, for example, occurs in some patients with aortic valve stenosis or coarctation of the descending thoracic aorta. Hemodynamic derangements, however, are only one piece of a complex puzzle.Atherosclerosis is commonly cited as a cause of thoracic aortic aneurysms. However, |
Surgery_Schwartz_5740 | Surgery_Schwartz | of the descending thoracic aorta. Hemodynamic derangements, however, are only one piece of a complex puzzle.Atherosclerosis is commonly cited as a cause of thoracic aortic aneurysms. However, although atherosclerotic disease often is found in conjunction with aortic aneurysms, the notion that atherosclerosis is a distinct cause of aneurysm formation has been challenged. In most thoracic aortic aneurysms, ath-erosclerosis appears to be a coexisting process, rather than the underlying cause.Research into the pathogenesis of abdominal aortic aneurysms has focused on the molecular mechanisms of aortic wall degeneration and dilatation.3 For example, imbalances between proteolytic enzymes (e.g., matrix metalloproteinases) and their inhibitors contribute to abdominal aortic aneurysm formation. Building on these advances, current investigations are attempting to determine whether similar inflammatory and proteolytic mechanisms are involved in thoracic aortic disease, in hope of identifying | Surgery_Schwartz. of the descending thoracic aorta. Hemodynamic derangements, however, are only one piece of a complex puzzle.Atherosclerosis is commonly cited as a cause of thoracic aortic aneurysms. However, although atherosclerotic disease often is found in conjunction with aortic aneurysms, the notion that atherosclerosis is a distinct cause of aneurysm formation has been challenged. In most thoracic aortic aneurysms, ath-erosclerosis appears to be a coexisting process, rather than the underlying cause.Research into the pathogenesis of abdominal aortic aneurysms has focused on the molecular mechanisms of aortic wall degeneration and dilatation.3 For example, imbalances between proteolytic enzymes (e.g., matrix metalloproteinases) and their inhibitors contribute to abdominal aortic aneurysm formation. Building on these advances, current investigations are attempting to determine whether similar inflammatory and proteolytic mechanisms are involved in thoracic aortic disease, in hope of identifying |
Surgery_Schwartz_5741 | Surgery_Schwartz | Building on these advances, current investigations are attempting to determine whether similar inflammatory and proteolytic mechanisms are involved in thoracic aortic disease, in hope of identifying potential molecular targets for pharmacologic therapy.Nonspecific Medial Degeneration. Nonspecific medial degeneration is the most common cause of thoracic aortic dis-ease. Histologic findings of mild medial degeneration, includ-ing fragmentation of elastic fibers and loss of smooth muscle cells, are expected in the aging aorta. However, an advanced, accelerated form of medial degeneration leads to progressive weakening of the aortic wall, aneurysm formation, and eventual dissection, rupture, or both. The underlying causes of medial degenerative disease remain poorly understood.Aortic Dissection. An aortic dissection usually begins as a tear in the inner aortic wall, which initiates a progressive sepa-ration of the medial layers and creates two channels within the aorta. This event | Surgery_Schwartz. Building on these advances, current investigations are attempting to determine whether similar inflammatory and proteolytic mechanisms are involved in thoracic aortic disease, in hope of identifying potential molecular targets for pharmacologic therapy.Nonspecific Medial Degeneration. Nonspecific medial degeneration is the most common cause of thoracic aortic dis-ease. Histologic findings of mild medial degeneration, includ-ing fragmentation of elastic fibers and loss of smooth muscle cells, are expected in the aging aorta. However, an advanced, accelerated form of medial degeneration leads to progressive weakening of the aortic wall, aneurysm formation, and eventual dissection, rupture, or both. The underlying causes of medial degenerative disease remain poorly understood.Aortic Dissection. An aortic dissection usually begins as a tear in the inner aortic wall, which initiates a progressive sepa-ration of the medial layers and creates two channels within the aorta. This event |
Surgery_Schwartz_5742 | Surgery_Schwartz | aortic dissection usually begins as a tear in the inner aortic wall, which initiates a progressive sepa-ration of the medial layers and creates two channels within the aorta. This event profoundly weakens the outer wall. As the most common catastrophe involving the aorta, dissection repre-sents a major, distinct cause of thoracic aortic aneurysms and is discussed in detail in the second half of this chapter.Heritable Conditions. Several heritable conditions cause thoracic aortic aneurysms. To better characterize these disorders, the National Institutes of Health (NIH) sponsored a longitudinal registry for individuals affected by genetically triggered thoracic aortic aneurysms and cardiovascular conditions (GenTAC) more than a decade ago.4 The registry enrollment includes adults and children in 13 clinical categories, including Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome, familial tho-racic aortic aneurysms and dissections, aneurysms-osteoarthritis syndrome, and | Surgery_Schwartz. aortic dissection usually begins as a tear in the inner aortic wall, which initiates a progressive sepa-ration of the medial layers and creates two channels within the aorta. This event profoundly weakens the outer wall. As the most common catastrophe involving the aorta, dissection repre-sents a major, distinct cause of thoracic aortic aneurysms and is discussed in detail in the second half of this chapter.Heritable Conditions. Several heritable conditions cause thoracic aortic aneurysms. To better characterize these disorders, the National Institutes of Health (NIH) sponsored a longitudinal registry for individuals affected by genetically triggered thoracic aortic aneurysms and cardiovascular conditions (GenTAC) more than a decade ago.4 The registry enrollment includes adults and children in 13 clinical categories, including Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome, familial tho-racic aortic aneurysms and dissections, aneurysms-osteoarthritis syndrome, and |
Surgery_Schwartz_5743 | Surgery_Schwartz | in 13 clinical categories, including Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome, familial tho-racic aortic aneurysms and dissections, aneurysms-osteoarthritis syndrome, and congenital bicuspid aortic valve.Marfan Syndrome Marfan syndrome is an autosomal domi-nant genetic disorder characterized by a specific connective tissue defect that leads to aneurysm formation. The phenotype of patients with Marfan syndrome typically includes a tall stat-ure, high palate, joint hypermobility, eye lens disorders, mitral valve prolapse, and aortic aneurysms. The aortic wall is weak-ened by fragmentation of elastic fibers and deposition of exten-sive amounts of mucopolysaccharides (a process previously called cystic medial degeneration or cystic medial necrosis). Patients with Marfan syndrome have a mutation in the fibrillin gene located on the long arm of chromosome 15. The tradi-tional view has been that abnormal fibrillin in the extracellular matrix decreases connective tissue | Surgery_Schwartz. in 13 clinical categories, including Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome, familial tho-racic aortic aneurysms and dissections, aneurysms-osteoarthritis syndrome, and congenital bicuspid aortic valve.Marfan Syndrome Marfan syndrome is an autosomal domi-nant genetic disorder characterized by a specific connective tissue defect that leads to aneurysm formation. The phenotype of patients with Marfan syndrome typically includes a tall stat-ure, high palate, joint hypermobility, eye lens disorders, mitral valve prolapse, and aortic aneurysms. The aortic wall is weak-ened by fragmentation of elastic fibers and deposition of exten-sive amounts of mucopolysaccharides (a process previously called cystic medial degeneration or cystic medial necrosis). Patients with Marfan syndrome have a mutation in the fibrillin gene located on the long arm of chromosome 15. The tradi-tional view has been that abnormal fibrillin in the extracellular matrix decreases connective tissue |
Surgery_Schwartz_5744 | Surgery_Schwartz | syndrome have a mutation in the fibrillin gene located on the long arm of chromosome 15. The tradi-tional view has been that abnormal fibrillin in the extracellular matrix decreases connective tissue strength in the aortic wall and produces abnormal elasticity, which predisposes the aorta to dilatation from wall tension caused by left ventricular ejec-tion impulses.5 More recent evidence, however, shows that the abnormal fibrillin causes degeneration of the aortic wall matrix by increasing the activity of transforming growth factor beta (TGF-β).6 Between 75% and 85% of patients with Marfan syn-drome have dilatation of the ascending aorta and annuloaortic ectasia (dilatation of the aortic sinuses and annulus).7 Marfan syndrome also is frequently associated with aortic dissection, and aortic complications are the most common cause of death among patients with Marfan syndrome.8Loeys-Dietz Syndrome Loeys-Dietz syndrome is phenotypi-cally distinct from Marfan syndrome. It is characterized | Surgery_Schwartz. syndrome have a mutation in the fibrillin gene located on the long arm of chromosome 15. The tradi-tional view has been that abnormal fibrillin in the extracellular matrix decreases connective tissue strength in the aortic wall and produces abnormal elasticity, which predisposes the aorta to dilatation from wall tension caused by left ventricular ejec-tion impulses.5 More recent evidence, however, shows that the abnormal fibrillin causes degeneration of the aortic wall matrix by increasing the activity of transforming growth factor beta (TGF-β).6 Between 75% and 85% of patients with Marfan syn-drome have dilatation of the ascending aorta and annuloaortic ectasia (dilatation of the aortic sinuses and annulus).7 Marfan syndrome also is frequently associated with aortic dissection, and aortic complications are the most common cause of death among patients with Marfan syndrome.8Loeys-Dietz Syndrome Loeys-Dietz syndrome is phenotypi-cally distinct from Marfan syndrome. It is characterized |
Surgery_Schwartz_5745 | Surgery_Schwartz | complications are the most common cause of death among patients with Marfan syndrome.8Loeys-Dietz Syndrome Loeys-Dietz syndrome is phenotypi-cally distinct from Marfan syndrome. It is characterized as an aneurysmal syndrome with widespread systemic involvement. Loeys-Dietz syndrome is an aggressive, autosomal dominant condition that is distinguished by the triad of arterial tortuosity and aneurysms, hypertelorism (widely spaced eyes), and bifid uvula or cleft palate. It is caused by heterozygous mutations in the genes encoding TGF-β receptors.9,10 Patients with Loeys-Dietz syndrome—including young children—are at increased risk of aortic rupture and aortic dissection; diameter-based thresholds of repair tend to be lower for patients with this syndrome than for patients with other heritable disorders.Ehlers-Danlos Syndrome Ehlers-Danlos syndrome includes a spectrum of inherited disorders of collagen synthesis. The sub-types represent differing defective steps of collagen production. | Surgery_Schwartz. complications are the most common cause of death among patients with Marfan syndrome.8Loeys-Dietz Syndrome Loeys-Dietz syndrome is phenotypi-cally distinct from Marfan syndrome. It is characterized as an aneurysmal syndrome with widespread systemic involvement. Loeys-Dietz syndrome is an aggressive, autosomal dominant condition that is distinguished by the triad of arterial tortuosity and aneurysms, hypertelorism (widely spaced eyes), and bifid uvula or cleft palate. It is caused by heterozygous mutations in the genes encoding TGF-β receptors.9,10 Patients with Loeys-Dietz syndrome—including young children—are at increased risk of aortic rupture and aortic dissection; diameter-based thresholds of repair tend to be lower for patients with this syndrome than for patients with other heritable disorders.Ehlers-Danlos Syndrome Ehlers-Danlos syndrome includes a spectrum of inherited disorders of collagen synthesis. The sub-types represent differing defective steps of collagen production. |
Surgery_Schwartz_5746 | Surgery_Schwartz | disorders.Ehlers-Danlos Syndrome Ehlers-Danlos syndrome includes a spectrum of inherited disorders of collagen synthesis. The sub-types represent differing defective steps of collagen production. Vascular type Ehlers-Danlos syndrome is characterized by an autosomal dominant defect in type III collagen synthesis, which can have life-threatening cardiovascular manifestations. Sponta-neous arterial rupture, usually involving the mesenteric vessels, is the most common cause of death in these patients. Thoracic aortic aneurysms and dissections are less commonly associated with Ehlers-Danlos syndrome, but when they do occur, they pose a particularly challenging surgical problem because of the reduced integrity of the aortic tissue.11 An Ehlers-Danlos variant of periventricular heterotopia associated with joint and skin hyperextensibility and aortic dilation has been described as being caused by mutations in the gene encoding filamin A Brunicardi_Ch22_p0853-p0896.indd 85501/03/19 5:40 PM | Surgery_Schwartz. disorders.Ehlers-Danlos Syndrome Ehlers-Danlos syndrome includes a spectrum of inherited disorders of collagen synthesis. The sub-types represent differing defective steps of collagen production. Vascular type Ehlers-Danlos syndrome is characterized by an autosomal dominant defect in type III collagen synthesis, which can have life-threatening cardiovascular manifestations. Sponta-neous arterial rupture, usually involving the mesenteric vessels, is the most common cause of death in these patients. Thoracic aortic aneurysms and dissections are less commonly associated with Ehlers-Danlos syndrome, but when they do occur, they pose a particularly challenging surgical problem because of the reduced integrity of the aortic tissue.11 An Ehlers-Danlos variant of periventricular heterotopia associated with joint and skin hyperextensibility and aortic dilation has been described as being caused by mutations in the gene encoding filamin A Brunicardi_Ch22_p0853-p0896.indd 85501/03/19 5:40 PM |
Surgery_Schwartz_5747 | Surgery_Schwartz | with joint and skin hyperextensibility and aortic dilation has been described as being caused by mutations in the gene encoding filamin A Brunicardi_Ch22_p0853-p0896.indd 85501/03/19 5:40 PM 856SPECIFIC CONSIDERATIONSPART II(FLNA), an actin-binding protein that links the smooth muscle cell contractile unit to the cell surface.12Familial Thoracic Aortic Aneurysm and Dissection Fami-lies without the heritable syndromes described earlier also can be affected by genetic conditions that cause thoracic aortic aneurysm. In fact, it is estimated that at least 20% of patients with thoracic aortic aneurysms and dissections have a genetic predisposition to them. The involved mutations are characterized by autosomal dominant inheritance with decreased penetrance and variable expression. The number of genes for which mutations have been identified as causes of familial thoracic aortic aneurysm and dissection is expanding rapidly; involved genes include those related to TGF-β receptors (TGFBR1 | Surgery_Schwartz. with joint and skin hyperextensibility and aortic dilation has been described as being caused by mutations in the gene encoding filamin A Brunicardi_Ch22_p0853-p0896.indd 85501/03/19 5:40 PM 856SPECIFIC CONSIDERATIONSPART II(FLNA), an actin-binding protein that links the smooth muscle cell contractile unit to the cell surface.12Familial Thoracic Aortic Aneurysm and Dissection Fami-lies without the heritable syndromes described earlier also can be affected by genetic conditions that cause thoracic aortic aneurysm. In fact, it is estimated that at least 20% of patients with thoracic aortic aneurysms and dissections have a genetic predisposition to them. The involved mutations are characterized by autosomal dominant inheritance with decreased penetrance and variable expression. The number of genes for which mutations have been identified as causes of familial thoracic aortic aneurysm and dissection is expanding rapidly; involved genes include those related to TGF-β receptors (TGFBR1 |
Surgery_Schwartz_5748 | Surgery_Schwartz | of genes for which mutations have been identified as causes of familial thoracic aortic aneurysm and dissection is expanding rapidly; involved genes include those related to TGF-β receptors (TGFBR1 and TGFBR2), TGF-β ligands (TGFB2 and TGFB3), myosin (MYH11 and MYLK), elastin (ELN), elastin microfibril interfacer 1 (EMLIN1), microfibril-associated glycoprotein 2 (MFAP5), fibrillin-2 (FBN2), fibulin-4 (FBLN4), lysyl oxidase (LOX), and α-smooth muscle cell actin (ACTA2).3,13-16 ACTA2 mutations are present in approximately 14% of families with familial thoracic aortic aneurysms and dissections.Aneurysms-Osteoarthritis Syndrome Aneurysmsosteoarthritis syndrome is an autosomal dominant disorder char-acterized by aortic and arterial aneurysms, arterial tortuosity, aor-tic dissection, mild craniofacial abnormalities, and early-onset osteoarthritis. Aneurysms-osteoarthritis syndrome is caused by mutations in the gene encoding SMAD3, a transcription factor for TGF-β. Affected patients have a | Surgery_Schwartz. of genes for which mutations have been identified as causes of familial thoracic aortic aneurysm and dissection is expanding rapidly; involved genes include those related to TGF-β receptors (TGFBR1 and TGFBR2), TGF-β ligands (TGFB2 and TGFB3), myosin (MYH11 and MYLK), elastin (ELN), elastin microfibril interfacer 1 (EMLIN1), microfibril-associated glycoprotein 2 (MFAP5), fibrillin-2 (FBN2), fibulin-4 (FBLN4), lysyl oxidase (LOX), and α-smooth muscle cell actin (ACTA2).3,13-16 ACTA2 mutations are present in approximately 14% of families with familial thoracic aortic aneurysms and dissections.Aneurysms-Osteoarthritis Syndrome Aneurysmsosteoarthritis syndrome is an autosomal dominant disorder char-acterized by aortic and arterial aneurysms, arterial tortuosity, aor-tic dissection, mild craniofacial abnormalities, and early-onset osteoarthritis. Aneurysms-osteoarthritis syndrome is caused by mutations in the gene encoding SMAD3, a transcription factor for TGF-β. Affected patients have a |
Surgery_Schwartz_5749 | Surgery_Schwartz | abnormalities, and early-onset osteoarthritis. Aneurysms-osteoarthritis syndrome is caused by mutations in the gene encoding SMAD3, a transcription factor for TGF-β. Affected patients have a high incidence of aortic dissection, which often occurs in a mildly dilated aorta and causes sudden death.17Congenital Bicuspid Aortic Valve Bicuspid aortic valve is the most common congenital malformation of the heart or great vessels, affecting up to 2% of Americans.18 Compared to patients with a normal, trileaflet aortic valve, patients with bicuspid aortic valve have an increased incidence of ascending aortic aneurysm formation and, often, a more rapid rate of aortic enlargement.19 The location of the fused leaflet, or raphe, may be predictive of aortic dilation and other abnormalities.20 Fifty to 70% of adults with bicuspid aortic valve, but without significant valve dysfunction, have echocardiographically detectable aortic dilatation.21,22 This dilatation usually is limited to the ascending | Surgery_Schwartz. abnormalities, and early-onset osteoarthritis. Aneurysms-osteoarthritis syndrome is caused by mutations in the gene encoding SMAD3, a transcription factor for TGF-β. Affected patients have a high incidence of aortic dissection, which often occurs in a mildly dilated aorta and causes sudden death.17Congenital Bicuspid Aortic Valve Bicuspid aortic valve is the most common congenital malformation of the heart or great vessels, affecting up to 2% of Americans.18 Compared to patients with a normal, trileaflet aortic valve, patients with bicuspid aortic valve have an increased incidence of ascending aortic aneurysm formation and, often, a more rapid rate of aortic enlargement.19 The location of the fused leaflet, or raphe, may be predictive of aortic dilation and other abnormalities.20 Fifty to 70% of adults with bicuspid aortic valve, but without significant valve dysfunction, have echocardiographically detectable aortic dilatation.21,22 This dilatation usually is limited to the ascending |
Surgery_Schwartz_5750 | Surgery_Schwartz | 70% of adults with bicuspid aortic valve, but without significant valve dysfunction, have echocardiographically detectable aortic dilatation.21,22 This dilatation usually is limited to the ascending aorta and root.23 Dilation occasionally is found in the arch and only rarely in the descending or abdominal aorta. In addition, aortic dissection occurs 10 times more often in patients with bicuspid valves than in the general population.24 Recent findings suggest that aneurysms associated with bicuspid aortic valve have a fundamentally different pathobiologic cause than aneu-rysms that occur in patients with trileaflet valves.25Although the exact mechanism responsible for aneu-rysm formation in patients with bicuspid aortic valve remains unclear, evidence suggests that these patients have a congeni-tal connective tissue abnormality that predisposes the aorta to medial degeneration.25-31 For example, fibrillin-1 content is sig-nificantly lower and matrix metalloproteinase activity is | Surgery_Schwartz. 70% of adults with bicuspid aortic valve, but without significant valve dysfunction, have echocardiographically detectable aortic dilatation.21,22 This dilatation usually is limited to the ascending aorta and root.23 Dilation occasionally is found in the arch and only rarely in the descending or abdominal aorta. In addition, aortic dissection occurs 10 times more often in patients with bicuspid valves than in the general population.24 Recent findings suggest that aneurysms associated with bicuspid aortic valve have a fundamentally different pathobiologic cause than aneu-rysms that occur in patients with trileaflet valves.25Although the exact mechanism responsible for aneu-rysm formation in patients with bicuspid aortic valve remains unclear, evidence suggests that these patients have a congeni-tal connective tissue abnormality that predisposes the aorta to medial degeneration.25-31 For example, fibrillin-1 content is sig-nificantly lower and matrix metalloproteinase activity is |
Surgery_Schwartz_5751 | Surgery_Schwartz | a congeni-tal connective tissue abnormality that predisposes the aorta to medial degeneration.25-31 For example, fibrillin-1 content is sig-nificantly lower and matrix metalloproteinase activity is signifi-cantly higher in the aortic media in patients with bicuspid aortic valve than in persons with a normal, tricuspid aortic valve.25-27 Further, the process of medial degeneration in patients with bicuspid aortic valve may be exacerbated by the presence of chronic turbulent flow through the deformed valve.Bovine Aortic Arch Bovine aortic arch—a common origin of the innominate and left common carotid arteries—has been con-sidered a normal anatomic variant. Studies from Yale University have identified a higher prevalence of bovine aortic arch in patients with thoracic aortic disease; an association was found between this anomaly and a generalized increase in aortic aneu-rysmal disease (without any predisposition to a particular aortic region). However, bovine aortic arch was not | Surgery_Schwartz. a congeni-tal connective tissue abnormality that predisposes the aorta to medial degeneration.25-31 For example, fibrillin-1 content is sig-nificantly lower and matrix metalloproteinase activity is signifi-cantly higher in the aortic media in patients with bicuspid aortic valve than in persons with a normal, tricuspid aortic valve.25-27 Further, the process of medial degeneration in patients with bicuspid aortic valve may be exacerbated by the presence of chronic turbulent flow through the deformed valve.Bovine Aortic Arch Bovine aortic arch—a common origin of the innominate and left common carotid arteries—has been con-sidered a normal anatomic variant. Studies from Yale University have identified a higher prevalence of bovine aortic arch in patients with thoracic aortic disease; an association was found between this anomaly and a generalized increase in aortic aneu-rysmal disease (without any predisposition to a particular aortic region). However, bovine aortic arch was not |
Surgery_Schwartz_5752 | Surgery_Schwartz | an association was found between this anomaly and a generalized increase in aortic aneu-rysmal disease (without any predisposition to a particular aortic region). However, bovine aortic arch was not associated dis-tinctly with bicuspid aortic valve or aortic dissection, but with a higher mean aortic growth rate: 0.29 cm per year in patients with bovine aortic arch, compared with 0.09 cm per year in controls. Therefore, bovine aortic arch may be better character-ized as a precursor of aortic aneurysm than as a simple normal anatomic variant.32 Further studies are needed to delineate the underlying mechanism for this association.Infection. Primary infection of the aortic wall resulting in aneurysm formation is rare. Although these lesions are termed mycotic aneurysms, the responsible pathogens usually are bac-teria rather than fungi. Bacterial invasion of the aortic wall may result from bacterial endocarditis, endothelial trauma caused by an aortic jet lesion, or extension from an | Surgery_Schwartz. an association was found between this anomaly and a generalized increase in aortic aneu-rysmal disease (without any predisposition to a particular aortic region). However, bovine aortic arch was not associated dis-tinctly with bicuspid aortic valve or aortic dissection, but with a higher mean aortic growth rate: 0.29 cm per year in patients with bovine aortic arch, compared with 0.09 cm per year in controls. Therefore, bovine aortic arch may be better character-ized as a precursor of aortic aneurysm than as a simple normal anatomic variant.32 Further studies are needed to delineate the underlying mechanism for this association.Infection. Primary infection of the aortic wall resulting in aneurysm formation is rare. Although these lesions are termed mycotic aneurysms, the responsible pathogens usually are bac-teria rather than fungi. Bacterial invasion of the aortic wall may result from bacterial endocarditis, endothelial trauma caused by an aortic jet lesion, or extension from an |
Surgery_Schwartz_5753 | Surgery_Schwartz | usually are bac-teria rather than fungi. Bacterial invasion of the aortic wall may result from bacterial endocarditis, endothelial trauma caused by an aortic jet lesion, or extension from an infected laminar clot within a preexisting aneurysm. The most common causative organisms are Staphylococcus aureus, Staphylococcus epider-midis, Salmonella, and Streptococcus.33,34 Unlike most other causes of thoracic aortic aneurysms, which generally produce fusiform aneurysms, infection often produces saccular aneu-rysms located in areas of aortic tissue destroyed by the infec-tious process.Although syphilis was once the most common cause of ascending aortic aneurysms, the advent of effective antibiotic therapy has made syphilitic aneurysms a rarity in developed nations. In other parts of the world, however, syphilitic aneu-rysms remain a major cause of morbidity and mortality. The spi-rochete Treponema pallidum causes an obliterative endarteritis of the vasa vasorum that results in medial | Surgery_Schwartz. usually are bac-teria rather than fungi. Bacterial invasion of the aortic wall may result from bacterial endocarditis, endothelial trauma caused by an aortic jet lesion, or extension from an infected laminar clot within a preexisting aneurysm. The most common causative organisms are Staphylococcus aureus, Staphylococcus epider-midis, Salmonella, and Streptococcus.33,34 Unlike most other causes of thoracic aortic aneurysms, which generally produce fusiform aneurysms, infection often produces saccular aneu-rysms located in areas of aortic tissue destroyed by the infec-tious process.Although syphilis was once the most common cause of ascending aortic aneurysms, the advent of effective antibiotic therapy has made syphilitic aneurysms a rarity in developed nations. In other parts of the world, however, syphilitic aneu-rysms remain a major cause of morbidity and mortality. The spi-rochete Treponema pallidum causes an obliterative endarteritis of the vasa vasorum that results in medial |
Surgery_Schwartz_5754 | Surgery_Schwartz | however, syphilitic aneu-rysms remain a major cause of morbidity and mortality. The spi-rochete Treponema pallidum causes an obliterative endarteritis of the vasa vasorum that results in medial ischemia and loss of the elastic and muscular elements of the aortic wall. The ascend-ing aorta and arch are the most commonly involved areas. The emergence of HIV infection in the 1980s was associated with a substantial increase in the incidence of syphilis in both HIV-positive and HIV-negative patients. Because syphilitic aortitis often presents 10 to 30 years after the primary infection, the inci-dence of associated aneurysms may increase in the near future.Aortitis. In patients with preexisting degenerative thoracic aortic aneurysms, localized transmural inflammation and subse-quent fibrosis can develop. The dense aortic infiltrate responsible for the fibrosis consists of lymphocytes, plasma cells, and giant cells. The cause of the intense inflammatory reaction is unknown. Although the | Surgery_Schwartz. however, syphilitic aneu-rysms remain a major cause of morbidity and mortality. The spi-rochete Treponema pallidum causes an obliterative endarteritis of the vasa vasorum that results in medial ischemia and loss of the elastic and muscular elements of the aortic wall. The ascend-ing aorta and arch are the most commonly involved areas. The emergence of HIV infection in the 1980s was associated with a substantial increase in the incidence of syphilis in both HIV-positive and HIV-negative patients. Because syphilitic aortitis often presents 10 to 30 years after the primary infection, the inci-dence of associated aneurysms may increase in the near future.Aortitis. In patients with preexisting degenerative thoracic aortic aneurysms, localized transmural inflammation and subse-quent fibrosis can develop. The dense aortic infiltrate responsible for the fibrosis consists of lymphocytes, plasma cells, and giant cells. The cause of the intense inflammatory reaction is unknown. Although the |
Surgery_Schwartz_5755 | Surgery_Schwartz | can develop. The dense aortic infiltrate responsible for the fibrosis consists of lymphocytes, plasma cells, and giant cells. The cause of the intense inflammatory reaction is unknown. Although the severe inflammation is a superimposed problem rather than a primary cause, its onset within an aneurysm can further weaken the aortic wall and precipitate expansion.Systemic autoimmune disorders also cause thoracic aor-titis. Aortic Takayasu arteritis generally produces obstructive lesions related to severe intimal thickening, but associated medial necrosis can lead to aneurysm formation. In patients with giant cell arteritis (temporal arteritis), granulomatous inflam-mation may develop that involves the entire thickness of the aortic wall, causing intimal thickening and medial destruction. Rheumatoid aortitis is an uncommon systemic disease that is associated with rheumatoid arthritis and ankylosing spondylitis. The resulting medial inflammation and fibrosis can affect the aortic root, | Surgery_Schwartz. can develop. The dense aortic infiltrate responsible for the fibrosis consists of lymphocytes, plasma cells, and giant cells. The cause of the intense inflammatory reaction is unknown. Although the severe inflammation is a superimposed problem rather than a primary cause, its onset within an aneurysm can further weaken the aortic wall and precipitate expansion.Systemic autoimmune disorders also cause thoracic aor-titis. Aortic Takayasu arteritis generally produces obstructive lesions related to severe intimal thickening, but associated medial necrosis can lead to aneurysm formation. In patients with giant cell arteritis (temporal arteritis), granulomatous inflam-mation may develop that involves the entire thickness of the aortic wall, causing intimal thickening and medial destruction. Rheumatoid aortitis is an uncommon systemic disease that is associated with rheumatoid arthritis and ankylosing spondylitis. The resulting medial inflammation and fibrosis can affect the aortic root, |
Surgery_Schwartz_5756 | Surgery_Schwartz | Rheumatoid aortitis is an uncommon systemic disease that is associated with rheumatoid arthritis and ankylosing spondylitis. The resulting medial inflammation and fibrosis can affect the aortic root, causing annular dilatation, aortic valve regurgitation, and ascending aortic aneurysm formation.Pseudoaneurysms. Pseudoaneurysms of the thoracic aorta usually represent chronic leaks that are contained by surrounding Brunicardi_Ch22_p0853-p0896.indd 85601/03/19 5:40 PM 857THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22tissue and fibrosis. By definition, the wall of a pseudoaneurysm is not formed by intact aortic tissue; rather, the wall devel-ops from organized thrombus and associated fibrosis. Pseu-doaneurysms can arise from primary defects in the aortic wall (e.g., after trauma or contained aneurysm rupture) or from anas-tomotic or cannulation site leaks that occur after cardiovascular surgery. Anastomotic pseudoaneurysms can be caused by tech-nical problems or by deterioration | Surgery_Schwartz. Rheumatoid aortitis is an uncommon systemic disease that is associated with rheumatoid arthritis and ankylosing spondylitis. The resulting medial inflammation and fibrosis can affect the aortic root, causing annular dilatation, aortic valve regurgitation, and ascending aortic aneurysm formation.Pseudoaneurysms. Pseudoaneurysms of the thoracic aorta usually represent chronic leaks that are contained by surrounding Brunicardi_Ch22_p0853-p0896.indd 85601/03/19 5:40 PM 857THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22tissue and fibrosis. By definition, the wall of a pseudoaneurysm is not formed by intact aortic tissue; rather, the wall devel-ops from organized thrombus and associated fibrosis. Pseu-doaneurysms can arise from primary defects in the aortic wall (e.g., after trauma or contained aneurysm rupture) or from anas-tomotic or cannulation site leaks that occur after cardiovascular surgery. Anastomotic pseudoaneurysms can be caused by tech-nical problems or by deterioration |
Surgery_Schwartz_5757 | Surgery_Schwartz | aneurysm rupture) or from anas-tomotic or cannulation site leaks that occur after cardiovascular surgery. Anastomotic pseudoaneurysms can be caused by tech-nical problems or by deterioration of the native aortic tissue, graft material, or suture. Commonly, they occur in patients with Marfan syndrome, Loeys-Dietz syndrome, or other heritable conditions that markedly weaken the vessel wall.35 Tissue dete-rioration usually is related to either progressive degenerative disease or infection. Improvements in sutures, graft materials, and surgical techniques have decreased the incidence of tho-racic aortic pseudoaneurysm. Should thoracic aortic pseudoan-eurysms occur, they typically require expeditious open surgical or catheter-based repair because they are associated with a high incidence of morbidity and rupture.Clinical HistoryTreatment decisions in cases of thoracic aortic aneurysm are guided by our current understanding of the clinical history of these aneurysms, which classically is | Surgery_Schwartz. aneurysm rupture) or from anas-tomotic or cannulation site leaks that occur after cardiovascular surgery. Anastomotic pseudoaneurysms can be caused by tech-nical problems or by deterioration of the native aortic tissue, graft material, or suture. Commonly, they occur in patients with Marfan syndrome, Loeys-Dietz syndrome, or other heritable conditions that markedly weaken the vessel wall.35 Tissue dete-rioration usually is related to either progressive degenerative disease or infection. Improvements in sutures, graft materials, and surgical techniques have decreased the incidence of tho-racic aortic pseudoaneurysm. Should thoracic aortic pseudoan-eurysms occur, they typically require expeditious open surgical or catheter-based repair because they are associated with a high incidence of morbidity and rupture.Clinical HistoryTreatment decisions in cases of thoracic aortic aneurysm are guided by our current understanding of the clinical history of these aneurysms, which classically is |
Surgery_Schwartz_5758 | Surgery_Schwartz | morbidity and rupture.Clinical HistoryTreatment decisions in cases of thoracic aortic aneurysm are guided by our current understanding of the clinical history of these aneurysms, which classically is characterized as progres-sive aortic dilatation and eventual dissection, rupture, or both. An analysis by Elefteriades of data from 1600 patients with thoracic aortic disease has helped quantify these well-recognized risks.36 Average expansion rates were 0.07 cm per year in ascending aortic aneurysms and 0.19 cm per year in descending thoracic aortic aneurysms. As expected, aortic diam-eter was a strong predictor of rupture, dissection, and mortality. For thoracic aortic aneurysms >6 cm in diameter, annual rates of catastrophic complications were 3.6% for rupture, 3.7% for dissection, and 10.8% for death. Critical “hinge-point” diame-ters, at which the incidence of expected complications signifi-cantly increased, were 6.0 cm for aneurysms of the ascending aorta and 7.0 cm for aneurysms of | Surgery_Schwartz. morbidity and rupture.Clinical HistoryTreatment decisions in cases of thoracic aortic aneurysm are guided by our current understanding of the clinical history of these aneurysms, which classically is characterized as progres-sive aortic dilatation and eventual dissection, rupture, or both. An analysis by Elefteriades of data from 1600 patients with thoracic aortic disease has helped quantify these well-recognized risks.36 Average expansion rates were 0.07 cm per year in ascending aortic aneurysms and 0.19 cm per year in descending thoracic aortic aneurysms. As expected, aortic diam-eter was a strong predictor of rupture, dissection, and mortality. For thoracic aortic aneurysms >6 cm in diameter, annual rates of catastrophic complications were 3.6% for rupture, 3.7% for dissection, and 10.8% for death. Critical “hinge-point” diame-ters, at which the incidence of expected complications signifi-cantly increased, were 6.0 cm for aneurysms of the ascending aorta and 7.0 cm for aneurysms of |
Surgery_Schwartz_5759 | Surgery_Schwartz | for death. Critical “hinge-point” diame-ters, at which the incidence of expected complications signifi-cantly increased, were 6.0 cm for aneurysms of the ascending aorta and 7.0 cm for aneurysms of the descending thoracic aorta; the corresponding risks of rupture after reaching these diameters were 31% and 43%, respectively.37Certain types of aneurysms have an elevated propensity for expansion and rupture. For example, aneurysms in patients with Marfan or Loeys-Dietz syndrome tend to dilate at an accelerated rate and rupture or dissect at smaller diameters than sporadic, nonheritable aneurysms. Before the era of surgical treatment for aortic aneurysms, the aggressive form of aortic disease in Marfan patients resulted in an average life expectancy of 32 years, with aortic root complications causing the majority of deaths.38 Saccular aneurysms, which commonly are associated with aortic infection and typically affect only a discrete small section of the aorta, tend to grow more rapidly | Surgery_Schwartz. for death. Critical “hinge-point” diame-ters, at which the incidence of expected complications signifi-cantly increased, were 6.0 cm for aneurysms of the ascending aorta and 7.0 cm for aneurysms of the descending thoracic aorta; the corresponding risks of rupture after reaching these diameters were 31% and 43%, respectively.37Certain types of aneurysms have an elevated propensity for expansion and rupture. For example, aneurysms in patients with Marfan or Loeys-Dietz syndrome tend to dilate at an accelerated rate and rupture or dissect at smaller diameters than sporadic, nonheritable aneurysms. Before the era of surgical treatment for aortic aneurysms, the aggressive form of aortic disease in Marfan patients resulted in an average life expectancy of 32 years, with aortic root complications causing the majority of deaths.38 Saccular aneurysms, which commonly are associated with aortic infection and typically affect only a discrete small section of the aorta, tend to grow more rapidly |
Surgery_Schwartz_5760 | Surgery_Schwartz | causing the majority of deaths.38 Saccular aneurysms, which commonly are associated with aortic infection and typically affect only a discrete small section of the aorta, tend to grow more rapidly than fusiform aneurysms, which are associated with more widespread degen-erative changes and generally affect a larger section of the aorta.One common clinical scenario deserves special attention. A moderately dilated ascending aorta (i.e., 4 to 5 cm) often is encountered during aortic valve replacement or coronary artery bypass operations. The clinical history of these ectatic ascend-ing aortas has been defined by several studies. Michel and colleagues39 studied patients whose ascending aortic diameters were >4 cm at the time of aortic valve replacement; 25% of these patients required reoperation for ascending aortic replacement. Prenger and colleagues40 reported that aortic dissection occurred in 27% of patients who had aortic diameters of >5 cm at the time of aortic valve replacement. | Surgery_Schwartz. causing the majority of deaths.38 Saccular aneurysms, which commonly are associated with aortic infection and typically affect only a discrete small section of the aorta, tend to grow more rapidly than fusiform aneurysms, which are associated with more widespread degen-erative changes and generally affect a larger section of the aorta.One common clinical scenario deserves special attention. A moderately dilated ascending aorta (i.e., 4 to 5 cm) often is encountered during aortic valve replacement or coronary artery bypass operations. The clinical history of these ectatic ascend-ing aortas has been defined by several studies. Michel and colleagues39 studied patients whose ascending aortic diameters were >4 cm at the time of aortic valve replacement; 25% of these patients required reoperation for ascending aortic replacement. Prenger and colleagues40 reported that aortic dissection occurred in 27% of patients who had aortic diameters of >5 cm at the time of aortic valve replacement. |
Surgery_Schwartz_5761 | Surgery_Schwartz | for ascending aortic replacement. Prenger and colleagues40 reported that aortic dissection occurred in 27% of patients who had aortic diameters of >5 cm at the time of aortic valve replacement. Attention has been directed toward whether or not a mildly dilated aortic root should be replaced in patients with bicuspid aortic valve who are undergoing iso-lated valve replacement, and at what threshold to intervene. Although this is a controversial issue, many surgeons believe that the tendency toward late aortic dilatation in these patients war-rants aggressive treatment.41,42 According to a recent guidelines clarification,43 in patients with bicuspid aortic valve who are undergoing aortic valve replacement or repair, replacing the ascending aorta is reasonable when the diameter of the ascending aorta is greater than 4.5 cm (Class IIa, Level C recommendation).Clinical ManifestationsIn many patients with thoracic aortic aneurysms, the aneurysm is discovered incidentally when imaging | Surgery_Schwartz. for ascending aortic replacement. Prenger and colleagues40 reported that aortic dissection occurred in 27% of patients who had aortic diameters of >5 cm at the time of aortic valve replacement. Attention has been directed toward whether or not a mildly dilated aortic root should be replaced in patients with bicuspid aortic valve who are undergoing iso-lated valve replacement, and at what threshold to intervene. Although this is a controversial issue, many surgeons believe that the tendency toward late aortic dilatation in these patients war-rants aggressive treatment.41,42 According to a recent guidelines clarification,43 in patients with bicuspid aortic valve who are undergoing aortic valve replacement or repair, replacing the ascending aorta is reasonable when the diameter of the ascending aorta is greater than 4.5 cm (Class IIa, Level C recommendation).Clinical ManifestationsIn many patients with thoracic aortic aneurysms, the aneurysm is discovered incidentally when imaging |
Surgery_Schwartz_5762 | Surgery_Schwartz | ascending aorta is greater than 4.5 cm (Class IIa, Level C recommendation).Clinical ManifestationsIn many patients with thoracic aortic aneurysms, the aneurysm is discovered incidentally when imaging studies are performed for unrelated reasons. Therefore, patients often are asymptom-atic at the time of diagnosis. However, thoracic aortic aneurysms that initially go undetected eventually create symptoms and signs that correspond with the segment of aorta that is involved. These aneurysms have a wide variety of manifestations, includ-ing compression or erosion of adjacent structures, aortic valve regurgitation, distal embolism, and rupture.Local Compression and Erosion. Initially, aneurysmal expan-sion and impingement on adjacent structures causes mild, chronic pain. The most common symptom in patients with ascending aor-tic aneurysms is anterior chest discomfort; the pain is frequently precordial in location but may radiate to the neck and jaw, mim-icking angina. Aneurysms of the | Surgery_Schwartz. ascending aorta is greater than 4.5 cm (Class IIa, Level C recommendation).Clinical ManifestationsIn many patients with thoracic aortic aneurysms, the aneurysm is discovered incidentally when imaging studies are performed for unrelated reasons. Therefore, patients often are asymptom-atic at the time of diagnosis. However, thoracic aortic aneurysms that initially go undetected eventually create symptoms and signs that correspond with the segment of aorta that is involved. These aneurysms have a wide variety of manifestations, includ-ing compression or erosion of adjacent structures, aortic valve regurgitation, distal embolism, and rupture.Local Compression and Erosion. Initially, aneurysmal expan-sion and impingement on adjacent structures causes mild, chronic pain. The most common symptom in patients with ascending aor-tic aneurysms is anterior chest discomfort; the pain is frequently precordial in location but may radiate to the neck and jaw, mim-icking angina. Aneurysms of the |
Surgery_Schwartz_5763 | Surgery_Schwartz | in patients with ascending aor-tic aneurysms is anterior chest discomfort; the pain is frequently precordial in location but may radiate to the neck and jaw, mim-icking angina. Aneurysms of the ascending aorta and transverse aortic arch can cause symptoms related to compression of the superior vena cava, the pulmonary artery, the airway, or the ster-num. Rarely, these aneurysms erode into the superior vena cava or right atrium, causing acute high-output failure. Expansion of the distal aortic arch can stretch the recurrent laryngeal nerve, which results in left vocal cord paralysis and hoarseness. Descending thoracic and thoracoabdominal aneurysms frequently cause back pain localized between the scapulae. When the aneurysm is larg-est in the region of the aortic hiatus, it may cause middle back and epigastric pain. Thoracic or lumbar vertebral body erosion typically causes severe, chronic back pain; extreme cases can present with spinal instability and neurologic deficits from spinal | Surgery_Schwartz. in patients with ascending aor-tic aneurysms is anterior chest discomfort; the pain is frequently precordial in location but may radiate to the neck and jaw, mim-icking angina. Aneurysms of the ascending aorta and transverse aortic arch can cause symptoms related to compression of the superior vena cava, the pulmonary artery, the airway, or the ster-num. Rarely, these aneurysms erode into the superior vena cava or right atrium, causing acute high-output failure. Expansion of the distal aortic arch can stretch the recurrent laryngeal nerve, which results in left vocal cord paralysis and hoarseness. Descending thoracic and thoracoabdominal aneurysms frequently cause back pain localized between the scapulae. When the aneurysm is larg-est in the region of the aortic hiatus, it may cause middle back and epigastric pain. Thoracic or lumbar vertebral body erosion typically causes severe, chronic back pain; extreme cases can present with spinal instability and neurologic deficits from spinal |
Surgery_Schwartz_5764 | Surgery_Schwartz | back and epigastric pain. Thoracic or lumbar vertebral body erosion typically causes severe, chronic back pain; extreme cases can present with spinal instability and neurologic deficits from spinal cord compression. Although mycotic aneurysms have a peculiar propensity to destroy vertebral bodies, spinal erosion also occurs with degenerative aneurysms. Descending thoracic aortic aneu-rysms may cause varying degrees of airway obstruction, mani-festing as cough, wheezing, stridor, or pneumonitis. Pulmonary or airway erosion presents as hemoptysis. Compression and ero-sion of the esophagus cause dysphagia and hematemesis, respec-tively. Thoracoabdominal aortic aneurysms can cause duodenal obstruction or, if they erode through the bowel wall, gastrointes-tinal bleeding. Jaundice due to compression of the liver or porta hepatis is uncommon. Erosion into the inferior vena cava or iliac vein presents with an abdominal bruit, widened pulse pressure, edema, and heart failure.Aortic Valve | Surgery_Schwartz. back and epigastric pain. Thoracic or lumbar vertebral body erosion typically causes severe, chronic back pain; extreme cases can present with spinal instability and neurologic deficits from spinal cord compression. Although mycotic aneurysms have a peculiar propensity to destroy vertebral bodies, spinal erosion also occurs with degenerative aneurysms. Descending thoracic aortic aneu-rysms may cause varying degrees of airway obstruction, mani-festing as cough, wheezing, stridor, or pneumonitis. Pulmonary or airway erosion presents as hemoptysis. Compression and ero-sion of the esophagus cause dysphagia and hematemesis, respec-tively. Thoracoabdominal aortic aneurysms can cause duodenal obstruction or, if they erode through the bowel wall, gastrointes-tinal bleeding. Jaundice due to compression of the liver or porta hepatis is uncommon. Erosion into the inferior vena cava or iliac vein presents with an abdominal bruit, widened pulse pressure, edema, and heart failure.Aortic Valve |
Surgery_Schwartz_5765 | Surgery_Schwartz | of the liver or porta hepatis is uncommon. Erosion into the inferior vena cava or iliac vein presents with an abdominal bruit, widened pulse pressure, edema, and heart failure.Aortic Valve Regurgitation. Ascending aortic aneurysms can cause displacement of the aortic valve commissures and annular dilatation. The resulting deformation of the aortic valve leads to progressively worsening aortic valve regurgitation. In response to the volume overload, the heart remodels and becomes increasingly dilated. Patients with this condition may present with progressive heart failure, a widened pulse pressure, and a diastolic murmur.Distal Embolization. Thoracic aortic aneurysms—particularly those involving the descending and thoracoabdominal aorta—are commonly lined with friable, atheromatous plaque and 1Brunicardi_Ch22_p0853-p0896.indd 85701/03/19 5:40 PM 858SPECIFIC CONSIDERATIONSPART IIFigure 22-2. Chest radiographs showing a calcified rim (arrows) in the aortic wall of a thoracoabdominal | Surgery_Schwartz. of the liver or porta hepatis is uncommon. Erosion into the inferior vena cava or iliac vein presents with an abdominal bruit, widened pulse pressure, edema, and heart failure.Aortic Valve Regurgitation. Ascending aortic aneurysms can cause displacement of the aortic valve commissures and annular dilatation. The resulting deformation of the aortic valve leads to progressively worsening aortic valve regurgitation. In response to the volume overload, the heart remodels and becomes increasingly dilated. Patients with this condition may present with progressive heart failure, a widened pulse pressure, and a diastolic murmur.Distal Embolization. Thoracic aortic aneurysms—particularly those involving the descending and thoracoabdominal aorta—are commonly lined with friable, atheromatous plaque and 1Brunicardi_Ch22_p0853-p0896.indd 85701/03/19 5:40 PM 858SPECIFIC CONSIDERATIONSPART IIFigure 22-2. Chest radiographs showing a calcified rim (arrows) in the aortic wall of a thoracoabdominal |
Surgery_Schwartz_5766 | Surgery_Schwartz | and 1Brunicardi_Ch22_p0853-p0896.indd 85701/03/19 5:40 PM 858SPECIFIC CONSIDERATIONSPART IIFigure 22-2. Chest radiographs showing a calcified rim (arrows) in the aortic wall of a thoracoabdominal aortic aneurysm. A. Anteroposterior view. B. Lateral view.mural thrombus. This debris may embolize distally, caus-ing occlusion and thrombosis of the visceral, renal, or lower-extremity branches.Rupture. Patients with ruptured thoracic aortic aneurysms often experience sudden, severe pain in the anterior chest (ascending aorta), upper back or left chest (descending thoracic aorta), or left flank or abdomen (thoracoabdominal aorta). When ascending aortic aneurysms rupture, they usually bleed into the pericardial space, producing acute cardiac tamponade and death. Descending thoracic aortic aneurysms rupture into the pleural cavity, producing a combination of severe hemorrhagic shock and respiratory compromise. External rupture is extremely rare; saccular syphilitic aneurysms have been | Surgery_Schwartz. and 1Brunicardi_Ch22_p0853-p0896.indd 85701/03/19 5:40 PM 858SPECIFIC CONSIDERATIONSPART IIFigure 22-2. Chest radiographs showing a calcified rim (arrows) in the aortic wall of a thoracoabdominal aortic aneurysm. A. Anteroposterior view. B. Lateral view.mural thrombus. This debris may embolize distally, caus-ing occlusion and thrombosis of the visceral, renal, or lower-extremity branches.Rupture. Patients with ruptured thoracic aortic aneurysms often experience sudden, severe pain in the anterior chest (ascending aorta), upper back or left chest (descending thoracic aorta), or left flank or abdomen (thoracoabdominal aorta). When ascending aortic aneurysms rupture, they usually bleed into the pericardial space, producing acute cardiac tamponade and death. Descending thoracic aortic aneurysms rupture into the pleural cavity, producing a combination of severe hemorrhagic shock and respiratory compromise. External rupture is extremely rare; saccular syphilitic aneurysms have been |
Surgery_Schwartz_5767 | Surgery_Schwartz | aneurysms rupture into the pleural cavity, producing a combination of severe hemorrhagic shock and respiratory compromise. External rupture is extremely rare; saccular syphilitic aneurysms have been observed to rupture externally after eroding through the sternum.Diagnostic EvaluationDiagnosis and characterization of thoracic aneurysms require imaging studies, which also provide critical information that guides the selection of treatment options. Although the best choice of imaging technique for the thoracic and thoracoab-dominal aorta is somewhat institution-specific, varying with the availability of imaging equipment and expertise, efforts have been made to standardize key elements of image acquisition and reporting. Recent practice guidelines44 recommend that aortic imaging reports plainly state the location of aortic abnormalities (including calcification and the extent to which abnormalities extend into branch vessels), the maximum external aortic diam-eters (rather than | Surgery_Schwartz. aneurysms rupture into the pleural cavity, producing a combination of severe hemorrhagic shock and respiratory compromise. External rupture is extremely rare; saccular syphilitic aneurysms have been observed to rupture externally after eroding through the sternum.Diagnostic EvaluationDiagnosis and characterization of thoracic aneurysms require imaging studies, which also provide critical information that guides the selection of treatment options. Although the best choice of imaging technique for the thoracic and thoracoab-dominal aorta is somewhat institution-specific, varying with the availability of imaging equipment and expertise, efforts have been made to standardize key elements of image acquisition and reporting. Recent practice guidelines44 recommend that aortic imaging reports plainly state the location of aortic abnormalities (including calcification and the extent to which abnormalities extend into branch vessels), the maximum external aortic diam-eters (rather than |
Surgery_Schwartz_5768 | Surgery_Schwartz | plainly state the location of aortic abnormalities (including calcification and the extent to which abnormalities extend into branch vessels), the maximum external aortic diam-eters (rather than internal, lumen-based diameters), internal fill-ing defects, and any evidence of rupture. Whenever possible, all results should be compared with those of prior imaging studies.Plain Radiography. Plain radiographs of the chest, abdomen, or spine often provide enough information to support the initial diag-nosis of thoracic aortic aneurysm. Ascending aortic aneurysms produce a convex shadow to the right of the cardiac silhouette. The anterior projection of an ascending aneurysm results in the loss of the retrosternal space in the lateral view. An aneurysm may be indistinguishable from elongation and tortuosity.45 Impor-tantly, chest radiographs (CXRs) may appear normal in patients with thoracic aortic disease and thus cannot exclude the diagnosis of aortic aneurysm. Aortic root aneurysms, for | Surgery_Schwartz. plainly state the location of aortic abnormalities (including calcification and the extent to which abnormalities extend into branch vessels), the maximum external aortic diam-eters (rather than internal, lumen-based diameters), internal fill-ing defects, and any evidence of rupture. Whenever possible, all results should be compared with those of prior imaging studies.Plain Radiography. Plain radiographs of the chest, abdomen, or spine often provide enough information to support the initial diag-nosis of thoracic aortic aneurysm. Ascending aortic aneurysms produce a convex shadow to the right of the cardiac silhouette. The anterior projection of an ascending aneurysm results in the loss of the retrosternal space in the lateral view. An aneurysm may be indistinguishable from elongation and tortuosity.45 Impor-tantly, chest radiographs (CXRs) may appear normal in patients with thoracic aortic disease and thus cannot exclude the diagnosis of aortic aneurysm. Aortic root aneurysms, for |
Surgery_Schwartz_5769 | Surgery_Schwartz | tortuosity.45 Impor-tantly, chest radiographs (CXRs) may appear normal in patients with thoracic aortic disease and thus cannot exclude the diagnosis of aortic aneurysm. Aortic root aneurysms, for example, often are hidden within the cardiac silhouette. Plain CXRs may reveal convexity in the right superior mediastinum, loss of the retroster-nal space, or widening of the descending thoracic aortic shadow, which may be highlighted by a rim of calcification outlining the dilated aneurysmal aortic wall. Aortic calcification also may be seen in the upper abdomen on a standard radiograph made in the anteroposterior or lateral projection (Fig. 22-2). Once a thoracic aortic aneurysm is detected on plain radiographs, additional stud-ies are required to define the extent of aortic involvement.Echocardiography and Abdominal Ultrasonography. Ascending aortic aneurysms are commonly discovered during echocardiography in patients presenting with symptoms or signs of aortic valve regurgitation. Both | Surgery_Schwartz. tortuosity.45 Impor-tantly, chest radiographs (CXRs) may appear normal in patients with thoracic aortic disease and thus cannot exclude the diagnosis of aortic aneurysm. Aortic root aneurysms, for example, often are hidden within the cardiac silhouette. Plain CXRs may reveal convexity in the right superior mediastinum, loss of the retroster-nal space, or widening of the descending thoracic aortic shadow, which may be highlighted by a rim of calcification outlining the dilated aneurysmal aortic wall. Aortic calcification also may be seen in the upper abdomen on a standard radiograph made in the anteroposterior or lateral projection (Fig. 22-2). Once a thoracic aortic aneurysm is detected on plain radiographs, additional stud-ies are required to define the extent of aortic involvement.Echocardiography and Abdominal Ultrasonography. Ascending aortic aneurysms are commonly discovered during echocardiography in patients presenting with symptoms or signs of aortic valve regurgitation. Both |
Surgery_Schwartz_5770 | Surgery_Schwartz | and Abdominal Ultrasonography. Ascending aortic aneurysms are commonly discovered during echocardiography in patients presenting with symptoms or signs of aortic valve regurgitation. Both transthoracic and transesophageal echocardiography provide excellent visualization of the ascending aorta, including the aortic root.46 Transesophageal echocardiography also allows visualization of the descending thoracic aorta but is not ideal for evaluating the transverse aortic arch (which is obscured by air in the tracheobronchial tree) or the upper abdominal aorta. Effective echocardiography requires considerable technical skill, both in obtaining adequate images and in interpreting them. This imaging modality has the added Brunicardi_Ch22_p0853-p0896.indd 85801/03/19 5:40 PM 859THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22Figure 22-3. Current practice guidelines44 seek to standardize the reporting of aortic diameters by indicating key locations of mea-surement. These include (1) the | Surgery_Schwartz. and Abdominal Ultrasonography. Ascending aortic aneurysms are commonly discovered during echocardiography in patients presenting with symptoms or signs of aortic valve regurgitation. Both transthoracic and transesophageal echocardiography provide excellent visualization of the ascending aorta, including the aortic root.46 Transesophageal echocardiography also allows visualization of the descending thoracic aorta but is not ideal for evaluating the transverse aortic arch (which is obscured by air in the tracheobronchial tree) or the upper abdominal aorta. Effective echocardiography requires considerable technical skill, both in obtaining adequate images and in interpreting them. This imaging modality has the added Brunicardi_Ch22_p0853-p0896.indd 85801/03/19 5:40 PM 859THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22Figure 22-3. Current practice guidelines44 seek to standardize the reporting of aortic diameters by indicating key locations of mea-surement. These include (1) the |
Surgery_Schwartz_5771 | Surgery_Schwartz | AND AORTIC DISSECTIONCHAPTER 22Figure 22-3. Current practice guidelines44 seek to standardize the reporting of aortic diameters by indicating key locations of mea-surement. These include (1) the sinuses of Valsalva, (2) the sinotu-bular junction, (3) the mid-ascending aorta, (4) the proximal aortic arch at the origins of the innominate artery, (5) the mid-aortic arch, which is between the left common carotid and left subclavian arter-ies, (6) the proximal descending thoracic aorta, which begins at the isthmus (approximately 2 cm distal to the origins of the left subcla-vian artery), (7) the mid-descending thoracic artery, (8) the aorta at the diaphragm, and (9) the abdominal aorta at the origins of the celiac axis. (Used with permission of Baylor College of Medicine.)benefit of assessing cardiac function and revealing any other abnormalities that may be present. During ultrasound evaluation of a suspected infrarenal abdominal aortic aneurysm, if a definitive neck cannot be identified | Surgery_Schwartz. AND AORTIC DISSECTIONCHAPTER 22Figure 22-3. Current practice guidelines44 seek to standardize the reporting of aortic diameters by indicating key locations of mea-surement. These include (1) the sinuses of Valsalva, (2) the sinotu-bular junction, (3) the mid-ascending aorta, (4) the proximal aortic arch at the origins of the innominate artery, (5) the mid-aortic arch, which is between the left common carotid and left subclavian arter-ies, (6) the proximal descending thoracic aorta, which begins at the isthmus (approximately 2 cm distal to the origins of the left subcla-vian artery), (7) the mid-descending thoracic artery, (8) the aorta at the diaphragm, and (9) the abdominal aorta at the origins of the celiac axis. (Used with permission of Baylor College of Medicine.)benefit of assessing cardiac function and revealing any other abnormalities that may be present. During ultrasound evaluation of a suspected infrarenal abdominal aortic aneurysm, if a definitive neck cannot be identified |
Surgery_Schwartz_5772 | Surgery_Schwartz | cardiac function and revealing any other abnormalities that may be present. During ultrasound evaluation of a suspected infrarenal abdominal aortic aneurysm, if a definitive neck cannot be identified at the level of the renal arteries, the possibility of thoracoabdominal aortic involvement should be suspected and investigated by using other imaging modalities. Caution should be exercised while interpreting aneurysm dimensions from ultrasound imaging because intraluminal measurements are often reported, whereas external measurements are usually used in other imaging modalities.Computed Tomography. Computed tomographic (CT) scan-ning is widely available, provides visualization of the entire thoracic and abdominal aorta, and permits multiplanar and 3-dimensional aortic reconstructions. Consequently, CT is the most common—and arguably the most useful—imaging modal-ity for evaluating thoracic aortic aneurysms.47 In addition to establishing the diagnosis, CT provides information about an | Surgery_Schwartz. cardiac function and revealing any other abnormalities that may be present. During ultrasound evaluation of a suspected infrarenal abdominal aortic aneurysm, if a definitive neck cannot be identified at the level of the renal arteries, the possibility of thoracoabdominal aortic involvement should be suspected and investigated by using other imaging modalities. Caution should be exercised while interpreting aneurysm dimensions from ultrasound imaging because intraluminal measurements are often reported, whereas external measurements are usually used in other imaging modalities.Computed Tomography. Computed tomographic (CT) scan-ning is widely available, provides visualization of the entire thoracic and abdominal aorta, and permits multiplanar and 3-dimensional aortic reconstructions. Consequently, CT is the most common—and arguably the most useful—imaging modal-ity for evaluating thoracic aortic aneurysms.47 In addition to establishing the diagnosis, CT provides information about an |
Surgery_Schwartz_5773 | Surgery_Schwartz | CT is the most common—and arguably the most useful—imaging modal-ity for evaluating thoracic aortic aneurysms.47 In addition to establishing the diagnosis, CT provides information about an aneurysm’s location, extent, anatomic anomalies, and relation-ship to major branch vessels. CT is particularly useful in deter-mining the absolute diameter of the aorta, especially in the presence of laminated clot, and also detects aortic calcification. Contrast-enhanced CT provides information about the aortic lumen and can detect mural thrombus, aortic dissection, inflam-matory periaortic fibrosis, and mediastinal or retroperitoneal hematoma due to contained aortic rupture. To increase consis-tency and ensure uniform reporting, current practice guidelines suggest that measurements be taken perpendicular to blood flow and at standard anatomic locations44 (Fig. 22-3); this should reduce the likelihood of erroneous measurements, espe-cially during serial imaging surveillance .The major disadvantage | Surgery_Schwartz. CT is the most common—and arguably the most useful—imaging modal-ity for evaluating thoracic aortic aneurysms.47 In addition to establishing the diagnosis, CT provides information about an aneurysm’s location, extent, anatomic anomalies, and relation-ship to major branch vessels. CT is particularly useful in deter-mining the absolute diameter of the aorta, especially in the presence of laminated clot, and also detects aortic calcification. Contrast-enhanced CT provides information about the aortic lumen and can detect mural thrombus, aortic dissection, inflam-matory periaortic fibrosis, and mediastinal or retroperitoneal hematoma due to contained aortic rupture. To increase consis-tency and ensure uniform reporting, current practice guidelines suggest that measurements be taken perpendicular to blood flow and at standard anatomic locations44 (Fig. 22-3); this should reduce the likelihood of erroneous measurements, espe-cially during serial imaging surveillance .The major disadvantage |
Surgery_Schwartz_5774 | Surgery_Schwartz | to blood flow and at standard anatomic locations44 (Fig. 22-3); this should reduce the likelihood of erroneous measurements, espe-cially during serial imaging surveillance .The major disadvantage of contrast-enhanced CT scanning is the possibility of contrast-induced acute renal failure in patients who are at risk (e.g., patients with preexisting renal disease or diabetes) even though the risk is smaller than was assumed in the past.48,49 If possible, surgery is performed at least 1 day after contrast administration to allow time to observe renal function and to permit diuresis. If renal insufficiency occurs or is worsened, elective surgery is postponed until renal function returns to normal or stabilizes.Magnetic Resonance Angiography. Magnetic resonance angiography (MRA) is becoming widely available and can facilitate visualization of the entire aorta. This modality pro-duces aortic images comparable to those produced by contrast-enhanced CT but does not necessitate exposure to | Surgery_Schwartz. to blood flow and at standard anatomic locations44 (Fig. 22-3); this should reduce the likelihood of erroneous measurements, espe-cially during serial imaging surveillance .The major disadvantage of contrast-enhanced CT scanning is the possibility of contrast-induced acute renal failure in patients who are at risk (e.g., patients with preexisting renal disease or diabetes) even though the risk is smaller than was assumed in the past.48,49 If possible, surgery is performed at least 1 day after contrast administration to allow time to observe renal function and to permit diuresis. If renal insufficiency occurs or is worsened, elective surgery is postponed until renal function returns to normal or stabilizes.Magnetic Resonance Angiography. Magnetic resonance angiography (MRA) is becoming widely available and can facilitate visualization of the entire aorta. This modality pro-duces aortic images comparable to those produced by contrast-enhanced CT but does not necessitate exposure to |
Surgery_Schwartz_5775 | Surgery_Schwartz | widely available and can facilitate visualization of the entire aorta. This modality pro-duces aortic images comparable to those produced by contrast-enhanced CT but does not necessitate exposure to ionizing radiation.50 In addition, MRA offers excellent visualization of branch-vessel details, and it is useful in detecting branch-vessel stenosis.51 However, MRA is limited by high expense and a sus-ceptibility to artifacts created by ferromagnetic materials, and gadolinium—the contrast agent for MRA—may be linked to nephrogenic systemic fibrosis and acute renal failure in patients with advanced renal insufficiency.52 Furthermore, the MRA environment is not appropriate for many critically ill patients, and unlike CT imaging, MRA imaging is suboptimal in patients with extensive aortic calcification.Invasive Aortography and Cardiac Catheterization. Although catheter-based contrast aortography was previously considered the gold standard for evaluating thoracic aortic dis-ease, | Surgery_Schwartz. widely available and can facilitate visualization of the entire aorta. This modality pro-duces aortic images comparable to those produced by contrast-enhanced CT but does not necessitate exposure to ionizing radiation.50 In addition, MRA offers excellent visualization of branch-vessel details, and it is useful in detecting branch-vessel stenosis.51 However, MRA is limited by high expense and a sus-ceptibility to artifacts created by ferromagnetic materials, and gadolinium—the contrast agent for MRA—may be linked to nephrogenic systemic fibrosis and acute renal failure in patients with advanced renal insufficiency.52 Furthermore, the MRA environment is not appropriate for many critically ill patients, and unlike CT imaging, MRA imaging is suboptimal in patients with extensive aortic calcification.Invasive Aortography and Cardiac Catheterization. Although catheter-based contrast aortography was previously considered the gold standard for evaluating thoracic aortic dis-ease, |
Surgery_Schwartz_5776 | Surgery_Schwartz | calcification.Invasive Aortography and Cardiac Catheterization. Although catheter-based contrast aortography was previously considered the gold standard for evaluating thoracic aortic dis-ease, cross-sectional imaging (i.e., CT and MRA) has largely replaced this modality. Technologic improvements have enabled CT and MRA to provide excellent aortic imaging while causing less morbidity than catheter-based studies do, so CT and 2MRA are now the primary modes for evaluating thoracic aortic disease. Today, the use of invasive aortography in patients with thoracic aortic disease is generally limited to those undergoing endovascular therapies or when other types of studies are con-traindicated or have not provided satisfactory results.Unlike standard aortography, cardiac catheterization con-tinues to play an important role in diagnosis and preoperative planning, especially in patients with ascending aortic involve-ment. Proximal aortography can reveal not only the status of the coronary | Surgery_Schwartz. calcification.Invasive Aortography and Cardiac Catheterization. Although catheter-based contrast aortography was previously considered the gold standard for evaluating thoracic aortic dis-ease, cross-sectional imaging (i.e., CT and MRA) has largely replaced this modality. Technologic improvements have enabled CT and MRA to provide excellent aortic imaging while causing less morbidity than catheter-based studies do, so CT and 2MRA are now the primary modes for evaluating thoracic aortic disease. Today, the use of invasive aortography in patients with thoracic aortic disease is generally limited to those undergoing endovascular therapies or when other types of studies are con-traindicated or have not provided satisfactory results.Unlike standard aortography, cardiac catheterization con-tinues to play an important role in diagnosis and preoperative planning, especially in patients with ascending aortic involve-ment. Proximal aortography can reveal not only the status of the coronary |
Surgery_Schwartz_5777 | Surgery_Schwartz | to play an important role in diagnosis and preoperative planning, especially in patients with ascending aortic involve-ment. Proximal aortography can reveal not only the status of the coronary arteries and left ventricular function but also the degree of aortic valve regurgitation, the extent of aortic root involvement, coronary ostial displacement, and the relationship of the aneurysm to the arch vessels.The value of the information one can obtain from catheter-based diagnostic studies should be weighed against Brunicardi_Ch22_p0853-p0896.indd 85901/03/19 5:40 PM 860SPECIFIC CONSIDERATIONSPART IIthe established limitations and potential complications of such studies. A key limitation of aortography is that it images only the lumen and may therefore underrepresent the size of large aneurysms that contain laminated thrombus. Manipulation of intraluminal catheters can result in embolization of laminated thrombus or atheromatous debris. Proximal aortography carries a 0.6% to 1.2% | Surgery_Schwartz. to play an important role in diagnosis and preoperative planning, especially in patients with ascending aortic involve-ment. Proximal aortography can reveal not only the status of the coronary arteries and left ventricular function but also the degree of aortic valve regurgitation, the extent of aortic root involvement, coronary ostial displacement, and the relationship of the aneurysm to the arch vessels.The value of the information one can obtain from catheter-based diagnostic studies should be weighed against Brunicardi_Ch22_p0853-p0896.indd 85901/03/19 5:40 PM 860SPECIFIC CONSIDERATIONSPART IIthe established limitations and potential complications of such studies. A key limitation of aortography is that it images only the lumen and may therefore underrepresent the size of large aneurysms that contain laminated thrombus. Manipulation of intraluminal catheters can result in embolization of laminated thrombus or atheromatous debris. Proximal aortography carries a 0.6% to 1.2% |
Surgery_Schwartz_5778 | Surgery_Schwartz | aneurysms that contain laminated thrombus. Manipulation of intraluminal catheters can result in embolization of laminated thrombus or atheromatous debris. Proximal aortography carries a 0.6% to 1.2% risk of stroke. Other risks include allergic reac-tion to the contrast agent, iatrogenic aortic dissection, and bleed-ing at the arterial access site. In addition, the volumes of contrast agent required to adequately fill large aneurysms can cause sig-nificant renal toxicity. To minimize the risk of contrast nephrop-athy, patients receive periprocedural intravenous (IV) fluids for hydration, mannitol for diuresis, and acetylcysteine.53,54 As with contrast-enhanced CT, surgery is performed ≥1 day after angiography whenever possible to ensure that renal func-tion has stabilized or returned to baseline.TreatmentSelecting the Appropriate Treatment. Once a thoracic aor-tic aneurysm is detected, management begins with patient edu-cation, particularly if the patient is asymptomatic, because | Surgery_Schwartz. aneurysms that contain laminated thrombus. Manipulation of intraluminal catheters can result in embolization of laminated thrombus or atheromatous debris. Proximal aortography carries a 0.6% to 1.2% risk of stroke. Other risks include allergic reac-tion to the contrast agent, iatrogenic aortic dissection, and bleed-ing at the arterial access site. In addition, the volumes of contrast agent required to adequately fill large aneurysms can cause sig-nificant renal toxicity. To minimize the risk of contrast nephrop-athy, patients receive periprocedural intravenous (IV) fluids for hydration, mannitol for diuresis, and acetylcysteine.53,54 As with contrast-enhanced CT, surgery is performed ≥1 day after angiography whenever possible to ensure that renal func-tion has stabilized or returned to baseline.TreatmentSelecting the Appropriate Treatment. Once a thoracic aor-tic aneurysm is detected, management begins with patient edu-cation, particularly if the patient is asymptomatic, because |
Surgery_Schwartz_5779 | Surgery_Schwartz | to baseline.TreatmentSelecting the Appropriate Treatment. Once a thoracic aor-tic aneurysm is detected, management begins with patient edu-cation, particularly if the patient is asymptomatic, because aortic disease may progress rapidly and unexpectedly in some patients. A detailed medical history is collected, a physical examination is performed, and a systematic review of medical records is car-ried out to clearly assess the presence or absence of pertinent symptoms and signs, despite any initial denial of symptoms by the patient. Signs of heritable conditions such as Marfan syn-drome or Loeys-Dietz syndrome are thoroughly reviewed. If clinical criteria are met for a heritable condition, confirmatory laboratory tests are conducted. Patients with heritable disorders are best treated in a dedicated aortic clinic where they can be appropriately followed up. Surveillance imaging and aggressive blood pressure control are the mainstays of initial management for asymptomatic patients. When | Surgery_Schwartz. to baseline.TreatmentSelecting the Appropriate Treatment. Once a thoracic aor-tic aneurysm is detected, management begins with patient edu-cation, particularly if the patient is asymptomatic, because aortic disease may progress rapidly and unexpectedly in some patients. A detailed medical history is collected, a physical examination is performed, and a systematic review of medical records is car-ried out to clearly assess the presence or absence of pertinent symptoms and signs, despite any initial denial of symptoms by the patient. Signs of heritable conditions such as Marfan syn-drome or Loeys-Dietz syndrome are thoroughly reviewed. If clinical criteria are met for a heritable condition, confirmatory laboratory tests are conducted. Patients with heritable disorders are best treated in a dedicated aortic clinic where they can be appropriately followed up. Surveillance imaging and aggressive blood pressure control are the mainstays of initial management for asymptomatic patients. When |
Surgery_Schwartz_5780 | Surgery_Schwartz | dedicated aortic clinic where they can be appropriately followed up. Surveillance imaging and aggressive blood pressure control are the mainstays of initial management for asymptomatic patients. When patients become symptomatic or their aneurysms grow to meet certain size criteria, the patients become surgical candidates.Endovascular therapy has become an accepted treatment for descending thoracic aortic aneurysm.55,56 Its role in treating proximal aortic disease and thoracoabdominal aortic aneurysm remains experimental;55 nonetheless, endoluminal stenting is approved by the U.S. Food and Drug Administration for the treatment of isolated descending thoracic aortic aneurysm, and several different devices have been approved for the treatment of blunt aortic injury and penetrating aortic ulcer. In practice, however, the off-label application of aortic stent grafts is widespread and accounts for well over half their use57; endovascular approaches may be helpful in emergent aneurysm | Surgery_Schwartz. dedicated aortic clinic where they can be appropriately followed up. Surveillance imaging and aggressive blood pressure control are the mainstays of initial management for asymptomatic patients. When patients become symptomatic or their aneurysms grow to meet certain size criteria, the patients become surgical candidates.Endovascular therapy has become an accepted treatment for descending thoracic aortic aneurysm.55,56 Its role in treating proximal aortic disease and thoracoabdominal aortic aneurysm remains experimental;55 nonetheless, endoluminal stenting is approved by the U.S. Food and Drug Administration for the treatment of isolated descending thoracic aortic aneurysm, and several different devices have been approved for the treatment of blunt aortic injury and penetrating aortic ulcer. In practice, however, the off-label application of aortic stent grafts is widespread and accounts for well over half their use57; endovascular approaches may be helpful in emergent aneurysm |
Surgery_Schwartz_5781 | Surgery_Schwartz | ulcer. In practice, however, the off-label application of aortic stent grafts is widespread and accounts for well over half their use57; endovascular approaches may be helpful in emergent aneurysm repair, such as for patients with aortic rupture.58 Endovascular therapy has evolved to include hybrid repairs, which combine open “debranching” techniques (to reroute branching vessels) with endovascular aortic repair.59,60 Despite these advances, for the repair of aneurysms with proximal aortic involvement and of thoracoabdominal aortic aneurysms, open procedures remain the gold standard and preferred approach.Determination of the Extent and Severity of Disease. Cross-sectional imaging with reconstruction is critical when one is evaluating a thoracic aneurysm, determining treatment strategy, and planning necessary procedures. Note that patients with a thoracic aortic aneurysm may also have a second, remote aneurysm.2 In such cases, the more threatening lesion usually is addressed first. | Surgery_Schwartz. ulcer. In practice, however, the off-label application of aortic stent grafts is widespread and accounts for well over half their use57; endovascular approaches may be helpful in emergent aneurysm repair, such as for patients with aortic rupture.58 Endovascular therapy has evolved to include hybrid repairs, which combine open “debranching” techniques (to reroute branching vessels) with endovascular aortic repair.59,60 Despite these advances, for the repair of aneurysms with proximal aortic involvement and of thoracoabdominal aortic aneurysms, open procedures remain the gold standard and preferred approach.Determination of the Extent and Severity of Disease. Cross-sectional imaging with reconstruction is critical when one is evaluating a thoracic aneurysm, determining treatment strategy, and planning necessary procedures. Note that patients with a thoracic aortic aneurysm may also have a second, remote aneurysm.2 In such cases, the more threatening lesion usually is addressed first. |
Surgery_Schwartz_5782 | Surgery_Schwartz | and planning necessary procedures. Note that patients with a thoracic aortic aneurysm may also have a second, remote aneurysm.2 In such cases, the more threatening lesion usually is addressed first. In many patients, staged operative procedures are necessary for complete repair of extensive aneurysms involving the ascending aorta, transverse arch, and descending thoracic or thoracoabdominal aorta.61 When the descending segment is not disproportionately large (compared with the proximal aorta) and is not causing symptoms, the proximal aortic repair is carried out first. An important benefit of this approach is that it allows treatment of valvular and coronary artery occlusive disease at the first operation.Proximal aneurysms (proximal to the left subclavian artery) usually are addressed via a sternotomy approach. Aneu-rysms involving the descending thoracic aorta are evaluated in terms of criteria (described in the following section) for poten-tial endovascular repair; those unsuitable | Surgery_Schwartz. and planning necessary procedures. Note that patients with a thoracic aortic aneurysm may also have a second, remote aneurysm.2 In such cases, the more threatening lesion usually is addressed first. In many patients, staged operative procedures are necessary for complete repair of extensive aneurysms involving the ascending aorta, transverse arch, and descending thoracic or thoracoabdominal aorta.61 When the descending segment is not disproportionately large (compared with the proximal aorta) and is not causing symptoms, the proximal aortic repair is carried out first. An important benefit of this approach is that it allows treatment of valvular and coronary artery occlusive disease at the first operation.Proximal aneurysms (proximal to the left subclavian artery) usually are addressed via a sternotomy approach. Aneu-rysms involving the descending thoracic aorta are evaluated in terms of criteria (described in the following section) for poten-tial endovascular repair; those unsuitable |
Surgery_Schwartz_5783 | Surgery_Schwartz | a sternotomy approach. Aneu-rysms involving the descending thoracic aorta are evaluated in terms of criteria (described in the following section) for poten-tial endovascular repair; those unsuitable for an endovascular approach are repaired with open techniques through a left thora-cotomy. A CT scan can reveal detailed information about aortic calcification and luminal thrombus. These details are important in preventing embolization during surgical manipulation.Indications for Operation Thoracic aortic aneurysms are repaired to prevent fatal rupture. Therefore, on the basis of clini-cal history studies and other data, practice guidelines for tho-racic aortic disease43,44,62 recommend elective operation in asymptomatic patients when the diameter of an ascending aortic aneurysm is >5.5 cm, when the diameter of a descending thoracic aortic aneurysm is >6.0 cm, or when the rate of dilata-tion is >0.5 cm per year. In patients with heritable disorders such as Marfan and Loeys-Dietz | Surgery_Schwartz. a sternotomy approach. Aneu-rysms involving the descending thoracic aorta are evaluated in terms of criteria (described in the following section) for poten-tial endovascular repair; those unsuitable for an endovascular approach are repaired with open techniques through a left thora-cotomy. A CT scan can reveal detailed information about aortic calcification and luminal thrombus. These details are important in preventing embolization during surgical manipulation.Indications for Operation Thoracic aortic aneurysms are repaired to prevent fatal rupture. Therefore, on the basis of clini-cal history studies and other data, practice guidelines for tho-racic aortic disease43,44,62 recommend elective operation in asymptomatic patients when the diameter of an ascending aortic aneurysm is >5.5 cm, when the diameter of a descending thoracic aortic aneurysm is >6.0 cm, or when the rate of dilata-tion is >0.5 cm per year. In patients with heritable disorders such as Marfan and Loeys-Dietz |
Surgery_Schwartz_5784 | Surgery_Schwartz | cm, when the diameter of a descending thoracic aortic aneurysm is >6.0 cm, or when the rate of dilata-tion is >0.5 cm per year. In patients with heritable disorders such as Marfan and Loeys-Dietz syndromes, the threshold for opera-tion is based on a smaller aortic diameter (5.0 cm for the ascend-ing aorta in patients with Marfan syndrome, 4.4 to 4.6 cm for the ascending aorta in patients with Loeys-Dietz syndrome, and <6.0 cm for the descending thoracic aorta in patients with either disorder). For women with heritable disorders who are consider-ing pregnancy, prophylactic aortic root replacement is considered because the risk of aortic dissection or rupture increases at an aortic diameter of 4.0 cm and greater. For patients with ascending aortic aneurysm and bicuspid aortic valve, repair is recommended if aortic diameter is 5.0 cm or greater and additional risk factors are present (e.g., family his-tory of dissection, expansion rate exceeding 0.5 cm per year), if aortic diameter is | Surgery_Schwartz. cm, when the diameter of a descending thoracic aortic aneurysm is >6.0 cm, or when the rate of dilata-tion is >0.5 cm per year. In patients with heritable disorders such as Marfan and Loeys-Dietz syndromes, the threshold for opera-tion is based on a smaller aortic diameter (5.0 cm for the ascend-ing aorta in patients with Marfan syndrome, 4.4 to 4.6 cm for the ascending aorta in patients with Loeys-Dietz syndrome, and <6.0 cm for the descending thoracic aorta in patients with either disorder). For women with heritable disorders who are consider-ing pregnancy, prophylactic aortic root replacement is considered because the risk of aortic dissection or rupture increases at an aortic diameter of 4.0 cm and greater. For patients with ascending aortic aneurysm and bicuspid aortic valve, repair is recommended if aortic diameter is 5.0 cm or greater and additional risk factors are present (e.g., family his-tory of dissection, expansion rate exceeding 0.5 cm per year), if aortic diameter is |
Surgery_Schwartz_5785 | Surgery_Schwartz | is recommended if aortic diameter is 5.0 cm or greater and additional risk factors are present (e.g., family his-tory of dissection, expansion rate exceeding 0.5 cm per year), if aortic diameter is 5.5 cm or larger and no additional risk factors are present, or if aortic diameter exceeds 4.5 cm and the patient is undergoing aortic valve replacement or repair.43 For low-risk patients with chronic aortic dissection, descending thoracic repair is recommended at an aortic diameter of 5.5 cm or greater.The acuity of presentation is a major factor in decisions about the timing of surgical intervention. Many patients are asymptomatic at the time of presentation, so there is time for thorough preoperative evaluation and improvement of their cur-rent health status, such as through smoking cessation and other optimization programs. In contrast, patients who present with symptoms may need urgent operation. Symptomatic patients are at increased risk of rupture and warrant expe-ditious evaluation. | Surgery_Schwartz. is recommended if aortic diameter is 5.0 cm or greater and additional risk factors are present (e.g., family his-tory of dissection, expansion rate exceeding 0.5 cm per year), if aortic diameter is 5.5 cm or larger and no additional risk factors are present, or if aortic diameter exceeds 4.5 cm and the patient is undergoing aortic valve replacement or repair.43 For low-risk patients with chronic aortic dissection, descending thoracic repair is recommended at an aortic diameter of 5.5 cm or greater.The acuity of presentation is a major factor in decisions about the timing of surgical intervention. Many patients are asymptomatic at the time of presentation, so there is time for thorough preoperative evaluation and improvement of their cur-rent health status, such as through smoking cessation and other optimization programs. In contrast, patients who present with symptoms may need urgent operation. Symptomatic patients are at increased risk of rupture and warrant expe-ditious evaluation. |
Surgery_Schwartz_5786 | Surgery_Schwartz | and other optimization programs. In contrast, patients who present with symptoms may need urgent operation. Symptomatic patients are at increased risk of rupture and warrant expe-ditious evaluation. The onset of new pain in patients with known aneurysms is especially concerning because it may herald sig-nificant expansion, leakage, or impending rupture. Emergent intervention is reserved for patients who present with aneurysm rupture or superimposed acute dissection.63Open Repair vs. Endovascular Repair As noted earlier, endo-vascular repair has become the standard approach for patients with isolated degenerative descending thoracic aortic aneurysm; in fact, practice guidelines recommend that endovascular repair be strongly considered for patients with descending thoracic aneurysm at an aortic diameter of 5.5 cm (which is slightly below the 6.0-cm threshold for open repair).44 For endovascular 3456Brunicardi_Ch22_p0853-p0896.indd 86001/03/19 5:40 PM 861THORACIC ANEURYSMS AND AORTIC | Surgery_Schwartz. and other optimization programs. In contrast, patients who present with symptoms may need urgent operation. Symptomatic patients are at increased risk of rupture and warrant expe-ditious evaluation. The onset of new pain in patients with known aneurysms is especially concerning because it may herald sig-nificant expansion, leakage, or impending rupture. Emergent intervention is reserved for patients who present with aneurysm rupture or superimposed acute dissection.63Open Repair vs. Endovascular Repair As noted earlier, endo-vascular repair has become the standard approach for patients with isolated degenerative descending thoracic aortic aneurysm; in fact, practice guidelines recommend that endovascular repair be strongly considered for patients with descending thoracic aneurysm at an aortic diameter of 5.5 cm (which is slightly below the 6.0-cm threshold for open repair).44 For endovascular 3456Brunicardi_Ch22_p0853-p0896.indd 86001/03/19 5:40 PM 861THORACIC ANEURYSMS AND AORTIC |
Surgery_Schwartz_5787 | Surgery_Schwartz | diameter of 5.5 cm (which is slightly below the 6.0-cm threshold for open repair).44 For endovascular 3456Brunicardi_Ch22_p0853-p0896.indd 86001/03/19 5:40 PM 861THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22repairs to produce optimal outcomes, several anatomic criteria must be met. For one, the proximal and distal neck diameters should fall within a range that will allow proper sealing. Also, the proximal and distal landing zones should ideally be at least 20 mm long so that an appropriate seal can be made. Note that the limiting structures proximally and distally are the brachio-cephalic vessels and celiac axis, respectively. Vascular access continues to be one of the most important determinants of suc-cessful deployment of the current endovascular devices. The femoral and iliac arteries have to be wide enough to accommo-date the sheaths used to deploy the stent grafts. As endovascular technology evolves, newer devices are using smaller sheaths (or are “sheathless” | Surgery_Schwartz. diameter of 5.5 cm (which is slightly below the 6.0-cm threshold for open repair).44 For endovascular 3456Brunicardi_Ch22_p0853-p0896.indd 86001/03/19 5:40 PM 861THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22repairs to produce optimal outcomes, several anatomic criteria must be met. For one, the proximal and distal neck diameters should fall within a range that will allow proper sealing. Also, the proximal and distal landing zones should ideally be at least 20 mm long so that an appropriate seal can be made. Note that the limiting structures proximally and distally are the brachio-cephalic vessels and celiac axis, respectively. Vascular access continues to be one of the most important determinants of suc-cessful deployment of the current endovascular devices. The femoral and iliac arteries have to be wide enough to accommo-date the sheaths used to deploy the stent grafts. As endovascular technology evolves, newer devices are using smaller sheaths (or are “sheathless” |
Surgery_Schwartz_5788 | Surgery_Schwartz | and iliac arteries have to be wide enough to accommo-date the sheaths used to deploy the stent grafts. As endovascular technology evolves, newer devices are using smaller sheaths (or are “sheathless” self-deployed stent grafts) to accommodate smaller arteries. Tortuosity of the iliac vessels and abdominal aorta can make these procedures technically challenging. Occa-sionally, an 8or 10-mm polyester “side graft” is anastomosed to the iliac artery through a retroperitoneal incision if the femo-ral vessels are too small to access easily.Of note, attempts have been made to extend the use of endovascular therapy to aortic arch aneurysms and thoracoab-dominal aortic aneurysms. Although reports of purely endovas-cular repair of the aortic arch remain limited, Greenberg and colleagues64 have reported their experience with a large series of purely endovascular thoracoabdominal aortic repairs. Addition-ally, there have been numerous reports of small series of off-label, experimental hybrid | Surgery_Schwartz. and iliac arteries have to be wide enough to accommo-date the sheaths used to deploy the stent grafts. As endovascular technology evolves, newer devices are using smaller sheaths (or are “sheathless” self-deployed stent grafts) to accommodate smaller arteries. Tortuosity of the iliac vessels and abdominal aorta can make these procedures technically challenging. Occa-sionally, an 8or 10-mm polyester “side graft” is anastomosed to the iliac artery through a retroperitoneal incision if the femo-ral vessels are too small to access easily.Of note, attempts have been made to extend the use of endovascular therapy to aortic arch aneurysms and thoracoab-dominal aortic aneurysms. Although reports of purely endovas-cular repair of the aortic arch remain limited, Greenberg and colleagues64 have reported their experience with a large series of purely endovascular thoracoabdominal aortic repairs. Addition-ally, there have been numerous reports of small series of off-label, experimental hybrid |
Surgery_Schwartz_5789 | Surgery_Schwartz | reported their experience with a large series of purely endovascular thoracoabdominal aortic repairs. Addition-ally, there have been numerous reports of small series of off-label, experimental hybrid procedures that involve debranching the aortic arch or the visceral vessels of the abdominal aorta, fol-lowed by endovascular exclusion of the aneurysm. The majority of hybrid approaches involve repairing the aortic arch.59,60 In its simplest form, hybrid arch repair involves an open bypass from the left subclavian to the left common carotid artery, which is followed by deliberate coverage of the origins of the left subcla-vian artery by the stent graft. In its most complex form, hybrid arch repair involves rerouting all of the brachiocephalic vessels, followed by proximal placement of the stent graft in the ascend-ing aorta and extending repair distally into the aortic arch and descending thoracic aorta.The patients who theoretically benefit the most from an endovascular approach are | Surgery_Schwartz. reported their experience with a large series of purely endovascular thoracoabdominal aortic repairs. Addition-ally, there have been numerous reports of small series of off-label, experimental hybrid procedures that involve debranching the aortic arch or the visceral vessels of the abdominal aorta, fol-lowed by endovascular exclusion of the aneurysm. The majority of hybrid approaches involve repairing the aortic arch.59,60 In its simplest form, hybrid arch repair involves an open bypass from the left subclavian to the left common carotid artery, which is followed by deliberate coverage of the origins of the left subcla-vian artery by the stent graft. In its most complex form, hybrid arch repair involves rerouting all of the brachiocephalic vessels, followed by proximal placement of the stent graft in the ascend-ing aorta and extending repair distally into the aortic arch and descending thoracic aorta.The patients who theoretically benefit the most from an endovascular approach are |
Surgery_Schwartz_5790 | Surgery_Schwartz | stent graft in the ascend-ing aorta and extending repair distally into the aortic arch and descending thoracic aorta.The patients who theoretically benefit the most from an endovascular approach are those who are of advanced age or have significant comorbidities, as many of these patients face substantial risks when undergoing traditional open repair.65 For example, with regard to open repair of a descending thoracic aortic aneurysm, significant pulmonary morbidity can occur postoperatively; therefore, patients with borderline pulmonary reserve may better tolerate an endovascular procedure than a standard open repair. Patients with heritable syndromic condi-tions generally are not considered candidates for elective endo-vascular repair except in specific circumstances.66 Endovascular repair in patients with heritable syndromic conditions have pro-duced poor results, which are mainly due to progressive dilata-tion, stent graft migration, and endoleak.67,68Preoperative Assessment and | Surgery_Schwartz. stent graft in the ascend-ing aorta and extending repair distally into the aortic arch and descending thoracic aorta.The patients who theoretically benefit the most from an endovascular approach are those who are of advanced age or have significant comorbidities, as many of these patients face substantial risks when undergoing traditional open repair.65 For example, with regard to open repair of a descending thoracic aortic aneurysm, significant pulmonary morbidity can occur postoperatively; therefore, patients with borderline pulmonary reserve may better tolerate an endovascular procedure than a standard open repair. Patients with heritable syndromic condi-tions generally are not considered candidates for elective endo-vascular repair except in specific circumstances.66 Endovascular repair in patients with heritable syndromic conditions have pro-duced poor results, which are mainly due to progressive dilata-tion, stent graft migration, and endoleak.67,68Preoperative Assessment and |
Surgery_Schwartz_5791 | Surgery_Schwartz | in patients with heritable syndromic conditions have pro-duced poor results, which are mainly due to progressive dilata-tion, stent graft migration, and endoleak.67,68Preoperative Assessment and Preparation. Given the impact of comorbid conditions on perioperative complications, a careful preoperative assessment of physiologic reserve is criti-cal in assessing operative risk. Therefore, most patients undergo a thorough evaluation—with emphasis on cardiac, pulmonary, and renal function—before undergoing elective surgery.69,70Cardiac Evaluation Coronary artery disease is common in patients with thoracic aortic aneurysm and is responsible for a substantial proportion of early and late postoperative deaths in such patients. Similarly, valvular disease and myocardial dysfunction have important implications when one is planning anesthetic management and surgical approaches for aortic repair. Transthoracic echocardiography is a satisfactory noninvasive method for evaluating both valvular and | Surgery_Schwartz. in patients with heritable syndromic conditions have pro-duced poor results, which are mainly due to progressive dilata-tion, stent graft migration, and endoleak.67,68Preoperative Assessment and Preparation. Given the impact of comorbid conditions on perioperative complications, a careful preoperative assessment of physiologic reserve is criti-cal in assessing operative risk. Therefore, most patients undergo a thorough evaluation—with emphasis on cardiac, pulmonary, and renal function—before undergoing elective surgery.69,70Cardiac Evaluation Coronary artery disease is common in patients with thoracic aortic aneurysm and is responsible for a substantial proportion of early and late postoperative deaths in such patients. Similarly, valvular disease and myocardial dysfunction have important implications when one is planning anesthetic management and surgical approaches for aortic repair. Transthoracic echocardiography is a satisfactory noninvasive method for evaluating both valvular and |
Surgery_Schwartz_5792 | Surgery_Schwartz | implications when one is planning anesthetic management and surgical approaches for aortic repair. Transthoracic echocardiography is a satisfactory noninvasive method for evaluating both valvular and biventricular function. Dipyridamole-thallium myocardial scanning identifies regions of myocardium that have reversible ischemia, and this test is more practical than exercise testing in older patients with concomitant lower-extremity peripheral vascular disease. Cardiac catheteriza-tion and coronary arteriography are performed in patients who have evidence of coronary disease—as indicated by either the patient’s history or the results of noninvasive studies—or who have a left ventricular ejection fraction of ≤30%. If significant valvular or coronary artery disease is identified before a proxi-mal aortic operation, the disease can be addressed directly dur-ing the procedure. Patients who have asymptomatic distal aortic aneurysms and severe coronary occlusive disease undergo per-cutaneous | Surgery_Schwartz. implications when one is planning anesthetic management and surgical approaches for aortic repair. Transthoracic echocardiography is a satisfactory noninvasive method for evaluating both valvular and biventricular function. Dipyridamole-thallium myocardial scanning identifies regions of myocardium that have reversible ischemia, and this test is more practical than exercise testing in older patients with concomitant lower-extremity peripheral vascular disease. Cardiac catheteriza-tion and coronary arteriography are performed in patients who have evidence of coronary disease—as indicated by either the patient’s history or the results of noninvasive studies—or who have a left ventricular ejection fraction of ≤30%. If significant valvular or coronary artery disease is identified before a proxi-mal aortic operation, the disease can be addressed directly dur-ing the procedure. Patients who have asymptomatic distal aortic aneurysms and severe coronary occlusive disease undergo per-cutaneous |
Surgery_Schwartz_5793 | Surgery_Schwartz | aortic operation, the disease can be addressed directly dur-ing the procedure. Patients who have asymptomatic distal aortic aneurysms and severe coronary occlusive disease undergo per-cutaneous transluminal angioplasty or surgical revascularization before the aneurysmal aortic segment is replaced.Pulmonary Evaluation Pulmonary function screening with arterial blood gas measurement and spirometry is routinely per-formed before thoracic aortic operations. Patients with a forced expiratory volume in 1 second of >1.0 L and a partial pressure of carbon dioxide of <45 mmHg are considered appropriate can-didates for open surgical repair. In suitable patients, borderline pulmonary function can be improved by implementing a regi-men that includes smoking cessation, weight loss, exercise, and treatment of bronchitis for a period of 1 to 3 months before surgery. Although surgery is not withheld from patients with symptomatic aortic aneurysms and poor pulmonary function, adjustments in operative | Surgery_Schwartz. aortic operation, the disease can be addressed directly dur-ing the procedure. Patients who have asymptomatic distal aortic aneurysms and severe coronary occlusive disease undergo per-cutaneous transluminal angioplasty or surgical revascularization before the aneurysmal aortic segment is replaced.Pulmonary Evaluation Pulmonary function screening with arterial blood gas measurement and spirometry is routinely per-formed before thoracic aortic operations. Patients with a forced expiratory volume in 1 second of >1.0 L and a partial pressure of carbon dioxide of <45 mmHg are considered appropriate can-didates for open surgical repair. In suitable patients, borderline pulmonary function can be improved by implementing a regi-men that includes smoking cessation, weight loss, exercise, and treatment of bronchitis for a period of 1 to 3 months before surgery. Although surgery is not withheld from patients with symptomatic aortic aneurysms and poor pulmonary function, adjustments in operative |
Surgery_Schwartz_5794 | Surgery_Schwartz | of bronchitis for a period of 1 to 3 months before surgery. Although surgery is not withheld from patients with symptomatic aortic aneurysms and poor pulmonary function, adjustments in operative technique should be made to maximize these patients’ chances of recovery. In such patients, preserving the left recurrent laryngeal nerve, the phrenic nerves, and dia-phragmatic function is particularly important.Renal Evaluation Renal function is assessed preoperatively by measuring serum electrolyte, blood urea nitrogen, and cre-atinine levels. Information about kidney size and perfusion can be obtained from the imaging studies used to evaluate the aorta.Obtaining accurate information about baseline renal function has important therapeutic and prognostic implications. For exam-ple, perfusion strategies and perioperative medications are adjusted according to renal function. Patients with severely impaired renal function frequently require at least temporary hemodialysis after surgery. These | Surgery_Schwartz. of bronchitis for a period of 1 to 3 months before surgery. Although surgery is not withheld from patients with symptomatic aortic aneurysms and poor pulmonary function, adjustments in operative technique should be made to maximize these patients’ chances of recovery. In such patients, preserving the left recurrent laryngeal nerve, the phrenic nerves, and dia-phragmatic function is particularly important.Renal Evaluation Renal function is assessed preoperatively by measuring serum electrolyte, blood urea nitrogen, and cre-atinine levels. Information about kidney size and perfusion can be obtained from the imaging studies used to evaluate the aorta.Obtaining accurate information about baseline renal function has important therapeutic and prognostic implications. For exam-ple, perfusion strategies and perioperative medications are adjusted according to renal function. Patients with severely impaired renal function frequently require at least temporary hemodialysis after surgery. These |
Surgery_Schwartz_5795 | Surgery_Schwartz | and perioperative medications are adjusted according to renal function. Patients with severely impaired renal function frequently require at least temporary hemodialysis after surgery. These patients also have a mortality rate that is signifi-cantly higher than normal. Patients with thoracoabdominal aortic aneurysms and poor renal function secondary to severe proximal renal occlusive disease undergo renal artery endarterectomy, stent-ing, or bypass grafting during the aortic repair.Operative Repair Proximal Thoracic Aortic Aneurysms Open Repair Traditional open operations to repair proximal aortic aneurysms—which involve the ascending aorta, trans-verse aortic arch, or both—are performed through a midsternal incision and require cardiopulmonary bypass. The best choice of aortic replacement technique depends on the extent of the aneurysm and the condition of the aortic valve.71 The spectrum of operations (Fig. 22-4) ranges from simple graft replacement of the tubular portion of the | Surgery_Schwartz. and perioperative medications are adjusted according to renal function. Patients with severely impaired renal function frequently require at least temporary hemodialysis after surgery. These patients also have a mortality rate that is signifi-cantly higher than normal. Patients with thoracoabdominal aortic aneurysms and poor renal function secondary to severe proximal renal occlusive disease undergo renal artery endarterectomy, stent-ing, or bypass grafting during the aortic repair.Operative Repair Proximal Thoracic Aortic Aneurysms Open Repair Traditional open operations to repair proximal aortic aneurysms—which involve the ascending aorta, trans-verse aortic arch, or both—are performed through a midsternal incision and require cardiopulmonary bypass. The best choice of aortic replacement technique depends on the extent of the aneurysm and the condition of the aortic valve.71 The spectrum of operations (Fig. 22-4) ranges from simple graft replacement of the tubular portion of the |
Surgery_Schwartz_5796 | Surgery_Schwartz | technique depends on the extent of the aneurysm and the condition of the aortic valve.71 The spectrum of operations (Fig. 22-4) ranges from simple graft replacement of the tubular portion of the ascending aorta only (Fig. 22-4A) to replacement of the ascending aorta and the proximal aortic arch (Fig. 22-4B) to graft replacement of the entire proximal aorta, including the aortic root, and reattachment of the coronary Brunicardi_Ch22_p0853-p0896.indd 86101/03/19 5:40 PM 862SPECIFIC CONSIDERATIONSPART IIABCEFGHIJDKFigure 22-4. Illustrations of proximal aortic repairs in which the native aortic root is left intact. A. Graft replacement of the tubular portion of the ascending aorta with the aortic arch left intact. B. Hemiarch beveled graft replacement, in which the ascending aorta and a portion of the lesser curvature of the aortic arch are replaced. C. A modified arch with additional graft replacement of the innominate artery. D. Patch repair of the aortic arch. E. Traditional total | Surgery_Schwartz. technique depends on the extent of the aneurysm and the condition of the aortic valve.71 The spectrum of operations (Fig. 22-4) ranges from simple graft replacement of the tubular portion of the ascending aorta only (Fig. 22-4A) to replacement of the ascending aorta and the proximal aortic arch (Fig. 22-4B) to graft replacement of the entire proximal aorta, including the aortic root, and reattachment of the coronary Brunicardi_Ch22_p0853-p0896.indd 86101/03/19 5:40 PM 862SPECIFIC CONSIDERATIONSPART IIABCEFGHIJDKFigure 22-4. Illustrations of proximal aortic repairs in which the native aortic root is left intact. A. Graft replacement of the tubular portion of the ascending aorta with the aortic arch left intact. B. Hemiarch beveled graft replacement, in which the ascending aorta and a portion of the lesser curvature of the aortic arch are replaced. C. A modified arch with additional graft replacement of the innominate artery. D. Patch repair of the aortic arch. E. Traditional total |
Surgery_Schwartz_5797 | Surgery_Schwartz | of the lesser curvature of the aortic arch are replaced. C. A modified arch with additional graft replacement of the innominate artery. D. Patch repair of the aortic arch. E. Traditional total arch replacement using an island approach to reattach the brachiocephalic vessels. F. The branched graft approach, which replaces the brachiocephalic vessels by following their original anatomic location. G. The elephant trunk approach with a concomitant island brachiocephalic artery reattachment. Contemporary Y-graft arch repairs include (H) the single Y-graft approach, (I) the double Y-graft approach, (J) the elephant trunk approach with a single Y-graft, and (K) the elephant trunk approach with a double Y-graft.Brunicardi_Ch22_p0853-p0896.indd 86201/03/19 5:40 PM 863THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22arteries and brachiocephalic branches. The options for treating aortic valve disease, repairing aortic aneurysms, and maintain-ing perfusion during repair procedures each | Surgery_Schwartz. of the lesser curvature of the aortic arch are replaced. C. A modified arch with additional graft replacement of the innominate artery. D. Patch repair of the aortic arch. E. Traditional total arch replacement using an island approach to reattach the brachiocephalic vessels. F. The branched graft approach, which replaces the brachiocephalic vessels by following their original anatomic location. G. The elephant trunk approach with a concomitant island brachiocephalic artery reattachment. Contemporary Y-graft arch repairs include (H) the single Y-graft approach, (I) the double Y-graft approach, (J) the elephant trunk approach with a single Y-graft, and (K) the elephant trunk approach with a double Y-graft.Brunicardi_Ch22_p0853-p0896.indd 86201/03/19 5:40 PM 863THORACIC ANEURYSMS AND AORTIC DISSECTIONCHAPTER 22arteries and brachiocephalic branches. The options for treating aortic valve disease, repairing aortic aneurysms, and maintain-ing perfusion during repair procedures each |
Surgery_Schwartz_5798 | Surgery_Schwartz | AORTIC DISSECTIONCHAPTER 22arteries and brachiocephalic branches. The options for treating aortic valve disease, repairing aortic aneurysms, and maintain-ing perfusion during repair procedures each deserve detailed consideration (Table 22-2).Aortic Valve Disease and Root Aneurysms Many patients undergoing proximal aortic operations have aortic valve dis-ease that requires concomitant surgical correction. When such disease is present and the sinus segment is normal, separate repair or replacement of the aortic valve and graft replacement of the tubular segment of the ascending aorta are carried out. In such cases, mild to moderate valve regurgitation with annular dilatation can be addressed by plicating the annulus with mat-tress sutures placed below each commissure, thereby preserving the native valve. In patients with more severe valvular regur-gitation or with valvular stenosis, the valve is replaced with a stented biologic or mechanical prosthesis; mechanical prosthe-ses | Surgery_Schwartz. AORTIC DISSECTIONCHAPTER 22arteries and brachiocephalic branches. The options for treating aortic valve disease, repairing aortic aneurysms, and maintain-ing perfusion during repair procedures each deserve detailed consideration (Table 22-2).Aortic Valve Disease and Root Aneurysms Many patients undergoing proximal aortic operations have aortic valve dis-ease that requires concomitant surgical correction. When such disease is present and the sinus segment is normal, separate repair or replacement of the aortic valve and graft replacement of the tubular segment of the ascending aorta are carried out. In such cases, mild to moderate valve regurgitation with annular dilatation can be addressed by plicating the annulus with mat-tress sutures placed below each commissure, thereby preserving the native valve. In patients with more severe valvular regur-gitation or with valvular stenosis, the valve is replaced with a stented biologic or mechanical prosthesis; mechanical prosthe-ses |
Surgery_Schwartz_5799 | Surgery_Schwartz | the native valve. In patients with more severe valvular regur-gitation or with valvular stenosis, the valve is replaced with a stented biologic or mechanical prosthesis; mechanical prosthe-ses necessitate following a lifelong anticoagulation regimen. Separate replacement of the aortic valve and ascending aorta is Table 22-2Options for open surgical repair of proximal aortic aneurysmsOptions for treating aortic valve disease Aortic valve annuloplasty (annular plication) Aortic valve replacement (with mechanical or biologic prosthesis) Aortic root replacement Composite valve graft (with mechanical or biologic valve) Aortic homograft Stentless porcine root Pulmonary autograft (Ross procedure) Valve-sparing techniquesOptions for graft repair of the aortic aneurysm Patch aortoplasty Ascending replacement only Beveled hemiarch replacement Total arch replacement with reattachment of brachiocephalic branches (island technique) Elephant trunk technique with island reattachment Total arch | Surgery_Schwartz. the native valve. In patients with more severe valvular regur-gitation or with valvular stenosis, the valve is replaced with a stented biologic or mechanical prosthesis; mechanical prosthe-ses necessitate following a lifelong anticoagulation regimen. Separate replacement of the aortic valve and ascending aorta is Table 22-2Options for open surgical repair of proximal aortic aneurysmsOptions for treating aortic valve disease Aortic valve annuloplasty (annular plication) Aortic valve replacement (with mechanical or biologic prosthesis) Aortic root replacement Composite valve graft (with mechanical or biologic valve) Aortic homograft Stentless porcine root Pulmonary autograft (Ross procedure) Valve-sparing techniquesOptions for graft repair of the aortic aneurysm Patch aortoplasty Ascending replacement only Beveled hemiarch replacement Total arch replacement with reattachment of brachiocephalic branches (island technique) Elephant trunk technique with island reattachment Total arch |
Surgery_Schwartz_5800 | Surgery_Schwartz | replacement only Beveled hemiarch replacement Total arch replacement with reattachment of brachiocephalic branches (island technique) Elephant trunk technique with island reattachment Total arch replacement with bypass grafts to the brachiocephalic branches (including Y-graft approaches) Elephant trunk technique with Y-graft approach Hybrid aortic arch repairs (including “frozen elephant trunk technique”)Perfusion options Standard cardiopulmonary bypass Profound hypothermic circulatory arrest without adjuncts Hypothermic circulatory arrest with adjuncts Retrograde cerebral perfusion Antegrade cerebral perfusion Balloon perfusion catheters Right axillary artery cannulation Innominate artery cannulationnot performed in patients with Marfan syndrome or Loeys-Dietz syndrome, because progressive dilatation of the remaining sinus segment eventually leads to complications that necessitate reop-eration. Therefore, patients with Marfan syndrome, Loeys-Dietz syndrome, or annuloaortic | Surgery_Schwartz. replacement only Beveled hemiarch replacement Total arch replacement with reattachment of brachiocephalic branches (island technique) Elephant trunk technique with island reattachment Total arch replacement with bypass grafts to the brachiocephalic branches (including Y-graft approaches) Elephant trunk technique with Y-graft approach Hybrid aortic arch repairs (including “frozen elephant trunk technique”)Perfusion options Standard cardiopulmonary bypass Profound hypothermic circulatory arrest without adjuncts Hypothermic circulatory arrest with adjuncts Retrograde cerebral perfusion Antegrade cerebral perfusion Balloon perfusion catheters Right axillary artery cannulation Innominate artery cannulationnot performed in patients with Marfan syndrome or Loeys-Dietz syndrome, because progressive dilatation of the remaining sinus segment eventually leads to complications that necessitate reop-eration. Therefore, patients with Marfan syndrome, Loeys-Dietz syndrome, or annuloaortic |
Surgery_Schwartz_5801 | Surgery_Schwartz | progressive dilatation of the remaining sinus segment eventually leads to complications that necessitate reop-eration. Therefore, patients with Marfan syndrome, Loeys-Dietz syndrome, or annuloaortic ectasia require some form of aortic root replacement.72In many cases, the aortic root is replaced with a mechani-cal or biologic graft that has both a valve and an aortic conduit. Currently, the following graft options are commercially avail-able: composite valve grafts with a mechanical valve, which consist of a bileaflet mechanical valve attached to a polyester tube graft; composite valve grafts with a biological valve (avail-able in Europe only at this point); aortic root homografts, which are harvested from cadavers and cryopreserved73; and stentless porcine aortic root grafts.74,75 In the United States, because no biologic composite valve grafts are commercially available, another option for surgeons is to construct a bioprosthetic com-posite valve graft during the operation by | Surgery_Schwartz. progressive dilatation of the remaining sinus segment eventually leads to complications that necessitate reop-eration. Therefore, patients with Marfan syndrome, Loeys-Dietz syndrome, or annuloaortic ectasia require some form of aortic root replacement.72In many cases, the aortic root is replaced with a mechani-cal or biologic graft that has both a valve and an aortic conduit. Currently, the following graft options are commercially avail-able: composite valve grafts with a mechanical valve, which consist of a bileaflet mechanical valve attached to a polyester tube graft; composite valve grafts with a biological valve (avail-able in Europe only at this point); aortic root homografts, which are harvested from cadavers and cryopreserved73; and stentless porcine aortic root grafts.74,75 In the United States, because no biologic composite valve grafts are commercially available, another option for surgeons is to construct a bioprosthetic com-posite valve graft during the operation by |
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