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2,400 | Atrial fibrillation storms. | Evolving pacemaker and device technology now allows the onset pattern of arrhythmias to be identified. It is recognised that some cardiac arrhythmias have a circadian pattern of onset and that ventricular arrhythmias can occur in clusters of electrical storms. The long-term follow-up of patients with an atrial defibrillator suggests that in some patients persistent atrial fibrillation recurrences are not random, but can occur in clusters of 'atrial fibrillation storms'. A case report is used to demonstrate this newly recognised phenomenon. |
2,401 | Acute myocardial infarction complicated by early onset of heart failure: safety and feasibility of interhospital transfer for coronary angioplasty. Subanalysis of Killip II-IV patients from the PRAGUE-1 study. | The objective of this study is to assess the feasibility and safety of interhospital transfer (within up to 60 minutes) for primary/rescue coronary angioplasty of patients with myocardial infarction (AMI) complicated by an early onset of acute heart failure (AHF) admitted to a community hospital without PCI facilities.</AbstractText>From the multicenter randomized PRAGUE-1 study, a subgroup of 66 patients with AMI complicated by AHF on the first presentation to the community hospital were retrospectively analyzed. Group A patients (n = 21) were treated on site in community hospitals using thrombolysis (streptokinase), group B patients (n = 20) were transported with thrombolytic infusion to a PCI center for coronary angioplasty, and group C patients (n = 25) were immediately transported to a PCI center for primary angioplasty without thrombolysis.</AbstractText>No patient died during transportation. One group B patient developed ventricular fibrillation during transfer. The time delay from the onset of chest pain to reperfusion was > 142 minutes, and 253 and 251 minutes in groups A, B, and C, respectively. Hospital stay (16 vs 11 vs 10 days, P = NS) was shorter in the angioplasty groups. Transported patients (groups B, C) displayed a significant decrease in heart failure progression within the first 24 hours after treatment (48% vs 15% vs 8%, P < 0.05). The combined end point, i.e., mortality + nonfatal reinfarction (43% vs 25% vs 8%, P < 0.05), was significantly less frequent in the coronary angioplasty group.</AbstractText>Interhospital transfer for coronary angioplasty of patients with AMI complicated by an early onset of AHF is feasible and safe. Transport for angioplasty may even reduce the risk of heart failure progression and improve clinical outcome compared to immediate thrombolysis in the nearest community hospital.</AbstractText> |
2,402 | The administration of alpha-melanocyte-stimulating hormone protects the ischemic/reperfused myocardium. | The contribution of alpha-melanocyte-stimulating hormone (alpha-MSH) treatment, an active fragment of adrenocorticotropic hormone (ACTH), to the recovery of postischemic cardiac function, infarct size, the incidence of reperfusion-induced ventricular fibrillation and apoptotic cell death was studied in ischemic/reperfused isolated rat hearts. Rats were subcutaneously injected with 40, 200 and 400 microg/kg of alpha-MSH, and 12 h later, hearts were isolated, perfused and subjected to 30 min of ischemia followed by 120 min of reperfusion. Thus, after 120 min of reperfusion, with the concentration of 200 microg/kg alpha-MSH, coronary flow, aortic flow and left ventricular developed pressure were significantly improved from their control values of 14.6+/-0.6 ml/min, 7.5+/-0.5 ml/min and 9.1+/-0.4 kPa to 20.2+/-0.4 ml/min (p<0.05), 31.5+/-0.9 ml/min (p<0.05) and 15.9+/-0.6 (p<0.05) kPa, respectively. With the doses of 40, 200 and 400 microg/kg of alpha-MSH, infarct size was reduced from its control value of 38+/-5% to 33+/-6% (NS), 17+/-3% (p<0.05) and 19+/-4% (p<0.05), respectively. The reduction in the incidence of reperfusion-induced ventricular fibrillation followed the same pattern. It is reasonable to assume that a reduction in infarct size, in the alpha-MSH-treated myocardium, resulted in a reduction as well in apoptotic cell death. Although we did not specifically study the exact mechanism(s) of alpha-MSH-afforded postischemic protection, we assume that this protection may be related to alpha-MSH-induced corticosterone release and corticosterone-induced de novo protein synthesis, which reflected in the recovery of postischemic cardiac function in isolated hearts. Thus, interventions that are able to increase plasma corticosterone or glucocorticoid release may prevent the development of ischemia/reperfusion-induced damage. |
2,403 | Aldosterone receptor blockade improves left ventricular remodeling and increases ventricular fibrillation threshold in experimental heart failure. | To investigate the effects of aldosterone receptor blockade in postinfarction heart failure.</AbstractText>Eighty-seven rats with moderate myocardial infarction were randomized to receive either no drug or canrenone, the active metabolite of spironolactone, 20 mg/kg/day, or ramipril, 1 mg/kg/day, or a combination of the two drugs. Treatment was initiated 1 month after coronary ligation and lasted 4 weeks. Echocardiography was performed at baseline and after 4 weeks. LV catheterization, isolated heart studies, morphometric histology, myocardial norepinephrine and SERCA-2 mRNA were assessed at the end of the treatment period.</AbstractText>Infarct sizes were 33+/-3, 32+/-3, 34+/-3, and 34+/-4% in the placebo, canrenone, ramipril, and combination groups, respectively. Canrenone attenuated LV remodeling, improved LV systolic and diastolic function, and markedly reduced interstitial and perivascular fibrosis. These effects were increased by concomitant ramipril therapy. Moreover, myocardial norepinephrine content was decreased while ventricular fibrillation threshold significantly augmented by canrenone. SERCA-2 levels remained unchanged.</AbstractText>Canrenone attenuated LV dilation and interstitial remodeling, and improved LV filling dynamics and systolic function in the rat model of postinfarction heart failure. Addition of ramipril conferred further cardioprotection. Canrenone also reduced myocardial norepinephrine content and increased ventricular fibrillation threshold. The data provide a potential explanation for the decreased sudden death observed in the RALES study. The mechanisms of action of aldosterone inhibition are still poorly understood, despite its proven efficacy in heart failure. Rats with postinfarction heart failure were randomized to receive for 1 month either no drug or canrenone, or ramipril, or a combination of canrenone and ramipril. Canrenone treatment was associated with a significant attenuation of LV dilation, better LV diastolic and systolic dynamics, and a marked reduction of reactive fibrosis. These effects were enhanced by concomitant ramipril therapy. Moreover, canrenone increased ventricular fibrillation threshold and reduced myocardial norepinephrine content. The data may explain the reduced mortality demonstrated by the RALES.</AbstractText> |
2,404 | Activation of peripheral delta opioid receptors eliminates cardiac electrical instability in a rat model of post-infarction cardiosclerosis via mitochondrial ATP-dependent K+ channels. | The effects of the selective delta-1 (delta(1)) opioid receptor agonist, DPDPE, and the selective delta(2) opioid receptor agonist, DSLET, have been studied on the ventricular fibrillation threshold (VFT) in rats with an experimental post-infarction cardiosclerosis (CS). It has been found that CS induced a significant decrease in VFT. This CS-induced decrease in VFT was significantly reversed by intravenous administration of DPDPE (0.1 mg/kg) 10 min before VFT measurement. On the contrary, intravenous injection of DSLET (0.5 mg/kg) exacerbated the CS-induced cardiac electrical instability. Pretreatment with the selective delta opioid receptor antagonist, ICI 174,864 (0.5 mg/kg), completely abolished the changes in VFT produced by both DPDPE and DSLET. Previous administration of a nonselective peripherally acting opioid receptor antagonist, naloxone methiodide (5 mg/kg) also completely reversed the antifibrillatory action of DPDPE. Naloxone methiodide and ICI 174,864 alone had no effect on VFT. Pretreatment with the nonselective K(ATP) channel blocker, glibenclamide (0.3 mg/kg), or with the mitochondrial selective K(ATP) channel blocker, 5-hydroxydecanoic acid (5-HD, 5 mg/kg), completely abolished the DPDPE-induced increase in cardiac electrical stability. Glibenclamide and 5-HD alone had no effect on VFT. These results demonstrate that the delta opioid receptor plays an important role in the regulation of electrical stability in rats with post-infarction cardiosclerosis. We propose that peripheral delta(1) opioid receptor stimulation reverses CS-induced electrical instability via mitochondrial K(ATP) channels. On the contrary, delta(2) opioid receptor stimulation may exacerbate the CS-induced decrease in VFT. Further studies are necessary to determine the delta opioid receptor subtype which mediates the antifibrillatory effect of DPDPE and pro-fibrillatory effect of DSLET. |
2,405 | Stroke volumes and end-tidal carbon dioxide generated by precordial compression during ventricular fibrillation. | The objective of this study was to measure stroke volumes produced by precordial compression during cardiopulmonary resuscitation and to quantitate relationships of stroke volume to measurements of end-tidal carbon dioxide.</AbstractText>A prospective, observational animal study.</AbstractText>Medical research laboratory in a university-affiliated research and educational foundation.</AbstractText>Domestic pigs.</AbstractText>Eighteen anesthetized male, domestic pigs weighing between 40 and 45 kg were investigated. Ventricular fibrillation was electrically induced and continued for intervals ranging from 4 to 10 mins. Precordial compression was maintained at 80 per minute together with mechanical ventilation after endotracheal intubation.</AbstractText>Stroke volumes were measured with the aid of transesophageal echocardiographic imaging. End-tidal carbon dioxide was quantitated with conventional capnography. Baseline values of thermodilution cardiac output were highly correlated with echocardiographic measurements (r =.92). The stroke volume index produced by precordial compression averaged 0.45 mL/kg or approximately 37% of the average prearrest value of 1.22 mL/kg. The end-tidal carbon dioxide was highly predictive of stroke volume index (r =.88, p <.001) with a mean bias of 0.003 mL/kg.</AbstractText>We confirmed that precordial compression produces approximately one third of prearrest stroke volumes during cardiopulmonary resuscitation and demonstrated that end-tidal carbon dioxide was quantitatively predictive of stroke volume index estimated by transesophageal echocardiographic imaging.</AbstractText> |
2,406 | Study of sudden cardiac deaths in young athletes. | Sudden cardiac deaths in athletes are usually due to underlying cardiovascular disease. The final pathway is usually ventricular fibrillation following hypertrophic cardiomyopathy and coronary artery anomalies in young persons below the age of 30 years. Sudden cardiac death in young is rare but remains as a source of concern. A postmortem study was conducted to ascertain the cardiac causes of sudden death in persons below the age group 30 years following exercise in games or otherwise. Out of 15 cases in autopsy finding, hypertrophic cardiomyopathy (n=7) was the commonest cause followed by coronary artery anomalies (n=4). Sudden unexpected death is a source of concern and careful screening of history and physical examination for potential athletes should identify majority of people at risk. |
2,407 | [Early defibrillation in the treatment of sudden cardiac arrest]. | Recovery from nontraumatic cardiac arrest depends on the presence of all the elements in the chain of survival. "Early defibrillation" is critical because ventricular fibrillation is the most common initial dysrhythmia of sudden cardiac arrest. Defibrillation is the only treatment, and survival from ventricular fibrillation is determined by time. Out-of-hospital studies have demonstrated that defibrillation provided by first responders improves survival. Technologic advances have simplified defibrillation delivery through the development of automated external defibrillators (AEDs). Early defibrillation programs with AEDs are quickly becoming a standard of care for emergency medical service systems throughout the United States. Improvement in in-hospital survival rates from cardiac arrest is not as evident as in the emergency medical service community. Medical centers need to assess response times to cardiac arrest and implement AED programs. All the nurses should learn to use an AED as part of basic life support training. |
2,408 | Surgical myocardial revascularization without extracorporeal circulation. | To assess the immediate postoperative period of patients undergoing myocardial revascularization without extracorporeal circulation with different types of grafts.</AbstractText>One hundred and twelve patients, 89 (79.5%) of whom were males, were revascularized without extracorporeal circulation. Their ages ranged from 39 to 85 years. The criteria for indicating myocardial revascularization without extracorporeal circulation were as follows: revascularized coronary artery caliber > 1.5 mm, lack of intramyocardial trajectory on coronary angiography, noncalcified coronary arteries, and tolerance of the heart to the different rotation maneuvers.</AbstractText>Myocardial revascularization without extracorporeal circulation was performed in 112 patients. Three were converted to extracorporeal circulation, which required a longer hospital stay but did not impact mortality. During the procedure, the following events were observed: atrial fibrillation in 10 patients, ventricular fibrillation in 4, total transient atrioventricular block in 2, ventricular extrasystoles in 58, use of a device to retrieve red blood cells in 53, blood transfusion in 8, and arterial hypotension in 89 patients. Coronary angiography was performed in 20 patients on the seventh postoperative day when the grafts were patent.</AbstractText>Myocardial revascularization without extracorporeal circulation is a reproducible technique that is an alternative for treating ischemic heart disease.</AbstractText> |
2,409 | Dynamic pressure--flow velocity relationships in the human cerebral circulation. | The pressure-flow velocity relationship in the cerebral circulation is characterized by the critical closing pressure (CCP), which is the pressure at which flow ceases, and the linear slope of a plot between pressure and flow velocity. It has been suggested, but not validated, that CCP can be determined from arterial blood pressure (ABP) and transcranial Doppler (TCD) recordings during the cardiac cycle. We studied a group of patients in whom ventricular fibrillation (VF) was induced. The time interval before defibrillation enabled calculation of CCP from data in which flow approached zero. These estimates were compared with values calculated before and after fibrillation and during regular heartbeats.</AbstractText>TCD velocities and ABP in the radial artery were recorded before, during, and after 28 episodes of VF in 13 patients. CCPs were calculated by 3 different methods: (1) linear extrapolation from data during VF (gold standard); (2) linear extrapolation from normal heartbeat data; and (3) first harmonic Fourier filtering of normal heartbeat data.</AbstractText>The CCP during VF calculated from long diastoles was 32.9+/-11 mm Hg (mean+/-SD). The regular heartbeat estimate was 6.0+/-4.3 mm Hg lower (P<0.05). The CCP estimate with the use of a Fourier filter was 1.4+/-3.9 mm Hg (P=NS) lower than during VF. During hyperemia after defibrillation, the CCP decreased by 13.3 mm Hg, while velocity increased by 63%. The decrease in CCP could explain half of the increase in flow velocity during hyperemia.</AbstractText>CCP can be accurately estimated from regular heartbeat data and is an important factor in regulation of the cerebral circulation.</AbstractText> |
2,410 | Characterization of fibrillatory rhythms by ensemble vector directional analysis. | Recent studies have demonstrated that fibrillatory rhythms are not random phenomena but have definable patterns. However, standard mapping techniques may have limitations in their ability to identify the organization of fibrillation. The purpose of this study was to develop and apply a method, "ensemble vector mapping," for characterizing the spatiotemporal organization of fibrillation. Ventricular fibrillation was induced by burst pacing in normal mongrel dogs. In a separate protocol, atrial fibrillation was induced by epicardial aconitine application. Epicardial electrograms were recorded from a 112-electrode plaque array using a computerized mapping system. Vectors were created by summing orthogonal bipolar electrograms. The magnitude of the vectors was transformed using a logarithmic function, integrated over time, and normalized for local electrogram amplitude to produce an "ensemble vector" index whose magnitude is high when beat-to-beat activation direction is consistent and low when activation direction is variable. The mean index was 137 +/- 36 mV/s during ventricular pacing at a cycle length of 300 ms but only 39 +/- 23 mV/s during ventricular fibrillation (P < 0.001). The ensemble vector index was also lower during atrial fibrillation (60 +/- 54 mV/s) than during atrial pacing (115 +/- 27 mV/s, P < 0.01 vs. atrial fibrillation) but not as low as during ventricular fibrillation (P < 0.05, atrial vs. ventricular fibrillation). The index was also capable of distinguishing atrial tachycardia from atrial fibrillation. Ensemble vector mapping produces an objective assessment of the consistency of myocardial activation during fibrillation. The consistency of activation direction differs in different models of fibrillation and is higher during atrial than ventricular fibrillation. This technique has the potential to rapidly characterize repetitive activation patterns in fibrillatory rhythms and may help distinguish among different characteristics of fibrillatory rhythms. |
2,411 | Adenosine-sensitive wide-complex tachycardia: an uncommon variant of idiopathic fascicular ventricular tachycardia--a case report. | Most wide-complex tachycardias encountered in the emergency department (ED) are ventricular in origin, most commonly associated with structural heart disease. Ventricular tachyarrhythmias range in severity from life-threatening rhythms (eg, ventricular fibrillation and hemodynamically compromising ventricular tachycardia [VT]) to idiopathic forms of VT, which have a benign clinical course and a more favorable prognosis. The authors present the case of a 34-year-old woman who presented to the ED, with a wide-complex tachycardia with a right-bundle-branch block (RBBB) morphology and a right inferior axis, which was terminated with adenosine. The patient was previously misdiagnosed as suffering from a paroxysmal supraventricular tachycardia (SVT), which was unresponsive to beta-blocker therapy. Although the tachycardia responded to adenosine, suggestive of an SVT, the patient was referred to the arrhythmia service, where further work-up revealed an uncommon form of an idiopathic VT, originating from the left anterior fascicle. The authors discuss the unique electrocardiographic and electrophysiologic properties and useful diagnostic maneuvers required to properly identify this form of VT. |
2,412 | [Antithrombotic prophylaxis in patients with ventricular dysfunction: critical review of the literature and new perspectives]. | Recent observational data suggest that mild or moderate heart failure is associated with an annual risk of stroke of approximately 1.2%. Indeed, it is possible that the major cause of sudden death in chronic heart failure is not related to arrhythmias, but to vascular occlusion. Anticoagulation may reduce the rate of embolic events, but there is controversy about the mandatory use of antithrombotic therapy for all patients with ventricular dysfunction in sinus rhythm. At present antithrombotic therapy is indicated only in "high risk" subgroups of patients: atrial fibrillation, mobile/protruding/irregular thrombi, acute post-myocardial infarction thrombi or a recent history of thromboembolism. Actually there is no evidence to recommend the use of aspirin to prevent thromboembolism in patients with ventricular dysfunction in sinus rhythm. Further trials of both antiplatelet agents and anticoagulation are sorely needed and we are waiting for the results of large trials such as the WATCH trial (Warfarin and Antiplatelet Therapy in Chronic Heart Failure) and the WARCEF trial (Warfarin Versus Aspirin in Reduced Ejection Fraction). The future appears promising due to the advent of a new oral direct thrombin inhibitor, ximelagatran, with good efficacy and safety profile for the treatment and prevention of thromboembolism. |
2,413 | Ongoing trials of cardiac resynchronisation. | Heart failure is an increasingly common and debilitating condition for which pharmacological therapy has, so far, provided only partial relief. Despite medical therapy the overall prognosis remains poor with high rates of sudden death and death from progressive heart failure. Device based therapies offer considerable promise both for the relief of symptoms and for improving prognosis. Cardiac resynchronisation therapy (CRT) has already been shown to improve the symptoms of heart failure when optimal pharmacological therapy (including aggressive diuretic therapy, ACE inhibitors, b-blockers and spironolactone) has failed. Two large trials (CARE-HF and COMPANION) are currently investigating the effects of CRT on morbidity and mortality in patients with heart failure and sinus rhythm who have left ventricular systolic dysfunction and ventricular dyssynchrony. A series of small and medium sized studies are assessing the effects of CRT in patients similar to the above but who also have atrial fibrillation. Other potential indications for CRT that are being explored include heart failure due to left ventricular diastolic function and for the prevention of iatrogenic dyssynchrony caused by conventional pacing. The MADIT-II study suggests a small benefit from routine implantation of defibrillators in patients with heart failure who have a markedly depressed (<30%) ejection fraction due to prior myocardial infarction even in the absence of specific marker of risk for sudden arrhythmic death. Much greater benefit was observed in patients with QRS >150 msec, an ECG marker for cardiac dyssynchrony. The COMPANION trial will not only assess the effects of CRT alone but also the effects of a combined CRT and defibrillator device. Premature over-interpretation of the limited amount of existing data threatens to undermine the evidence that will form the basis of future guidelines and funding decisions. Those involved in trials have an ethical duty to minimise device implantation into patients who have been randomised to the control group (cross-overs). Doctors may have difficulty explaining to patients why they implanted a CRT device should the current trials not show benefit. Patients should be warned that CRT is still an experimental therapy that has not yet been proven to alter outcome substantially. |
2,414 | Ventricular fibrillation during electrical cardioversion of pre-excited atrial fibrillation. | The Wolff-Parkinson-White syndrome can rarely present with pre-excited atrial fibrillation. In this condition the short refractory period of the accessory pathway can lead to rapid atrioventricular conduction. There is then a danger that at high heart rates the irregular broad complex tachycardia that results can deteriorate into ventricular fibrillation. The initial management of patients presenting in pre-excited atrial fibrillation requires cardioversion to sinus rhythm. This can be performed by DC cardioversion or pharmacological means. This paper describes the case of a patient presenting in pre-excited atrial fibrillation where electrical DC cardioversion lead to transient iatrogenic ventricular fibrillation. |
2,415 | Adverse effect of ventricular pacing on heart failure and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. | Dual-chamber (DDDR) pacing preserves AV synchrony and may reduce heart failure (HF) and atrial fibrillation (AF) compared with ventricular (VVIR) pacing in sinus node dysfunction (SND). However, DDDR pacing often results in prolonged QRS durations (QRSd) as the result of right ventricular stimulation, and ventricular desynchronization may result. The effect of pacing-induced ventricular desynchronization in patients with normal baseline QRSd is unknown.</AbstractText>Baseline QRSd was obtained from 12-lead ECGs before pacemaker implantation in MOST, a 2010-patient, 6-year, randomized trial of DDDR versus VVIR pacing in SND. Cumulative percent ventricular paced (Cum%VP) was determined from stored pacemaker data. Baseline QRSd <120 ms was observed in 1339 patients (707 DDDR, 632 VVIR). Cum%VP was greater in DDDR versus VVIR (90% versus 58%, P=0.001). Cox models demonstrated that the time-dependent covariate Cum%VP was a strong predictor of HF hospitalization in DDDR (hazard ratio [HR], 2.99 [95% CI, 1.15 to 7.75] for Cum%VP >40%) and VVIR (HR 2.56 [95% CI, 1.48 to 4.43] for Cum%VP >80%). The risk of AF increased linearly with Cum%VP from 0% to 85% in both groups (DDDR, HR 1.36 [95% CI, 1.09, 1.69]; VVIR, HR 1.21 [95% CI 1.02, 1.43], for each 25% increase in Cum%VP). Model results were unaffected by adjustment for known baseline predictors of HF hospitalization and AF.</AbstractText>Ventricular desynchronization imposed by ventricular pacing even when AV synchrony is preserved increases the risk of HF hospitalization and AF in SND with normal baseline QRSd.</AbstractText> |
2,416 | Atrial fibrillation: hypertension as a causative agent, risk factor for complications, and potential therapeutic target. | Atrial fibrillation and hypertension are 2 prevalent, and often coexistent, conditions in the North American population. Their incidence increases with advancing age, and they are responsible for considerable morbidity and mortality. Although the relation between the 2 conditions has long been known, the treatment of hypertension is not currently a focus in the clinical management of atrial fibrillation. Hypertension is associated with left ventricular hypertrophy, impaired ventricular filling, left atrial enlargement, and slowing of atrial conduction velocity. These changes in cardiac structure and physiology favor the development of atrial fibrillation, and they increase the risk of thromboembolic complications. Conventional therapy of atrial fibrillation has focused on interventions to control heart rate and rhythm and the prevention of stroke through the use of anticoagulant medications. In patients with atrial fibrillation, aggressive treatment of hypertension may reverse the structural changes in the heart, reduce thromboembolic complications, and retard or prevent the occurrence of atrial fibrillation. Specific pharmacotherapy could potentially play a major role in the primary and secondary prevention of atrial fibrillation and its complications. |
2,417 | Suppressing arrhythmias in cardiac models using overdrive pacing and calcium channel blockers. | Recent findings indicate that ventricular fibrillation might arise from spiral wave chaos. Our objective in this computational study was to investigate wave interactions in excitable media and to explore the feasibility of using overdrive pacing to suppress spiral wave chaos. This work is based on the finding that in excitable media, propagating waves with the highest excitation frequency eventually overtake all other waves. We analyzed the effects of low-amplitude, high-frequency pacing in one-dimensional and two-dimensional networks of coupled, excitable cells governed by the Luo-Rudy model. In the one-dimensional cardiac model, we found narrow high-frequency regions of 1:1 synchronization between the input stimulus and the system's response. The frequencies in this region were higher than the intrinsic spiral wave frequency of cardiac tissue. When we paced the two-dimensional cardiac model with frequencies from this region, we found that spiral wave chaos could, in some cases, be suppressed. When we coupled the overdrive pacing with calcium channel blockers, we found that spiral wave chaos could be suppressed in all cases. These findings suggest that low-amplitude, high-frequency overdrive pacing, in combination with calcium channel inhibitors (e.g., class II or class IV antiarrhythmic drugs), may be useful for eliminating fibrillation. (c) 2002 American Institute of Physics. |
2,418 | Enhanced self-termination of re-entrant arrhythmias as a pharmacological strategy for antiarrhythmic action. | Ventricular tachycardia and fibrillation are potentially lethal cardiac arrhythmias generated by high frequency, irregular spatio-temporal electrical activity. Re-entrant propagation has been demonstrated as a mechanism generating these arrhythmias in computational and in vitro animal models of these arrhythmias. Re-entry can be idealised in homogenous isotropic virtual cardiac tissues as spiral and scroll wave solutions of reaction-diffusion equations. A spiral wave in a bounded medium can be terminated if its core reaches a boundary. Ventricular tachyarrhythmias in patients are sometimes observed to spontaneously self-terminate. One possible mechanism for self-termination of a spiral wave is meander of its core to an inexcitable boundary. We have previously proposed the hypothesis that the spatial extent of meander of a re-entrant wave in the heart can be directly related to its probability of self-termination, and so inversely related to its lethality. Meander in two-dimensional virtual ventricular tissues based on the Oxsoft family of cell models, with membrane excitation parameters simulating the inherited long Q-T syndromes has been shown to be consistent with this hypothesis: the largest meander is seen in the syndrome with the lowest probability of death per arrhythmic episode. Here we extend our previous results to virtual tissues based on the Luo-Rudy family of models. Consistent with our hypothesis, for both families of models, whose different ionic mechanisms produce different patterns of meander, the LQT virtual tissue with the larger meander simulates the syndrome with the lower probability of death per episode. Further, we search the parameter space of the repolarizing currents to find their conductance parameter values that give increased meander of spiral waves. These parameters may provide targets for antiarrhythmic drugs designed to act by increasing the likelihood of self-termination of re-entrant arrhythmias. (c) 2002 American Institute of Physics. |
2,419 | Wave front fragmentation due to ventricular geometry in a model of the rabbit heart. | The role of the heart's complex shape in causing the fragmentation of activation wave fronts characteristic of ventricular fibrillation (VF) has not been well studied. We used a finite element model of cardiac propagation capable of simulating functional reentry on curved two-dimensional surfaces to test the hypothesis that uneven surface curvature can cause local propagation block leading to proliferation of reentrant wave fronts. We found that when reentry was induced on a flat sheet, it rotated in a repeatable meander pattern without breaking up. However, when a model of the rabbit ventricles was formed from the same medium, reentrant wave fronts followed complex, nonrepeating trajectories. Local propagation block often occurred when wave fronts propagated across regions where the Gaussian curvature of the surface changed rapidly. This type of block did not occur every time wave fronts crossed such a region; rather, it only occurred when the wave front was very close behind the previous wave in the cycle and was therefore propagating into relatively inexcitable tissue. Close wave front spacing resulted from nonstationary reentrant propagation. Thus, uneven surface curvature and nonstationary reentrant propagation worked in concert to produce wave front fragmentation and complex activation patterns. None of the factors previously thought to be necessary for local propagation block (e.g., heterogeneous refractory period, steep action potential duration restitution) were present. We conclude that the complex geometry of the heart may be an important determinant of VF activation patterns. (c) 2002 American Institute of Physics. |
2,420 | Characterization of patterned irregularity in locally interacting, spatially extended systems: Ventricular fibrillation. | The re-entrant ventricular arrhythmias of monomorphic ventricular tachycardia and fibrillation are produced by abnormal spatio-temporal patterns of propagation in the ventricular myocardium. These behaviors can be described by solutions of reaction-diffusion equation excitable medium models. The direct comparison of such solutions with existing experimental observations is virtually impossible as there are too many factors to be taken into account, including not only the complicated dynamics of the re-entrant waves of excitation in the tissue, but also the way the appearance of these waves on the surface is modified by the inhomogeneity, anisotropy and three-dimensional nature of heart tissue. One way of indirect comparison is to compare characteristics of the complexity of the model and the real data, that are invariant under these modifications of the signal. Karhunen-Loeve decomposition is a standard tool for evaluating the complexity of multidimensional signals. A comparison of the separate and conjoint complexities of the signals on the opposite sides of the preparation can be considered as an indicator how much three-dimensional effects are essential in the preparation behavior. (c) 2001 American Institute of Physics. |
2,421 | Alternans and higher-order rhythms in an ionic model of a sheet of ischemic ventricular muscle. | Life-threatening arrhythmias such as ventricular tachycardia and fibrillation often occur during acute myocardial ischemia. During the first few minutes following coronary occlusion, there is a gradual rise in the extracellular concentration of potassium ions ([K(+)](0)) within ischemic tissue. This elevation of [K(+)](0) is one of the main causes of the electrophysiological changes produced by ischemia, and has been implicated in inducing arrhythmias. We investigate an ionic model of a 3 cmx3 cm sheet of normal ventricular myocardium containing an ischemic zone, simulated by elevating [K(+)](0) within a centrally-placed 1 cmx1 cm area of the sheet. As [K(+)](0) is gradually raised within the ischemic zone from the normal value of 5.4 mM, conduction first slows within the ischemic zone and then, at higher [K(+)](0), an arc of block develops within that area. The area distal to the arc of block is activated in a delayed fashion by a retrogradely moving wavefront originating from the distal edge of the ischemic zone. With a further increase in [K(+)](0), the point eventually comes where a very small increase in [K(+)](0) (0.01 mM) results in the abrupt transition from a global period-1 rhythm to a global period-2 rhythm in the sheet. In the peripheral part of the ischemic zone and in the normal area surrounding it, there is an alternation of action potential duration, producing a 2:2 response. Within the core of the ischemic zone, there is an alternation between an action potential and a maintained small-amplitude response ( approximately 30 mV in height). With a further increase of [K(+)](0), the maintained small-amplitude response turns into a decrementing subthreshold response, so that there is 2:1 block in the central part of the ischemic zone. A still further increase of [K(+)](0) leads to a transition in the sheet from a global period-2 to a period-4 rhythm, and then to period-6 and period-8 rhythms, and finally to a complete block of propagation within the ischemic core. When the size of the sheet is increased to 4 cmx4 cm (with a 2 cmx2 cm ischemic area), one observes essentially the same sequence of rhythms, except that the period-6 rhythm is not seen. Very similar sequences of rhythms are seen as [K(+)](0) is increased in the central region (1 or 2 cm long) of a thin strand of tissue (3 or 4 cm long) in which propagation is essentially one-dimensional and in which retrograde propagation does not occur. While reentrant rhythms resembling tachycardia and fibrillation were not encountered in the above simulations, well-known precursors to such rhythms (e.g., delayed activation, arcs of block, two-component upstrokes, retrograde activation, nascent spiral tips, alternans) were seen. We outline how additional modifications to the ischemic model might result in the emergence of reentrant rhythms following alternans. (c) 2000 American Institute of Physics. |
2,422 | Deterministic nonlinearity in ventricular fibrillation. | We provide numerical evidence that the electrocardiogram data collected from pigs during induced ventricular fibrillation cannot be described by a monotonic nonlinear transformation of linearly filtered noise. To establish this we use surrogate techniques and apply two test statistics: (1) the Takens' maximum likelihood estimator of the Grassberger-Procaccia correlation dimension and (2) an improved correlation dimension estimation routine. The improved dimension estimates provide evidence that the correlation dimension of the underlying dynamics during the episode of VF in the first 30 s is slightly less than 6. This result is consistent and reproducible among subjects. (c) 2000 American Institute of Physics. |
2,423 | The correlation dimension of rat hearts in an experimentally controlled environment. | The electric response of several isolated rat hearts in a controlled environment was studied experimentally. The correlation dimension D(2) was estimated and was found to be between 4 and 6.5 when the response was nearly periodic. The variation of D(2) with the concentration of calcium was studied and a general trend of its increase with increasing concentration was found. Two types of ventricular fibrillation (VF) were observed, one that corresponds to a stochastic signal where D(2) is unbounded and the other to a low dimensional dynamical system with 3.5</=D(2)</=4. It was found also that for the heart the correlation dimension is only an approximate concept. A new method for the estimation of D(2), that is suitable for the case when it is only approximate was introduced. A surrogate data method suitable for the analysis of nearly periodic series was implemented. (c) 2000 American Institute of Physics. |
2,424 | Acute reductions in ventricular myocardial tissue velocities after direct current cardioversion of atrial fibrillation. | Cardioversion by direct current (DC) and other methods can cause atrial "stunning." There are case reports of acute pulmonary edema after DC cardioversion, but whether acute ventricular dysfunction is a general consequence of DC cardioversion is unknown. We have investigated whether DC cardioversion acutely affects myocardial velocity assessed by Doppler tissue imaging.</AbstractText>40 patients (30 with atrial fibrillation and 10 with atrial flutter) undergoing elective DC cardioversion underwent transthoracic echocardiography with Doppler tissue imaging before and immediately after cardioversion, and after follow-up. Peak systolic velocity was derived for 6 ventricular segments using Doppler tissue imaging.</AbstractText>Immediately after DC cardioversion of atrial fibrillation, peak systolic velocity decreased in basal lateral (4.3 +/- 2.0-3.3 +/- 1.7 cm/s, P <.001), mitral annulus-septal (3.8 +/- 1.0-3.5 +/- 0.9, P <.05), mitral annulus-lateral (4.9 +/- 1.6-4.1 +/- 1.7, P <.001), and tricuspid annular (7.8 +/- 2.0-7.0 +/- 1.2, P <.03) segments, even though left ventricular ejection fraction was unchanged. In contrast, for the atrial flutter group there were no significant changes in peak systolic velocity in any segment post-DC cardioversion. Follow up studies were performed after sustained in sinus rhythm in both atrial fibrillation and atrial flutter groups. For both groups, increased peak systolic velocity was found in all 6 segments on follow-up (all P <.05).</AbstractText>DC cardioversion causes subclinical, acute reversible reduction in left ventricular peak systolic velocity in patients with atrial fibrillation. The causes of this reduction in myocardial contractile velocity and the circumstances in which acute dysfunction become clinically significant warrant further investigation.</AbstractText> |
2,425 | Clinical and electrophysiologic predictors of ventricular tachyarrhythmia recurrence in patients with implantable cardioverter defibrillators. | Not all patients experience recurrent sustained ventricular tachyarrhythmias after placement of an implantable cardioverter defibrillator (ICD). We evaluated the clinical and electrophysiologic predictors of ventricular tachycardia (VT) and ventricular fibrillation (VF) recurrence following ICD implantation.</AbstractText>Consecutive patients (n = 133) underwent 4 +/- 3 serial electrophysiologic studies (EPS) over 50 +/- 26 months following ICD implantation. Sustained VT/VF could always be induced during follow-up EPS in 49 patients; sustained VT/VF was sometimes induced during follow-up EPS in 47 patients; and sustained VT/VF could never be induced during follow-up EPS in 37 patients. Spontaneous VT/VF requiring ICD therapy occurred in 107 patients during follow-up. Patients with sustained VT/VF that was always inducible or sometimes inducible during follow-up experienced more frequent episodes of VT/VF following ICD implant (20.5, 95% CI 12.7-33.0; and 17.8, 95% CI 11.3-28.1 episodes/patient respectively; vs 3.0, 95% CI 2.0-4.6 episodes/patient for patients with VT/VF never induced, P < 0.001). Inducibility of sustained VT/VF post-ICD implant (P < 0.001) and sustained VT as the presenting arrhythmia (P = 0.02) were independent predictors of spontaneous VT/VF recurrence.</AbstractText>Reproducibly inducible VT/VF following ICD implantation predicts a high probability of VT/VF recurrence and identifies a cohort of patients who experience frequent episodes of VT/VF over time. Persistent noninducibility of sustained VT/VF identifies a group of patients who experience no or very few episodes of VT/VF recurrence.</AbstractText> |
2,426 | Natural history of Brugada syndrome: the prognostic value of programmed electrical stimulation of the heart. | The prognostic value of electrophysiologic studies in individuals with the syndrome of right bundle branch block and ST segment elevation in precordial leads V1 to V3 (Brugada syndrome) remains controversial. Our previous data from 252 individuals with the syndrome suggested that programmed ventricular stimulation had a good overall accuracy to predict events. However, studies from independent investigators questioned our results. We report here the largest population with Brugada syndrome ever studied by programmed electrical stimulation of the heart.</AbstractText>Four hundred forty-three individuals with an ECG diagnostic of Brugada syndrome were studied by programmed electrical stimulation of the heart. The diagnosis was made because of the classic ECG showing a coved-type ST segment elevation in precordial leads V1 to V3. Of the 443 individuals, 180 had developed spontaneous symptoms (syncope or aborted sudden cardiac death) and 263 were asymptomatic at the time the diagnosis was made. The ventricular stimulation protocol included a minimum of two basic pacing cycle lengths with two ventricular premature beats from the right ventricular apex. A sustained ventricular arrhythmia was induced in 217 cases (49%). Symptomatic patients were more frequently inducible [126/180 (70%)] than asymptomatic individuals [91/263 (34%); P = 0.0001]. Males were more frequently inducible than females (54% vs 32%, P < 0.0001). Inducible individuals had a longer HV interval than noninducible patients (50 +/- 12 msec vs 46 +/- 10 msec, P < 0.002). HV interval and number of premature beats needed to induce VF were not related to outcome. Inducibility was statistically a powerful predictor of arrhythmic events during follow-up. Sixty of 217 inducible patients (28%) had spontaneous ventricular fibrillation compared with 5 of 221 noninducible patients (2%; P = 0.0001).</AbstractText>Inducibility of sustained ventricular arrhythmias during programmed ventricular stimulation of the heart is a good predictor of outcome in Brugada syndrome.</AbstractText> |
2,427 | Cardioprotection with sildenafil, a selective inhibitor of cyclic 3',5'-monophosphate-specific phosphodiesterase 5. | The effects of sildenafil (Viagra), a specific inhibitor of phosphodiesterase 5, on ischemic myocardium was examined using an isolated rat heart model. Rats were pretreated with sildenafil at doses ranging from 0.001 mg to 0.5 mg/kg body weight. After 60 min, isolated hearts were subjected to ischemia for 30 min followed by 2 h of reperfusion. The results demonstrated that at 0.05 mg/kg (and to some extent at 0.01 mg/kg), sildenafil provided significant cardioprotection as evidenced by improved ventricular recovery, a reduced incidence of ventricular fibrillation and decreased myocardial infarction. At higher doses, it caused a significant increase in the incidence of ventricular fibrillation while at very low doses it had no effect on cardiac function. As expected, sildenafil increased cyclic 3',5'-monophosphate (cGMP) content in the heart. The results demonstrate for the first time that within a narrow dose range, sildenafil can protect the heart from ischemia/reperfusion injury, probably through a cGMP-signaling pathway. |
2,428 | [Study on the compatibility of composite herbal medicines of the lingguizhugan decoction]. | To study the compatibility of composite herbal medicines of the Ling Gui Zhu Gan Decoction.</AbstractText>Ethanol extract test solutions of the different combinations were prepared according to the orthogonal layout L16(4(5)). Pharmacologic experiments, such as the time of surviving of mice in shortage of oxygen in regular air pressure, the antagonizing effect on arrhythmia induced by chloroform and diuresis were carried out with the solutions. Variance analysis, canonical correlation and stepwise regression analysis were applied to interrelate the amount of each drug and the pharmacologic data.</AbstractText>The results confirmed that Fuling and Guizhi are the basis, while Baizhuand Gancao are the adjuvans, which is conformed to the theory of TCM.</AbstractText>This study provides a significant try for studying the compatibility of composite herbal medicines.</AbstractText> |
2,429 | Defibrillatory action of glibenclamide is independent from ATP-sensitive K+ channels and free radicals. | This study investigated whether glibenclamide exerts a defibrillatory action and if this action is mediated by a blockade of ATP-sensitive K+ channels (K(ATP)) or by an anti-free radical mechanism. Aerobically perfused isolated rat hearts were subjected to 10 min of pacing-induced ventricular fibrillation (VF) followed by 10 min of perfusion without pacing (post-VF period), in the presence of solvent (controls), 1 microM K(ATP) blocker glibenclamide, 10 microM K(ATP) opener cromakalim, and their combination, respectively. In controls, pacing-induced VF caused a significant deterioration in cardiac function in the post-VF period. Spontaneous defibrillation was 42%. Glibenclamide improved post-VF cardiac function and resulted in 100% (P < 0.05) spontaneous defibrillation. Cromakalim did not significantly affect post-VF cardiac function and the incidence of spontaneous defibrillation as compared with controls. The combination of the compounds improved cardiac function and resulted in 83% (P < 0.05) spontaneous defibrillation. In separate experiments, 2,5-dihydroxybenzoic acid formation in the perfusate as a marker of hydroxyl radical formation was measured by high-performance liquid chromatography and cardiac superoxide production was assessed by lucigenin-enhanced chemiluminescence during pacing-induced VF. Glibenclamide did not affect hydroxyl radical generation or myocardial superoxide content during VF. The conclusion is that glibenclamide exerts a defibrillatory action and improves post-VF cardiac function in rat hearts and these effects are independent from K(ATP) and free radicals. |
2,430 | Modulation of ventricular fibrillation in isolated perfused heart by dofetilide. | The authors studied the involvement of IKr potassium current in ventricular fibrillation during perfusion. Electrophysiologic parameters were measured before and after dofetilide administration (2.5, 7.5, and 12.5 x 10-7 M, n = 8) in isolated perfused feline hearts. During pacing, these parameters included epicardial conduction time, refractoriness, and the fastest rate for 1:1 pacing/response capture. During 8 minutes of electrically induced tachyarrhythmias, they included heart rate and normalized entropy reflecting the degree of organization. In all groups, arrhythmia rate was slower in the right ventricle than in the left ventricle. Dofetilide decreased the arrhythmia rate more than it increased organization, reduced its maintenance, or increased difficulty in initiation. Refractoriness was prolonged in a reverse use-dependent way which was less than 1:1 pacing/response capture. Unexpectedly, a moderate prolongation of conduction time was observed. Inverse correlation was found between the arrhythmia rate and changes in refractoriness and conduction time and between the degree of organization and refractoriness (both ventricles) and conduction time (right ventricle). Dofetilide, which intensively blocks IKr current and unexpectedly suppressed conduction, has different quantitative effects on fibrillation features. These changes in fibrillation suggest that these effects are mainly associated with refractoriness prolongation and do not seem to be attenuated by conduction suppression. |
2,431 | Late outcomes of mitral valve repair for floppy valves: Implications for asymptomatic patients. | We sought to evaluate the long-term results of mitral valve repair in patients with mitral regurgitation caused by floppy mitral valves and compare the outcomes of asymptomatic patients with those of symptomatic patients.</AbstractText>A retrospective review of 488 consecutive patients who had mitral valve repair for floppy mitral valve disclosed 199 patients who were asymptomatic or had minimal symptoms and 289 patients who were symptomatic at the time of the operation. Asymptomatic patients were younger, had better ventricular function, had a lower incidence of coronary artery disease, and had higher rates of atrial fibrillation than symptomatic patients.</AbstractText>Survival at 15 years was 61% for all patients. Survival was 76% for asymptomatic patients, which was identical to that for the general population matched for age and sex, whereas the survival of symptomatic patients was 53% and significantly lower than that of the general population. Cox regression analyses validated by means of bootstrap methodology identified the following predictors of late death: age by increments of 5 years (risk ratio = 1.2), New York Heart Association functional classes 3 and 4 (risk ratio = 3.0), left ventricular ejection fraction of less than 40% (risk ratio = 2.7), preoperative stroke or transient ischemic attack (risk ratio = 3.1), previous cardiac operation (risk ratio = 4.6), and severe chronic obstructive pulmonary disease (risk ratio = 3.1). Freedom from reoperation at 15 years was 91%, and it was similar for asymptomatic and symptomatic patients. Freedom from mitral regurgitation of greater than 2+ at 15 years was 85% for all patients, 96% for asymptomatic patients, and 76% for symptomatic patients.</AbstractText>This study supports the recommendation of surgical intervention in asymptomatic patients with mitral regurgitation caused by a floppy mitral valve if mitral valve repair is feasible and associated with low operative mortality and morbidity.</AbstractText> |
2,432 | Cardiopulmonary Resuscitation Guidelines 2000 update: what's happened since? | To examine the literature for new resuscitation science since the publication of the Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiac Care.</AbstractText>The two and a half years since the publication of the Guidelines 2000 have seen the advent of a number of new and important resuscitation studies. Such studies highlight the importance of simplification of cardiopulmonary resuscitation techniques and guidelines, including the elimination of the layperson pulse check and the need for a simple form of basic life support cardiopulmonary resuscitation that decreases interruptions of chest compressions. Automatic external defibrillators, even in the hands of nontraditional first responders, are effective and safe. A second prospective, randomized clinical trial of amiodarone for refractory ventricular fibrillation has again shown positive results in improving survival to hospital admission. Finally, mild hypothermia appears to be the first effective therapy at decreasing central nervous system injury when administered after resuscitation.</AbstractText>In this report, we review these new studies and discuss how they corroborate or alter the published 2000 guidelines.</AbstractText> |
2,433 | Monitoring during cardiac arrest: are we there yet? | Advancements in electronic data acquisition have translated into improved monitoring of victims of cardiac arrest, but initial techniques remain direct observation of pulses and respirations. The most essential monitor continues to be the electrocardiogram. However, monitoring diastolic blood pressure, myocardial perfusion pressure, and end-tidal carbon dioxide are extremely useful. Most of the current research on monitoring during cardiopulmonary resuscitation focuses on methods for analyzing ventricular fibrillation waveforms. By analyzing the waveform, defibrillation shocks may be delivered at the time when the chance of success is optimal. Low-amplitude and low-frequency fibrillation waveforms are associated with increased rates of asystole and pulseless electrical activity after defibrillation. Methods of analyzing the ventricular fibrillation waveform include measuring the amplitude and frequency and combining the contributions of amplitude and frequency by various methods to improve discrimination. Other types of monitoring being studied for their usefulness during cardiac arrests include sonography, Bispectral Index monitoring, tissue carbon dioxide monitors, and pupil observation. The test of these monitoring techniques is ultimately their ability to improve patient survival to hospital discharge, which is a major challenge for resuscitation researchers. |
2,434 | Myocardial protection during resuscitation from cardiac arrest. | Successful treatment of cardiac arrest requires that an electrically stable and mechanically competent cardiac activity be promptly reestablished. However, many interventions used to attempt to reestablish cardiac activity may also inflict additional myocardial injury and, in turn, compromise resuscitability. In this review, we examine mechanisms of such myocardial injury and discuss potential new strategies for myocardial protection during resuscitation from cardiac arrest.</AbstractText>Efforts are currently directed at understanding underlying mechanisms of myocardial injury associated with current resuscitation methods, with the purpose of developing alternative approaches that are safer and more effective. These new approaches include, among others, the development of alternative low-energy defibrillation waveforms, methods for optimizing the timing for attempting defibrillation, and the use of vasopressor agents devoid of beta-agonist effects. There is also interest in understanding the role that activation of pathways of ischemic and reperfusion injury could play during resuscitation from cardiac arrest. To this end, activation of the sarcolemmal sodium-hydrogen exchanger isoform 1 seems to play an important role. Other potentially important pathways involve adenosine metabolism, activation of potassium ATP channels, and generation of oxygen radical species. These pathways may become novel pharmacologic targets for cardiac resuscitation.</AbstractText>The growing body of research in these areas is bringing hope that in a not so distant future new approaches and interventions for cardiac resuscitation could be available for resuscitation of humans in various clinical settings.</AbstractText> |
2,435 | Strategies for reversing shock-resistant ventricular fibrillation. | Shock-resistant ventricular fibrillation is defined as ventricular fibrillation persisting after three defibrillation attempts. In approximately 10 to 25% of all cardiac arrests, shock-resistant ventricular fibrillation develops, and 87 to 98% of these patients die.</AbstractText>In the treatment of shock-resistant ventricular fibrillation, defibrillation using biphasic waveforms is considered as an intervention of choice. Intravenous amiodarone is also acceptable, safe, and useful, based on evidence from two randomized clinical trials. Intravenous vasopressin is acceptable and probably safe and useful, but the evidence supporting this recommendation is coming from a small, randomized clinical trial. Procainamide is acceptable but not recommended. In the presence of acute myocardial infarction and recurrent ventricular fibrillation, if all other therapies fail, beta-blockers can be considered. Magnesium, lidocaine, and bretylium are not recommended in the treatment of shock-resistant ventricular fibrillation.</AbstractText>Biphasic defibrillation and intravenous amiodarone are useful in shock-resistant ventricular fibrillation.</AbstractText> |
2,436 | Combined cardiac resynchronization and implantable cardioversion defibrillation in advanced chronic heart failure: the MIRACLE ICD Trial. | Cardiac resynchronization therapy (CRT) through biventricular pacing is an effective treatment for heart failure (HF) with a wide QRS; however, the outcomes of patients requiring CRT and implantable cardioverter defibrillator (ICD) therapy are unknown.</AbstractText>To examine the efficacy and safety of combined CRT and ICD therapy in patients with New York Heart Association (NYHA) class III or IV congestive HF despite appropriate medical management.</AbstractText><AbstractText Label="DESIGN, SETTING, AND PARTICIPANTS" NlmCategory="METHODS">Randomized, double-blind, parallel-controlled trial conducted from October 1, 1999, to August 31, 2001, of 369 patients with left ventricular ejection fraction of 35% or less, QRS duration of 130 ms, at high risk of life-threatening ventricular arrhythmias, and in NYHA class III (n = 328) or IV (n = 41) despite optimized medical treatment.</AbstractText>Of 369 randomized patients who received devices with combined CRT and ICD capabilities, 182 were controls (ICD activated, CRT off) and 187 were in the CRT group (ICD activated, CRT on).</AbstractText>The primary double-blind study end points were changes between baseline and 6 months in quality of life, functional class, and distance covered during a 6-minute walk. Additional outcome measures included changes in exercise capacity, plasma neurohormones, left ventricular function, and overall HF status. Survival, incidence of ventricular arrhythmias, and rates of hospitalization were also compared.</AbstractText>At 6 months, patients assigned to CRT had a greater improvement in median (95% confidence interval) quality of life score (-17.5 [-21 to -14] vs -11.0 [-16 to -7], P =.02) and functional class (-1 [-1 to -1] vs 0 [-1 to 0], P =.007) than controls but were no different in the change in distance walked in 6 minutes (55 m [44-79] vs 53 m [43-75], P =.36). Peak oxygen consumption increased by 1.1 mL/kg per minute (0.7-1.6) in the CRT group vs 0.1 mL/kg per minute (-0.1 to 0.8) in controls (P =.04), although treadmill exercise duration increased by 56 seconds (30-79) in the CRT group and decreased by 11 seconds (-55 to 12) in controls (P<.001). No significant differences were observed in changes in left ventricular size or function, overall HF status, survival, and rates of hospitalization. No proarrhythmia was observed and arrhythmia termination capabilities were not impaired.</AbstractText>Cardiac resynchronization improved quality of life, functional status, and exercise capacity in patients with moderate to severe HF, a wide QRS interval, and life-threatening arrhythmias. These improvements occurred in the context of underlying appropriate medical management without proarrhythmia or compromised ICD function.</AbstractText> |
2,437 | Enalapril decreases the incidence of atrial fibrillation in patients with left ventricular dysfunction: insight from the Studies Of Left Ventricular Dysfunction (SOLVD) trials. | Atrial fibrillation (AF) is frequently encountered in patients with heart failure (HF) and is also a predictor of morbidity and mortality in this population. Recent experimental studies have shown electrical and structural atrial remodeling with increased fibrosis in animals with HF and have suggested a preventive effect of ACE inhibitors (ACEi) on the development of AF. To verify the hypothesis that ACEi prevent the development of AF in patients with HF, we conducted a retrospective analysis of the patients from the Montreal Heart Institute (MHI) included in the Studies Of Left Ventricular Dysfunction (SOLVD).</AbstractText>Clinical charts were reviewed and serial ECGs interpreted by a single cardiologist blinded to drug allocation. Patients with AF or flutter on the baseline ECG were excluded. Baseline characteristics were obtained from the SOLVD databases. The mean follow-up was 2.9+/-1.0 years. Of the 391 patients randomly assigned at MHI, 374 were in sinus rhythm at the time of random assignment, with 186 taking enalapril and 188 taking placebo. Baseline characteristics were similar in the two groups except for a higher incidence of previous myocardial infarction in the enalapril group. Fifty-five patients had AF during the follow-up: 10 (5.4%) in the enalapril group and 45 (24%) in the placebo group (P<0.0001). By Cox multivariate analysis, enalapril was the most powerful predictor for risk reduction of AF (hazard ratio, 0.22; 95% CI, 0.11 to 0.44; P<0.0001).</AbstractText>Treatment with the ACEi enalapril markedly reduces the risk of development of atrial fibrillation in patients with left ventricular dysfunction.</AbstractText> |
2,438 | Results of early defibrillation program in Piacenza. | Defibrillation as soon as possible is the mainstay of modern emergency system in the treatment of sudden cardiac death. The emergency medical system (EMS) should be integrated with first responders in the community trained to use the semiautomatic external defibrillators (AED). Piacenza Progetto Vita is a European project of early defibrillation through lay first responders integrated within the EMS. After 22 months of the project 1 285 first responders were trained to the use of AED. Survival from sudden cardiac arrest significantly increased (from 3.3% to 10.5%, p<0.01). In particular in the group of patients treated by first responders survival from ventricular fibrillation was 44.1% vs 21.2% of EMS treated group (p < 0.05). A simple training for the use of AED without cardiopulmonary resuscitation training increased survival and created a group of competent AED operator integrated within the EMS. |
2,439 | Potent antifibrillatory effects of intrapericardial nitroglycerin in the ischemic porcine heart. | We investigated the antiarrhythmic effects of intrapericardial nitroglycerin (NTG) during acute myocardial ischemia in the porcine heart.</AbstractText>Nitroglycerin is a nitric oxide donor that exerts potent effects on the cardiovascular system. Intrapericardial administration allows investigation of pharmacologic actions on cardiac tissue in an in vivo system while minimizing the confounding influences of systemic effects.</AbstractText>In 29 closed-chest pigs, myocardial ischemia was induced by intraluminal balloon occlusion of the left anterior descending coronary artery. Arrhythmia incidence was monitored during 5-min balloon inflations performed without drug and at 15, 45, 75, and 105 min after NTG (4,000 microg bolus) administered by percutaneous transatrial access into the pericardial space. Electrocardiograms were monitored for ischemia-induced T-wave alternans (TWA), a marker of electrical instability. The antiadrenergic potential of NTG was investigated by examining the drug's suppression of dobutamine-induced increase in myocardial contractility.</AbstractText>Control coronary artery occlusion provoked ventricular fibrillation (VF) in all animals. Intrapericardial NTG suppressed VF at 45 min in all six pigs (p < 0.05) and reduced TWA across a parallel time course (from 459.1 +/- 144.4 microV before drug to 42.22 +/- 13.96 microV at 45 min, p = 0.047). The antifibrillatory effect occurred as early as 15 min and persisted for up to 75 min. Augmentation of maximum of the first time derivative of left ventricular pressure by dobutamine was blunted by intrapericardial NTG (from 3,999 +/- 196 mm Hg/s before NTG to 3,543 +/- 220 mm Hg/s at 15 min, p = 0.012).</AbstractText>Intrapericardial NTG exerts a robust antifibrillatory action. Potential mechanisms include reduction in electrical instability and blunting of adrenergic effects.</AbstractText> |
2,440 | Concomitant recovery of atrial mechanical and endocrine function after cardioversion in patients with persistent atrial fibrillation. | The purpose of this study was to evaluate left atrial mechanical function recovery and plasma atrial natriuretic peptide (ANP) release following successful cardioversion of persistent atrial fibrillation (AF).</AbstractText>Atrial fibrillation is characterized by functional deterioration, loss of atrial contraction, and elevation of plasma ANP levels. The response of ANP release toward atrial mechanical function after cardioversion of AF has not been fully examined.</AbstractText>We examined 29 patients with successfully cardioverted persistent AF in whom sinus rhythm was maintained for at least 30 days after cardioversion. We assessed mechanical function of the left atrium at 24 h and 7 and 30 days after cardioversion and evaluated plasma ANP level at the same time. Atrial mechanical function was assessed during echocardiographic examination by means of the peak velocity of the transmitral A-wave, early transmitral to atrial flow velocity ratio, and atrial filling fraction (AFF). The plasma ANP level was determined by the radioimmunoassay method.</AbstractText>Plasma ANP levels were significantly reduced from 59.4 +/- 16.6 pg/ml to 31.1 +/- 9.2 pg/ml at 24 h after successful cardioversion. Within 30 days, we noted progressive improvement of atrial systolic function (increase in AFF from 21% to 31%, p < 0.05). At the same time, plasma ANP levels gradually increased from 31.1 +/- 9.2 pg/ml at 24 h to 36.9 +/- 12.8 pg/ml on day 30 following cardioversion (p < 0.05).</AbstractText>Plasma ANP levels significantly decreased in patients with persistent AF after successful cardioversion. In the 30 days after cardioversion, gradual elevation of plasma ANP concentration was observed concomitantly with an increase of AFF. Plasma ANP release after successful cardioversion of persistent AF might be due to recovery of atrial mechanical function.</AbstractText> |
2,441 | The Australian Intervention Randomized Control of Rate in Atrial Fibrillation Trial (AIRCRAFT). | The Australian Intervention Randomized Control of Rate in Atrial Fibrillation Trial was a multicenter trial of atrioventricular junction ablation and pacing (AVJAP) compared with pharmacologic ventricular rate control (medication [MED]) in patients with mild to moderately symptomatic permanent atrial fibrillation (AF).</AbstractText>There have been very few prospective randomized trials, undertaken in highly symptomatic patients, comparing AVJAP with pharmacologic methods of ventricular rate control for patients with permanent AF.</AbstractText>There were 99 patients (70 men, mean age 68 +/- 8.6 years) at five centers. Forty-nine patients were randomized to AVJAP while 50 patients were randomized to pharmacologic control. The primary end point was cardiac function measured by echocardiography and exercise tolerance. The secondary end points were ventricular rate control, evaluated by 24-h ambulatory electrocardiographic monitoring, and quality of life. Data were collected at randomization and then at one month, six months, and 12 months post-randomization.</AbstractText>At 12 months follow-up there was no significant difference in left ventricular ejection fraction (AVJAP: 54 +/- 17%; MED: 61 +/- 13% [p = ns]) or exercise duration on treadmill testing (AVJAP: 4.1 +/- 2 min; MED: 4.6 +/- 2 min [p = ns]); however, the peak ventricular rate was lower in the AVJAP group during exercise (112 +/- 17 beats/min vs. 153 +/- 36 beats/min, p < 0.05) and activities of daily life (117 +/- 16 beats/min vs. 152 +/- 37 beats/min, p < 0.05). The CAST quality-of-life questionnaire revealed that patients in the AVJAP group had fewer symptoms at six months (p = 0.003) and at 12 months (p = 0.004). The observed relative risk reduction in symptoms at 12 months was 18%. Global subjective semiquantitative measurement of quality of life using the "ladder of life" revealed that the AVJAP group reported a 6% better quality of life at six months (p = 0.011).</AbstractText>In this trial, AVJAP for patients with mild to moderately symptomatic permanent AF did not worsen cardiac function during long-term follow-up, and quality of life was improved.</AbstractText> |
2,442 | Amiodarone for pharmacological cardioversion of recent-onset atrial fibrillation. | The efficacy and safety of amiodarone for pharmacological cardioversion of recent-onset atrial fibrillation was examined by reviewing the trials on the subject identified through a comprehensive literature search. Amiodarone has been used both intravenously (i.v.) and orally for the pharmacological cardioversion of recent-onset atrial fibrillation. Intravenous amiodarone has been used as a bolus only or as a bolus followed by a continuous i.v. infusion until conversion or up to 24 h. The dose of i.v. bolus given ranged from 3 to 7 mg/kg body weight and that of infusion from 900 to 3000 mg/day. The efficacy reported is 34-69% with the bolus only regimens, and 55-95% with the bolus followed by infusion regimens. Only the higher dose (>1500 mg/day) amiodarone is superior to placebo in converting recent-onset atrial fibrillation to sinus rhythm. The highest 24-h conversion rates have been reported with the i.v. regimen of 125 mg/h until conversion or a maximum of 3 g and the oral regimen of 25-30 mg/kg body weight administered as a single loading-dose (>90% and >85%, respectively). Most of the conversions occur after 6-8 h of the initiation of therapy. Predictors of successful conversion are shorter duration of atrial fibrillation, smaller left atrial size, and higher amiodarone dose. Amiodarone is not superior to the other antiarrhythmic drugs conventionally used for the pharmacological cardioversion of recent-onset atrial fibrillation but is relatively safe in patients with structural heart disease and in those with depressed left ventricle function. Therefore, amiodarone could be used particularly in patients with structural heart disease and in those with left ventricular systolic dysfunction as the use of class IC drugs, propafenone and flecainide, for cardioversion of atrial fibrillation is contraindicated in such patients. |
2,443 | Atrial stunning: determinants and cellular mechanisms. | Atrial stunning is a transient depression of atrial and atrial-appendage mechanical function after successful cardioversion of atrial fibrillation compared with its precardioversion state.</AbstractText>Atrial stunning associated with different methods of cardioversion of atrial fibrillation and the determinants and cellular mechanisms of atrial stunning were elaborated by thoroughly examining the studies on the subject identified through a comprehensive literature search.</AbstractText>Atrial stunning has been reported with all methods of cardioversion of atrial fibrillation, including transthoracic electrical, low-energy internal electrical, pharmacological, and spontaneous. It is a function of the underlying atrial fibrillation becoming apparent at the restoration of sinus rhythm, regardless of the method used for conversion. Unsuccessful cardioversion does not result in atrial stunning. The duration of the preceding atrial fibrillation, atrial size, and underlying structural heart disease are the determinants of atrial stunning. A shorter duration of atrial fibrillation and smaller atrial diameters are associated with a relatively less severe stunning, lasting for a shorter duration. Atrial stunning after cardioversion of atrial fibrillation of <1 week usually resolves within 24 hours, and atrial stunning after cardioversion of chronic atrial fibrillation usually resolves within 4 weeks. Tachycardia-induced atrial cardiomyopathy, atrial cytosolic calcium alterations with down-regulation of the L-type Ca2+ channels and up-regulation of the Na+/Ca2+ exchanger, atrial hibernation with myocyte dedifferentiation and myolysis, and atrial fibrosis are the suggested mechanisms underlying atrial stunning. Atrial stunning determines the risk of postcardioversion thrombus formation in atria and atrial appendages, the duration of postcardioversion anticoagulation therapy, the recovery of the atrial contribution to the ventricular function, and the functional recovery of the patients after successful cardioversion of atrial fibrillation.</AbstractText> |
2,444 | Quality of life evidence in the management of the individual patient with atrial fibrillation. | It is remarkable that in patients with paroxysmal AF not sufficiently controlled by pharmacological therapy, ablation and pacemaker treatment is highly effective and superior to drug therapy in controlling symptoms and improving quality of life. The discontinuation of drug therapy exposes patients to further recurrences of paroxysmal AF and the risk of developing permanent AF. However, both pharmacological and electrical treatment can enhance quality of life in AF patients. Long-term survival after ablation of the atrioventricular node and implantation of a permanent pacemaker in patients with AF is similar for AF patients whether they receive ablation or drug therapy; i.e. control of the ventricular rate by ablation of the atrioventricular node and permanent pacing do not adversely affect long-term survival. |
2,445 | Utility of patient-activated cardiac event recorders in the detection of cardiac arrhythmias. | Patient-activated event recorders are useful for the diagnosis of arrhythmia in patients with palpitation and presyncope. However, the utility of event recorders in patients suspected of arrhythmia but presenting with other symptoms is not clear. Furthermore, the factors influencing their utility have not been evaluated.</AbstractText>Event recorder reports of six hundred and sixty consecutive patients referred due to clinical suspicion of cardiac arrhythmia were reviewed. We divided symptoms into four groups: palpitation, presyncope, chest tightness, and dyspnea. We calculated the diagnostic yield according to patients' symptoms reported on the record, and analyzed the factors affecting the utility of event recorders.</AbstractText>The overall diagnostic yield was 64%, and those of palpitation, presyncope, chest tightness, and dyspnea were 66%, 57%, 51% and 60%, respectively. The most common five findings in our patients were sinus rhythm (36%), sinus tachycardia (30%), atrial premature complex (14%), ventricular premature complex (12%), and atrial fibrillation/atrial flutter (7%). The recording duration (8 +/- 4 days) was short in the present study, but the overall diagnostic yield was similar to those of previous ones. Women had lower diagnostic yields than men, especially in atrial flutter-fibrillation. The diagnostic yield was not influenced by age, ordered doctors, or history of cardiovascular disease. CONCLUSIONS; Patient-activated event recorders provided a good diagnostic yield in patients with different presentations of cardiac arrhythmia, and women had lower diagnostic yield in atrial flutter-fibrillation.</AbstractText> |
2,446 | [Systemic embolism after reversion to sinusal rhythm of persistent atrial flutter]. | The incidence of embolism in atrial flutter has been underestimated in the routine clinical practice.</AbstractText>In this study the incidence of thromboembolic events after restoration of sinus rhythm (by catheter ablation or cardioversion) was compared in two groups of consecutive patients, with a different anticoagulation protocol. A total of 169 patients were evaluated. A first retrospective analysis of 79 non anticoagulated patients (group I). A second prospective group of 90 patients who were treated with an anticoagulation protocol (group II) similar to that for patients with atrial fibrillation. All had typical atrial flutter of at least one month's duration before the procedure.</AbstractText>The mean age of patients in group I was 61 12 years and the mean left ventricular ejection fraction was 57 6%. Patients in group II had a mean age of 61 10 years and the mean left ventricular ejection fraction was 56 9%. No differences were observed regarding prevalence of structural cardiopathy, arterial hypertension, diabetes mellitus, left ventricular dysfunction, atrial size or atrial fibrillation between the two groups of patients. Four patients in the retrospective analysis (5%) had an embolic event associated with the procedure, compared with 0 (0%) in the group of patients treated with the anticoagulation protocol. The efficient anticoagulation was associated with a lower risk of thromboembolic events (p < 0.05).</AbstractText>The incidence of embolic events after reversion to sinusal rhythm of persistent atrial flutter can be decreased. These patients should follow the same recommendations of anticoagulation that apply for patients with persistent atrial fibrillation that are going to be reverted to sinus rhythm.</AbstractText> |
2,447 | Significance of the morphological patterns of electrograms recorded during ventricular fibrillation: an experimental study. | Mapping techniques are used to study the significance of the morphological patterns of the electrograms (EGMs) obtained during VF in an experimental model. In 24 isolated rabbit heart preparations recordings were made of activation during VF using a multiple electrode (121 unipolar electrodes) positioned on the lateral wall of the left ventricle. Three types of activation maps were selected: (A) with functional block of an activation front; (B) with epicardial breakthrough; and (C) with a single broad wavefront without block lines. The EGMs were classified as negative (Q), positive-negative with a predominance of the negative (rS) or positive wave (Rs), and positive (R). In 60 type A maps the morphology in the zone limiting the block line corresponded to an R wave in 55 (92%) cases and to Rs in 5 (8%) cases. In 67 type B maps, the EGM in the earliest activation zone most often showed Q wave morphology (48 [72%] cases), followed by rS (18 [27%] cases), and Rs morphology (1 [1%] case); in no case was R wave morphology seen. Finally, in 78 type C maps the morphology corresponded to a Q wave in 15 (19%) cases, rS in 38 (49%), Rs in 24 (31%), and R in a 1 (1%) case. The differences between the three types of maps were significant (P < 0.0001). Q wave EGM sensitivity for indicating the existence of an epicardial breakthrough pattern was 72%, with a specificity of 89%, and positive and negative predictive values of 76% and 87%, respectively. R wave EGM sensitivity for indicating the existence of conduction block was 92%, with a specificity of 99%, and positive and negative predictive values of 98% and 97%, respectively. R wave morphology is highly sensitive and specific for indicating conduction block. EGM recordings with initial positivity predominance are infrequent in the earliest activation zones of epicardial breakthrough during VF. The recording of the EGM with Q wave morphology indicates centrifugal activation from the explored zone. |
2,448 | Effects of sulfonylurea hypoglycemic agents and adenosine triphosphate dependent potassium channel antagonists on ventricular arrhythmias in patients with decompensated heart failure. | Hypoglycemic sulfonylureas block cardiac ATP-sensitive potassium channels (K(ATP)). The opening of these channels in cardiomyocytes can induce arrhythmias. In animal studies, sulfonylureas exert an antiarrhythmic effect on the ischemic myocardium, but data on human arrhythmic events are lacking. The study population included 207 patients (age 61 +/- 14 years) admitted for decompensated CHF. The severity of ventricular arrhythmias was assessed by 24-hour Holter monitoring. None of the patients were on parenteral vasoactive therapy or antiarrhythmics during Holter recording. Diabetic patients comprised 48% of the study population, and 34% of diabetic patients were prescribed sulfonylureas. The mean hourly ventricular pairs (3.6 +/- 0.5 vs 1.8 +/- 0.3, P = 0.03), the mean hourly repetitive ventricular beats (5.7 +/- 1.0 vs 2.6 +/- 0.1, P = 0.03), and the frequency of ventricular tachycardia episodes per 24 hours (4.7 +/- 0.8 vs 2.2 +/- 0.4, P = 0.03) were significantly lower in patients with diabetes who were receiving sulfonylureas compared with nondiabetics. No significant difference occurred between patients with diabetes who were not receiving sulfonylureas and nondiabetic patients. Multivariate regression revealed a negative independent relationship between sulfonylurea therapy and hourly ventricular pairs (P = 0.03), the mean hourly repetitive ventricular beats (P = 0.03), and ventricular tachycardia episodes (P = 0.04). In a multiple logistic regression, sulfonylurea therapy was a negative predictor of repetitive ventricular beats (P = 0.01, adjusted OR, 0.31; 95% CI, 0.12-0.78). Concomitant sulfonylurea therapy may reduce the occurrence of complex ventricular ectopy in the setting of severe CHF. These results suggest that cardiac K(ATP) channel activation may be involved in the genesis of ventricular arrhythmias in CHF. |
2,449 | Late improvement in ventricular performance following internal cardioversion for persistent atrial fibrillation: an argument in support of concealed cardiomyopathy. | The aim of the study was to evaluate the time course of atrial and ventricular function improvement following internal atrial cardioversion in patients with structural heart disease. Twenty-nine patients with chronic persistent atrial fibrillation (AF) and underlying structural heart disease were followed by serial echocardiograms performed at 1 and 6 hours, 1 day, 1, 2, and 3 weeks, and 1, 2, 3, and 6 months after successful cardioversion. Sinus rhythm was maintained at 6 months in 24 patients. Following cardioversion the time course of left atrial mechanical function (peak A wave, percent A wave filling) differed from that of left ventricular ejection fraction: peak A wave values (cm/s) increased significantly at 1 week (51 +/- 23 vs 35 +/- 15 at 1 hour, P < 0.05), percent A wave filling (%) increased significantly at 2 weeks (34 +/- 12 vs 22 +/- 9 at 1 hour, P < 0.05), whereas left ventricular ejection fraction (%) increased later (at 1 month 60 +/- 14 vs 55 +/- 14 at baseline, P < 0.05 and at 2 months 60 +/- 14 vs 56 +/- 14 at 1 hour, P < 0.05). In conclusion, restoration of sinus rhythm results in an improvement in left ventricular ejection fraction during follow-up, even in patients with structural heart disease without fast ventricular rates at baseline. The dissociation between the time course of atrial and ventricular function improvement suggests that the latter was partly due to regression of a concealed form of cardiomyopathy and/or of a ventricular dysfunction due to chronic AF. |
2,450 | Cycle length-dependent repolarization changes during atrial fibrillation in the Brugada syndrome. | This is a case report of a patient with Brugada syndrome who developed paroxysmal atrial fibrillation. During the episode, beat-to-beat changes in ventricular repolarization were observed. These changes were a paradoxical ST-segment alteration after a short-coupled ventricular beat. These findings, not reported before, may be helpful for the diagnosis of this syndrome. |
2,451 | Two-dimensional analysis of ventricular fibrillation in the guinea pig. | Cardiac arrhythmias are undesirable electrical activity in the heart. Ventricular fibrillation (VF) is a fatal cardiac arrhythmia and is characterized by the breakdown of organized electrical activity in the ventricular myocardium. However, little is known about VF, partially because it is difficult to study and understand an apparently disorganized activity. One method for discovering the nature of VF is processing the epicardial electrical signals by using cardiac mapping techniques. These techniques involve the study of propagation patterns seen in VF. In this project, we used guinea pigs to study the spatial organization of the epicardial electrical activity during VF. VF was induced in 9 open chest guinea pigs and epicardial electrode data were acquired by using a square array of 192 electrodes for 4 seconds every minute. The mean correlation length and dominant frequency were measured in each recorded segment. Correlation length is a measure of the spatial order in a system and dominant frequency is the frequency corresponding to the spectral maximum. The mean correlation length was found to vary between 1-7 mm and the dominant frequency was in the range of 1-14 Hz. This study suggests that guinea pig VF exhibits a level of organization equivalent to or greater than that seen in previous studies. |
2,452 | Increased cycle length variability during ventricular fibrillation: a novel predictor of arrhythmia recurrence. | To evaluate the clinical value of cycle length (CL) variability during ventricular fibrillation (VF), 26 patients who underwent implantable cardioverter defibrillator (ICD) implantation were enrolled. In VF induced for defibrillation testing, mean and SD of VFCL, mean successive differences (MSD) of VFCL, and coefficient of variations of the VFCL (CV(FF)) (SD x 100/mean VFCL) were calculated. During the follow-up period of 20 +/- 2 months, ventricular arrhythmias recurred in 13 patients. MSD and CV(FF) were 31 +/- 3(*) ms and 15.6 +/- 1.3(**) in recurrence group (n = 13), and 17 +/- 2 ms and 9.0 +/-1.1 in non-recurrence group (n = 13) ((*)P <.005, (**)P <.001 vs. nonrecurrence group). Relatively good repeatability of mean VFCL, MSD and CV(FF) in each patient was confirmed by the Bland-Altman method. In VF induced by programmed ventricular stimulation before ICD implantation, MSD and CV(FF) in recurrence group were also increased significantly. Kaplan-Meier estimates revealed that MSD >or= 20 ms and CV(FF) >or= 12 predicted higher arrhythmia recurrence (MSD, P =.039; CV(FF), P =.0069 by the log-rank test). By multivariate analysis, CV(FF) >or= 12 was a significant predictor of recurrent arrhythmic events (P =.019). In conclusion, the CL variability of VF, which was evaluated as MSD and CV(FF), is increased in patients with arrhythmia recurrence. These values may reflect the degree of electrical heterogeneity, and appears to be useful indexes of the future arrhythmic events. |
2,453 | Patients with chronic heart failure encountered in daily clinical practice are different from the "typical" patient enrolled in therapeutic trials. | The aim of this study was to compare the clinical characteristics of patients enrolled in randomized clinical trials on congestive heart failure treatment with those of real-world patients encountered in daily clinical practice.</AbstractText>We searched the Cochrane review methodology, Medline and SilverPlatter databases to obtain the clinical characteristics of both patients enrolled in therapeutic clinical trials and real-world patients with heart failure. We selected 27 clinical trials, and 8 prospective epidemiological studies or registries published between 1987 and 2001 which enrolled 53,859 and 18,207 patients, respectively.</AbstractText>On average, compared to real-world heart failure patients, patients enrolled in clinical trials were younger (63 +/- 10 vs 75 +/- 11 years respectively, p < 0.0001), and more likely to be male (72 vs 54% respectively, p < 0.0001). Clinical trial patients showed a lower ejection fraction (26 +/- 7 vs 38 +/- 15% respectively, p < 0.0001) but a lower prevalence of NYHA functional class III-IV (62 vs 75% respectively, p < 0.0001) than real-world patients. In clinical trial patients, the prevalence of ischemic heart disease (67 vs 42% respectively, p < 0.0001) and a history of previous myocardial infarction (62 vs 42% respectively, p < 0.0001) were higher than in real-world patients. Conversely, the prevalence of chronic atrial fibrillation (12 vs 31% respectively, p < 0.0001) and of diabetes (22 vs 24% respectively, p < 0.02) was lower in trial patients than in real-world patients.</AbstractText>Our data suggest that most clinical trials on congestive heart failure, on which the guidelines for clinical practice are based, have generally included patients who are not representative of the whole spectrum of patients actually managed in clinical practice.</AbstractText> |
2,454 | Survival with full neurologic recovery after prolonged cardiopulmonary resuscitation with a combination of vasopressin and epinephrine in pigs. | We sought to determine the effects of a combination of vasopressin and epinephrine on neurologic recovery in comparison with epinephrine alone and saline placebo alone in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive, every 5 min, either a combination of vasopressin and epinephrine (vasopressin [IU/kg]/epinephrine [ micro g/kg]: 0.4/45, 0.4/45, and 0.8/45; n = 6), epinephrine alone (45, 45, and 200 micro g/kg; n = 6), or saline placebo alone (n = 5). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve the return of spontaneous circulation. Aortic diastolic pressure was significantly (P < 0.01) increased 90 s after each of 3 vasopressin/epinephrine injections versus epinephrine alone versus saline placebo alone (mean +/- SEM: 69 +/- 3 mm Hg versus 45 +/- 3 mm Hg versus 29 +/- 2 mm Hg, 63 +/- 4 mm Hg versus 27 +/- 3 mm Hg versus 23 +/- 1 mm Hg, and 52 +/- 4 mm Hg versus 21 +/- 3 mm Hg versus 16 +/- 3 mm Hg, respectively). Spontaneous circulation was restored in six of six vasopressin/epinephrine pigs, whereas six of six epinephrine and five of five saline placebo pigs died (P < 0.01). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait and was normal 5 days after the experiment in all vasopressin/epinephrine-treated animals. In conclusion, in this porcine model of prolonged CPR, repeated vasopressin/epinephrine administration, but not epinephrine or saline placebo alone, ensured long-term survival with full neurologic recovery.</AbstractText>We present a study to evaluate the effects of a combination of vasopressin and epinephrine during prolonged cardiopulmonary resuscitation on neurological outcome in pigs. We found that all pigs treated with a combination of vasopressin and epinephrine could be resuscitated and had full neurologic recovery observed over an entire period of 5 days.</AbstractText> |
2,455 | [Sudden death in a normal heart. Idiopathic ventricular fibrillation. Review of the literature concerning one case]. | Idiopathic ventricular fibrillation is that which is produced in the absence of structural cardiac disease and of other identifiable causes of ventricular fibrillation such as cardiotoxicity, electrolytical alterations or hereditary predisposition. The case of a healthy male, aged 37, who was asymptomatic until the day he was admitted to hospital where he showed numerous episodes of ventricular fibrillation without any previous triggering, is discussed. In the examination no cause was found to explain this, and an automatic defibrillator was implanted. The requirements for its diagnosis, risk stratification and the usefulness of the tests employed, as well as the treatments proposed are discussed. |
2,456 | [Cardiac arrhythmias during pregnancy--what to do?]. | Atrial premature beats are frequently diagnosed during pregnancy, supraventricular tachycardia (atrial tachycardia, AV nodal reentrant tachycardia, circus movement tachycardia) less frequently. For acute therapy, electrical cardioversion with 50-100 J is indicated in all unstable patients. In stable supraventricular tachycardia, initial therapy includes vagal maneuvers to terminate breakthrough tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the drug of first choice and may safely terminate the arrhythmia. For long-term therapy, beta-blocking agents with beta(1) selectivity are first-line drugs; class Ic agents or the class III drug sotalol represent effective and therapeutic alternatives. Ventricular premature beats are also frequently present during pregnancy and benign in most of the unstable patients; however, malignant ventricular tachyarrhythmias (sustained ventricular tachycardia, ventricular flutter, ventricular fibrillation) are less frequently observed. Electrical cardioversion is necessary in all patients with hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable patients, initial therapy with ajmaline, procainamide or lidocaine is indicated. If prophylactic therapy is needed, beta-blocking agents with beta(1) selectivity are regarded as drugs of first choice. If this therapy proves ineffective, class Ic agents or sotalol can be considered. In patients with syncopal ventricular tachycardia, ventricular fibrillation, ventricular flutter or aborted sudden death, an implantable cardioverter-defibrillator is indicated. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of pregnancy.</AbstractText>The treatment of the pregnant patient with cardiac arrhythmias requires important modifications of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered.</AbstractText> |
2,457 | [Pregnancy and cardiomyopathies]. | This overview on the topic of cardiomyopathy and gestation comprises the diagnostic and therapeutic options of patients with preexistent cardiomyopathies (dilated, hypertrophic, inflammatory, and others) and with cardiomyopathies which have been discovered during or in the 6 months following delivery. CARDIOMYOPATHIES PREEXISTENT BEFORE GESTATION: If cardiomyopathy is present before an intended gestation, the couple should be advised against pregnancy because of the high risk of deterioration both during gestation and peripartum. If pregnancy occurs, according to ESC (European Society of Cardiology) recommendations termination should be advised if the ejection fraction is < 50% and/or the LV dimensions are definitely above normal. If termination is refused, the patient must be checked regularly by both gynecologist and cardiologist, by the latter to perform regular echocardiograms. Termination is not recommended for the hypertrophic (nonobstructive) cardiomyopathies. If atrial fibrillation occurs, anticoagulation with low molecular weight heparin and digoxin and/or Betablockers are recommended for rhythm and rate control. PERIPARTUM CARDIOMYOPATHIES: In peripartum cardiomyopathies, which are discovered clinically postpartum, inflammation of the myocardium sometimes associated with pericarditis is frequently found. For those patients, we recommend heart catheterization with endomyocardial biopsy to allow for the exact diagnosis of the underlying cardiac process (inflammatory and/or viral vs autoreactive myocarditis or noninflammatory or nonviral [= idiopathic] forms). This diagnostic algorithm, which we recommend for any form of dilated cardiomyopathy, bears impact on treatment options beyond the mere heart failure therapy that should be instigated anyhow. |
2,458 | Temporal trends in sudden cardiac arrest: a 25-year emergency medical services perspective. | Little is known about temporal trends in survival and prognostic characteristics of patients with out-of-hospital cardiac arrest treated by emergency medical services (EMS). We hypothesized that an evolving combination of beneficial and adverse factors may contribute to temporal patterns of survival.</AbstractText>We evaluated a population-based cohort of EMS-treated adult patients with cardiac arrest (n=12 591) from 1977 to 2001 in King County, Washington. Time was grouped into an initial 5-year period and 5 successive 4-year periods. We sought to determine the potential impact of temporal changes in prognostic factors typically beyond EMS control termed "fate" factors (for example, patient age) and factors implemented by EMS termed "program" factors (programs of dispatcher-assisted cardiopulmonary resuscitation and basic life support defibrillation). Several characteristics associated with survival changed over time. Observed survival did not change over time among all patients with cardiac arrest (OR=0.98 [0.95, 1.01], trend for each successive time period) and improved over time among patients with witnessed ventricular fibrillation (OR=1.05 [1.01, 1.09]). In models that included all patients with cardiac arrest and controlled for fate factors, advancing time period was associated with an increase in survival (OR=1.08 [1.05, 1.11]). Conversely, in models that controlled for program factors, advancing time period was associated with a decrease in survival (OR=0.95 [0.93, 0.98]). Results were similar among patients with witnessed ventricular fibrillation.</AbstractText>The static temporal pattern of survival from cardiac arrest appeared to result from an evolving balance of prognostic factors. Programs implemented by EMS appeared to counter adverse temporal trends in prognostic factors typically beyond EMS control.</AbstractText> |
2,459 | Nonrheumatic atrial fibrillation and left ventricular hypertrophy in the prognosis of reversible ischaemic neurological deficit. | Nonrheumatic atrial fibrillation (NRAF) and left ventricular hypertrophy (LVH) have long been recognised as risk factors for cerebral ischaemia and as predictors of recurrent vascular events. In the present study we aimed at determining the value of NRAF and LVH as predictors of recurrent vascular events in a cohort of patients with a first-ever episode of reversible ischemic neurological deficit (RIND). The study included 54 patients (37 men and 17 women, aged 62 +/- 9.6 yrs) who had suffered RIND; they were followed up for 30 days after the stroke in clinical conditions and for 12 months as outpatients. The patients were studied during the hospital stay by means of routine tests (electrocardiography, standard laboratory tests) and specialised studies (computer tomography, echocardiography). By the end of the one-year outpatient follow up there were 8 (14.8%) recurrent cerebrovascular events. By combining the statistically significant cerebrovascular risk factors (male sex, sudden onset of the event and moderately high systolic and diastolic blood pressure) with factors not reaching statistical significance (LVH, NRAF) we developed a statistically significant prediction model for patients with RIND. |
2,460 | Prognosis of congestive heart failure in patients with normal versus reduced ejection fractions: results from a cohort of 2,258 hospitalized patients. | Patients with congestive heart failure have an annual mortality of 10% to 20% depending on disease severity. Though one third of these patients have normal left ventricular (LV) ejection fraction (EF), their natural history is poorly defined. Small population-based studies have suggested a more benign prognosis for patients with preserved LVEF. However, prognosis in hospitalized patients, who form a higher risk group, is not known.</AbstractText>We investigated the survival patterns of 2,258 patients with a primary hospital discharge diagnosis of congestive heart failure between 1990 and 1999. Survival was analyzed and patients with normal and reduced LVEF were compared.</AbstractText>Their age was 71 +/- 11 years, and 97% were men. There were 1,535 deaths over a mean follow up of 786 days. Of these, 963 (43%) patients had a normal LVEF (>/=55%). Patients with normal LVEF were of the same age as those with reduced LVEF, but had a lower prevalence of atrial fibrillation (20 versus 26%, P =.03), left bundle branch block (2 versus 12%, P <.0001), significant mitral regurgitation (5 versus 31%, P <.0001) and electrocardiographic evidence of myocardial infarction (38 versus 60%, P <.0001). Despite lesser comorbidities, they had a higher mortality hazard, with a 5-year survival of 22% compared with 28% for those with systolic heart failure (P =.007). Proportional hazards model showed presence of normal EF as a categoric variable to be an independent predictor of mortality in those with heart failure after correcting for age and rhythm.</AbstractText>Prognosis of hospitalized patients with congestive heart failure and normal LVEF is worse than those with reduced EF despite lesser comorbidities. Studies addressing optimal management of these patients are warranted.</AbstractText> |
2,461 | Long-term follow-up of single-lead VDD pacing. | Long-term outcomes of single-lead VDD pacing were studied retrospectively and partly prospectively. Records were analysed of 81 patients out of 133 in whom a single-lead VDD pacemaker was implanted between January 1993 and December 1997 and who attended a follow-up clinic more than two years after the implant. Forty-eight of them attended a prospective follow-up 54 +/- 15 months after the implant. Sinus rhythm was present in 91.5% of the patients and atrial fibrillation in the remaining 8.5%. A-V synchronous pacing was documented in 91.9 to 94.9% at different follow-up periods; however, an intermittent asynchronous ventricular (VVI) pacing of more than 10% occurred intermittently in 19.1% of the patients. Chronic sensed P-wave amplitude was significantly lower than the implant P-wave amplitude (by 70%) and did not correlate with the implant amplitude. Postural changes (supine, sitting, standing, with normal breathing and during deep inspiration) did not have a significant impact on sensed P-wave amplitude more than four years after the implant. Rate histograms were remarkably stable over the years, with dominant heart rate 70 to 79 beats per minute observed for 25 to 30% of the monitored periods. Single-lead VDD pacing was found to be a reliable method of long-term physiological pacing in patients with heart block who returned for follow-up. Routine testing more than four years after the implant does not require postural manoeuvres. |
2,462 | Comparative follow up of patients with implanted cardioverter-defibrillators after induction of sustained monomorphic ventricular tachycardias or ventricular fibrillation by programmed stimulation. | To investigate the prognostic value of induced monomorphic ventricular tachycardia (VT) and ventricular flutter or fibrillation (VF) during programmed electrical stimulation in patients with a high risk for sudden arrhythmogenic cardiac death.</AbstractText>Prospective cohort study.</AbstractText>102 patients at high risk for arrhythmogenic sudden cardiac death who received an automated implantable cardioverter-defibrillator (AICD) were evaluated. 56 patients received the AICD for primary prevention and 46 for secondary prevention. 58 patients had induction of a monomorphic VT (VT group) and 44 had induction of a polymorphic VT, ventricular flutter, or ventricular fibrillation (VF group) during programmed electrical stimulation. Average follow up was 20 months in both groups.</AbstractText>Appropriate AICD protocol.</AbstractText>In patients who received the AICD for primary prevention, 16 of 32 patients in the VT group, compared with only four of 24 patients in the VF group, received an appropriate AICD protocol (p = 0.02). In the entire study population, 479 appropriate AICD protocols were recorded in 28 (48%) patients in the VT group and 28 appropriate protocols in 11 (25%) patients in the VF group. Cumulative Kaplan-Meier event-free survival curves were significantly different (p = 0.02).</AbstractText>Induction of VF during programmed electrical stimulation is of no prognostic value even in high risk patients without previously documented ventricular fibrillation.</AbstractText> |
2,463 | Successful resuscitation of a patient with electrical storm. | A 41 year old woman with type 2 diabetes, hypertension, and hyperlipidaemia but no known heart disease received 130 DC shocks for repeated cardiac arrests due to ventricular tachyarrhythmias over 48 hours. She was stabilised by intravenous amiodarone and had a defibrillator implanted. Serial ECGs did not change, but raised troponin I confirmed myocardial infarction as the underlying cause. Electrical storm is an uncommon and dramatic but usually treatable syndrome of recurrent ventricular arrhythmias. Frequent precipitants of electrical storm include recent worsening heart failure, hypokalaemia, hypomagnesaemia and myocardial ischaemia. Amiodarone is the antiarrhythmic agent of choice and implantable cardioverter defibrillator improves long term outcome. |
2,464 | Tedisamil in coronary disease: additional benefits in the therapy of atrial fibrillation? | Atrial fibrillation has recently come into clinical and research focus. In particular, ventricular rate control has been carefully compared with atrial rhythm control. Additionally, the recent discovery of atrial stunning has initiated clinical and research interest in atrial remodeling. Atrial fibrillation is more likely to occur when the atria are damaged by increased fibrosis. The ideal way to prevent atrial fibrillation and the risk of repetition is by tackling the root causes, such as ischemic heart disease, heart failure, and left ventricular hypertrophy. Tedisamil is an unusual antifibrillatory compound that has a novel mechanism of action by inhibiting the transient outward current (Ito) and the repolarizing potassium currents in the sinoatrial node. Tedisamil works acutely against atrial fibrillation. Importantly, atrial fibrillation is often caused by or related to cardiac ischemia, and conversely, ischemia is caused by the increased oxygen demand of atrial fibrillation. Hence, the double properties of tedisamil as a drug that both inhibits atrial fibrillation and acts in an anti-ischemic mode are an attractive basis for future clinical research. |
2,465 | Predicting defibrillation success by 'genetic' programming in patients with out-of-hospital cardiac arrest. | In some patients with ventricular fibrillation (VF) there may be a better chance of successful defibrillation after a period of chest compression and ventilation before the defibrillation attempt. It is therefore important to know whether a defibrillation attempt will be successful. The predictive power of a model developed by 'genetic' programming (GP) to predict defibrillation success was studied.</AbstractText>203 defibrillations were administered in 47 patients with out-of-hospital cardiac arrest due to a cardiac cause. Maximal amplitude, a total energy of power spectral density, and the Hurst exponent of the VF electrocardiogram (ECG) signal were included in the model developed by GP. Positive and negative likelihood ratios of the model for testing data were 35.5 and 0.00, respectively. Using a model developed by GP on the complete database, 120 of the 124 unsuccessful defibrillations would have been avoided, whereas all of the 79 successful defibrillations would have been administered.</AbstractText>The VF ECG contains information predictive of defibrillation success. The model developed by GP, including data from the time-domain, frequency-domain and nonlinear dynamics, could reduce the incidence of unsuccessful defibrillations.</AbstractText> |
2,466 | Age and sex analyses of out-of-hospital cardiac arrest in Osaka, Japan. | To determine effective interventional targets for out-of-hospital cardiac arrests by analyzing the distribution characteristics of arrest patients according to age and sex with special emphasis on ventricular fibrillation (VF).</AbstractText>All patients who suffered out-of-hospital cardiac arrest in Osaka Prefecture, Japan during 2 years, were prospectively recorded based on the Utstein style. The number and the incidence rate of cases of arrest, witnessed arrest, and witnessed VF were evaluated according to age and sex. The percentage of resuscitation attempts in arrest cases was also calculated.</AbstractText>We recorded 10139 consecutive out-of-hospital cardiac arrest cases. Resuscitation was attempted in 97.0% of 10139 and showed no significant differences by age and sex. The incidence rate of cardiac arrests increased exponentially with age. Men showed a significantly higher incidence rate of out-of-hospital arrests than women in every age group. Most of the witnessed VF cases showed cardiac a aetiology and were predominantly observed in men in their 50s, 60s and 70s. The incidence rates of witnessed VF were also greater in them.</AbstractText>Our study provides evidence that there are significant age and sex related epidemiological differences in cardiac arrests and we need to understand them better. Strategies that focus on high yielded patients, those in witnessed VF, should be pursued. These efforts should be expected to yield sex and age related differences in survivors.</AbstractText> |
2,467 | Myocardial injury in children following resuscitation after cardiac arrest. | Myocardial dysfunction occurs immediately after successful cardiac resuscitation. Our purpose was to determine whether measurement of cardiac troponin I in children with acute out-of-hospital cardiac arrest predicts the severity of myocardial injury.</AbstractText>This prospective, observational study was performed in the Pediatric Intensive Care Unit (PICU) on 24 patients following arrest, ranging in age from 8 months to 17 years. Troponin measurements were obtained on admission, and at 12, 24, and 48 h. Transthoracic echocardiograms were performed within 24 h after admission. Survival to hospital discharge was 29% (7/24). The mean age was 5.9+/-4.6 years for survivors and 4.2+/-5.3 years for non-survivors. The median (range) duration of cardiac arrest times for survivors was 6 min (3 to 63 min) versus 34 min (4 to 70 min) for nonsurvivors (P=0.02). Survivors received 1.3+/-2.2 doses of epinephrine (adrenaline) compared with 2.9+/-1.6 doses for non-survivors (P=0.02). Only one patient had ventricular fibrillation and defibrillation was unsuccessful. The ejection fraction for survivors averaged 73.2+/-11.2%, but for nonsurvivors only 55.4+/-19.8% (P=0.04). Ejection fraction correlated inversely with troponin at 12 h (r=-0.54, P=0.01) and at 24 h (r=-0.59, P=0.02). Circumferential fiber shortening for survivors was 37.5+/-7.8 and 25.5+/-10.7% for nonsurvivors (P=0.02). It also correlated inversely with troponin (r=-0.46, P=0.03 for survivors and r=-0.65, P=0.01, for nonsurvivors).</AbstractText>After cardiac arrest and resuscitation in pediatric patients, the severity of myocardial dysfunction was reflected in troponin I levels.</AbstractText> |
2,468 | Frequency of acute coronary syndrome in patients presenting to the emergency department with chest pain after methamphetamine use. | We reviewed the frequency of acute coronary syndrome (ACS) in patients presenting to our emergency department (ED) with chest pain after methamphetamine (MAP) use during a 2-year interval. Thirty-three patients (25 males, 8 females; average age 40.4 +/- 8.0 years) with a total of 36 visits met study inclusion criteria: 1) non-traumatic chest pain, 2) positive MAP urine toxicology screen, 3) admission to "rule-out" myocardial infarction, 4) chest radiograph demonstrating no infiltrates. An ACS was diagnosed in 9 patients (25%). Three patients (8%) (2 ACS and 1 non-ACS) suffered cardiac complications (ventricular fibrillation, ventricular tachycardia, supraventricular tachycardia, respectively). Age, gender, cardiac risk factors, prior coronary artery disease, initial systolic blood pressure and heart rate did not differ significantly in the ACS and non-ACS groups. The initial and subsequent electrocardiograms (EKG) were normal in 1/9 (11%) patients with ACS and 16/27 (59%) without ACS (p < 0.05). Our findings suggest that: 1) ACS is common in patients hospitalized for chest pain after MAP use, and 2) the frequency of other potentially life-threatening cardiac complications is not negligible. A normal EKG lowers the likelihood of ACS, but an abnormal EKG is not helpful in distinguishing patients with or without ACS. |
2,469 | [ECG changes in aortic valve defects]. | ECG is nowadays no longer the dominant way of diagnosing aortic valve diseases. The basis of accurate diagnosis of these diseases is clinical examination, ECHO and catheterization of the heart, which is essential in the great majority of valve diseases, in particular to rule out coronary changes. ECG is however important for the primary evaluation of left ventricular hypertrophy, left ventricular overburdening, for detection of enlargement or overloading of the left atrium. It is irreplaceable for evaluation of impaired rhythm, or impaired conduction of the impulse. Thus we can prove atrial fibrillation, or flutter bundle branch block, disorders of AV conduction (block of AV transmission grade one to three), supraventricular and ventricular extrasystoles etc. Changes of the ECG tracing provide also some information which cannot be obtained by other means. |
2,470 | [Electrocardiographic changes after heart transplantation]. | Electrocardiographic (ECG) changes are described after heart transplantation in almost 75% patients. During the early postoperative period the usual finding are conduction disorders which in 3-5% call for implantation of a pacemaker. The most frequent persisting disorder is bundle branch block which is of clinical importance only when it has a progressive character. The incidence of postoperative atrial fibrillation or flutter is lower as compared with other cardiosurgical operations and their sudden development may be associated with acute rejection. Ventricular arrhythmias develop as a rule as a complication of advanced coronary disease of the graft and are frequently the cause of sudden death. Before the introduction of cyclosporin A a relatively reliable sign of acute rejection was a reduction of the QRS complex voltage. During contemporary treatment ECG changes develop only in severe forms of rejection, incipient changes can be recorded only by an intracardial electrogram. |
2,471 | Sudden death in noncoronary heart disease is associated with delayed paced ventricular activation. | Slowed or delayed myocardial activation and dispersed refractoriness predispose to reentrant excitation that may lead to ventricular fibrillation (VF). Increased ventricular electrogram duration (DeltaED) in response to extrastimuli and increased S1S2 coupling intervals at which electrogram duration starts to increase (S1S2delay) are seen both in hypertrophic cardiomyopathy (HCM) in those at risk of VF and in patients with idiopathic VF (IVF).</AbstractText>DeltaED and S1S2delay have been measured using paced electrogram fractionation analysis in 266 patients with noncoronary heart disease. Of these, one group of 61 patients had a history of VF and included 21 HCM, 17 IVF, 13 long-QT syndrome (LQTS), 5 dilated cardiomyopathy (DCM), and 5 others. These were compared with 205 patients with similar diseases with no VF history (non-VF group) and a control group (n=12) without heart disease. Results from HCM VF patients (DeltaED, 19+/-3.3 ms; S1S2delay, 350+/-9.7 ms) differed sharply from observations in HCM non-VF patients (DeltaED, 7.3+/-1.35 ms; S1S2delay, 312+/-6.7 ms; P<0.001). DCM VF patients had longer delays (DeltaED, 14.3+/-5.9; S1S2delay, 344+/-11.2) than DCM non-VF patients (DeltaED, 5.8+/-1.87 ms; S1S2delay, 311+/-5.7 ms; P<0.001), with major differences also seen comparing LQTS VF (DeltaED, 12.4+/-5.3 ms; S1S2delay, 343+/-13.8 ms) and LQTS non-VF patients (DeltaED, 11.0+/-2.7 ms; S1S2delay, 320+/-5.4 ms; P<0.001). IVF patients had both severely abnormal and normal areas of myocardium.</AbstractText>Slowed or delayed myocardial activation is a common feature in patients with noncoronary heart disease with a history of VF, and its assessment may allow the prospective prediction of VF risk in these patients.</AbstractText> |
2,472 | Inherited arrhythmic disorders in Japan. | The clinical and genetic characteristics of inherited arrhythmic disorders in Japan are briefly summarized. The incidence of hereditary long QT syndrome (LQTS) in Japan seems comparable to that in western countries. The genotypes are mainly LQT1 and LQT2; LQT3 and other types are rare. Mutations found in Japanese LQTS families are mostly novel compared to mutations reported in other countries and in different ethnic populations. Functional assays of the mutants in heterologous expression systems have disclosed novel mechanisms of current suppression in LQT1 and LQT2, and of gain of function in LQT3. Mutations in KCNJ2 may provide a new genotype (LQT7) of LQTS. In addition, mutations or single nucleotide polymorphisms in the channel genes responsible for LQTS (KvLQT1, HERG, and SCN5A) may predispose to drug-induced LQTS. A relatively high prevalence of Brugada syndrome is suspected in the Japanese population, and 1 of approximately 2,000 asymptomatic individuals present Brugada-type ECG changes upon annual examination. Genetic screening of the symptomatic Brugada syndrome and suspected cases has revealed SCN5A mutations in only approximately 12%. Therefore, the genetic basis of the majority of cases is not known. The expressed Na+ current of SCN5A mutant channels showed the phenotype of decreased channel function commonly seen in Brugada mutations. A case of idiopathic ventricular fibrillation was found to have a novel mutation in SCN5A, in which the expressed current showed marked suppression of channel function. |
2,473 | A newly characterized SCN5A mutation underlying Brugada syndrome unmasked by hyperthermia. | Febrile illness has been rarely reported to modulate ST segment elevation in right precordial leads on ECG or even precipitate ventricular fibrillation in patients with Brugada syndrome. We report the case of a patient whose Brugada ECG pattern was unmasked by hyperthermia secondary to acute cholangitis. Serial ECGs showed progressive attenuation of ST segment elevation as body temperature gradually returned to normal. Structural heart disease was ruled out. Intravenous flecainide injection reproduced a less remarkable ST segment elevation. Genetic screening demonstrated a single amino acid substitution (H681P) in the SCN5A gene, thus confirming the diagnosis of Brugada syndrome. In vitro expression of this newly characterized genetic defect revealed novel biophysical abnormalities consisting of a shift in both steady-state activation and inactivation, resulting in a 60% reduction of sodium window current. Thus, SCN5A-H681P mutation induces a significant loss of transmembrane current and is clinically associated with a pathologic phenotype that is elicited by hyperthermia. Overall the observed clinical features are in agreement with previous observations and strongly suggest that fever may be an environmental modifier among Brugada syndrome patients with a detrimental (and possibly arrhythmogenic) effect on cardiac repolarization. |
2,474 | Site-specific arrhythmogenesis in patients with Brugada syndrome. | It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome.</AbstractText>Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29%), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76%). PES at RVA induced VF in only 2 patients (12%), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64% of PVCs occurred at the free-wall region of the RVOT, 18% at the septal region of the RVOT, 9% at RVA, and 9% at LV.</AbstractText>VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.</AbstractText> |
2,475 | Arrhythmia surgery in association with complex congenital heart repairs excluding patients with fontan conversion. | Surgical arrhythmia therapy may be performed for patients failing the catheter ablation approach or incorporated into repair of complex congenital heart disease. Variations in atrial and ventricular anatomy that may limit the catheter approach can be directly addressed surgically assuring lesion depth and continuity of anatomic lines of block. Between July 1992 and August 2002, we performed arrhythmia surgery on 34 patients for refractory atrial (n = 29) or ventricular (n = 5) arrhythmias. Not included in this series are patients who had arrhythmia surgery during Fontan conversion. The majority of patients had various forms of complex congenital heart disease; two had structurally normal hearts. Median age at surgery was 13.0 years (range, 7 days to 45 years). Five patients were infants (mean age, 25 days). Twenty-two patients (65%) had an average of 2.8 previous cardiac procedures; all required resternotomy. Operative mortality was 5.9% (2 of 34 patients) because of low cardiac output in one patient following Mustard takedown and arterial switch operation and in one neonate with Ebstein's anomaly and pulmonary atresia. Ablative surgery for supraventricular tachycardia (atrial re-entry, automatic atrial, atrioventricular nodal re-entry, and atrial fibrillation) had a 93% success rate (25 of 27 patients). Clinical tachycardia recurred in two of 27 surviving patients (7%) with atrial arrhythmia, one after an arrhythmia-free interval of several years. Ventricular tachycardia was inducible postoperatively in two of three patients with ventricular arrhythmias and congenital heart disease. Patient size or anatomic complexity should not be limiting factors in the combined surgical arrhythmia approach. Because older patients undergoing surgical revision of prior surgical repairs of congenital heart disease are at increased risk for the later development of atrial arrhythmias, incorporation of arrhythmia therapy into any planned surgical revision should be routinely considered. |
2,476 | Administration of atrial natriuretic peptide attenuates reperfusion phenomena and preserves left ventricular regional wall motion after direct coronary angioplasty for acute myocardial infarction. | To evaluate the effects of synthetic human atrial natriuretic peptide (hANP) on myocardial reperfusion injury and left ventricular remodeling, 19 patients within 12 h of a first attack of anterior myocardial infarction (AMI) underwent intracoronary injection of 25 microg of hANP immediately after coronary angioplasty, combined with intravenous infusion of 0.025 microg x kg(-1) x min(-1) of hANP initiated on admission for 1 week (hANP group); 18 similar patients had saline administered (control group). The incidences of premature ventricular contraction, ventricular tachycardia and/or fibrillation in the hANP group were significantly less than in the control group after coronary angioplasty. Left ventricular ejection fraction was significantly greater and left ventricular end-diastolic volume index was significantly smaller 6 months after coronary angioplasty. Left ventricular regional wall motion of the infarcted segments significantly increased. Thus, hANP remarkably suppressed reperfusion phenomena and preserved left ventricular function through improvement of regional wall motion of the infarcted segments after coronary angioplasty. |
2,477 | Alterations in atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation. | Clinically, chronic atrial dilatation is associated with an increased incidence of atrial fibrillation (AF), but the underlying mechanism is not clear. We have investigated atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation (MR).</AbstractText>Thirteen control and 19 MR dogs (1 month after partial mitral valve avulsion) were studied. Dogs in the MR group were monitored using echocardiography and Holter recording. In open-chest follow-up experiments, electrode arrays were placed on the atria to investigate conduction patterns, effective refractory periods, and inducibility of AF. Alterations in tissue structure and ultrastructure were assessed in atrial tissue samples. At follow-up, left atrial length in MR dogs was 4.09+/-0.45 cm, compared with 3.25+/-0.28 at baseline (P<0.01), corresponding to a volume of 205+/-61% of baseline. At follow-up, no differences in atrial conduction pattern and conduction velocities were noted between control and MR dogs. Effective refractory periods were increased homogeneously throughout the left and right atrium. Sustained AF (>1 hour) was inducible in 10 of 19 MR dogs and none of 13 control dogs (P<0.01). In the dilated MR left atrium, areas of increased interstitial fibrosis and chronic inflammation were accompanied by increased glycogen ultrastructurally.</AbstractText>Chronic atrial dilatation in the absence of overt heart failure leads to an increased vulnerability to AF that is not based on a decrease in wavelength.</AbstractText> |
2,478 | Mechanical effects on arrhythmogenesis: from pipette to patient. | Mechanical stimuli delivered to the precordium can, if strong enough and timed at the beginning of the T-wave, induce ventricular premature beats or runs of ventricular tachycardia and even fibrillation. On the other hand, there are reports that a properly timed "chest thump" can terminate ventricular tachycardia, or can act as pacemaker stimuli during an episode of asystole. It is likely that in these cases mechanical energy is translated to an electrical stimulus. There are more subtle ways in which mechanical stimuli, mediated by stretch, can exert electrophysiological effects, and the most common name to describe these effects is mechanoelectrical feedback. Most studies have concentrated on acute stretch or dilatation, while the effects of chronic stretch, which may clinically be more important, are difficult to evaluate since they are accompanied by other factors, such as hypertrophy, heart failure, fibrosis, neurohumeral disturbances, and electrolyte abnormalities, all of which have arrhythmogenic effects. There are a number of ion channels that are activated following stretch. Stretch during diastole usually leads to a depolarization, resembling a delayed afterdepolarization, which may reach threshold and initiate a ventricular premature beat. Stretch during systole usually shortens the action potential, but action potential prolongation, resulting in early afterdepolarizations has been described as well. The arrhythmias during acute myocardial ischaemia occur in two phases: the 1A phase between 2 and 10 min following coronary artery occlusion, and the 1B phase between 18 and 30 min. Experiments will be described, indicating that the ventricular premature beats of the 1B phase, which may induce ventricular fibrillation, are caused by stretch of the border between ischaemic and normal myocardium. Briefly, 1B arrhythmias are much less frequent in the isolated perfused heart than in the heart in situ, but in working, ejecting isolated hearts, the number of 1B arrhythmias is similar to those in the in situ heart. The ventricular premature beats have a focal origin at the border, and they occur more often after a pause-induced potentiated contraction. |
2,479 | Mechanically induced sudden death in chest wall impact (commotio cordis). | Sudden death due to nonpenetrating chest wall impact in the absence of injury to the ribs, sternum and heart is known as commotio cordis. Although once thought rare, an increasing number of these events have been reported. Indeed, a significant percentage of deaths on the athletic field are due to chest wall impact. Commotio cordis is most frequently observed in young individuals (age 4-18 years), but may also occur in adults. Sudden death is instantaneous or preceded by several seconds of lightheadedness after the chest wall blow. Victims are most often found in ventricular fibrillation, and successful resuscitation is more difficult than expected given the young age, excellent health of the victims, and the absence of structural heart disease. Autopsy examination is notable for the lack of any significant cardiac or thoracic abnormalities. In an experimental model of commotio cordis utilizing anesthetized juvenile swine, ventricular fibrillation can be produced by a 30 mph baseball strike if the strike occurred during the vulnerable period of repolarization, on the upslope of the T-wave. Energy of the impact object was also found to be a critical variable with 40 mph baseballs more likely to cause ventricular fibrillation than velocities less or greater than 40 mph. In addition, more rigid impact objects and blows directly over the center of the chest were more likely to cause ventricular fibrillation. Peak left ventricular pressure generated by the chest wall blow correlated with the risk of ventricular fibrillation. Activation of the K(+)(ATP) channel is a likely cause of the ventricular fibrillation produced by chest wall blows. Successful resuscitation is attainable with early defibrillation. |
2,480 | Mechano-electrical feedback underlying arrhythmias: the atrial fibrillation case. | Mechanoelectrical feedback (MEF) has become firmly established as a mechanism in which mechanical forces experienced by myocardial tissue or cell membranes convey alterations in electrophysiologic characteristics of such tissue. Observations to date mainly concern mechanically induced changes in action potential duration, resting and active potential amplitude, enhanced pacemaker frequency, or afterdepolarizations. While some of these changes (i.e. after depolarizations) may give rise to premature beats, a role of MEF in explaining sustained ventricular tachyarrhythmias has so far been elusive. Here, we review recent findings showing that acute atrial dilatation facilitates atrial fibrillation (AF) and that two stretch-activated channel (SAC) blockers (gadolinium and GsMTx-4) are able to suppress stretch-facilitated AF. These findings strongly support a role of MEF and SACs in promoting sustained arrhythmias and point to a new class of antiarrhythmic drugs. |
2,481 | Combining electrical therapies for advanced heart failure: the Milan experience with biventricular pacing-defibrillation backup combination for primary prevention of sudden cardiac death. | Biventricular pacing (BVP) improves hemodynamics and symptoms in patients with heart failure with bundle branch block. Patients with a left ventricular ejection fraction <0.35 and ventricular tachyarrhythmias are at risk of sudden cardiac death, and they benefit most from implantable cardioverter defibrillators (ICDs). No study has evaluated the efficacy of the BVP-ICD combination in patients with heart failure with no history of syncope or sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Our prospective, observational study was performed on 135 consecutive patients with heart failure (aged, 64 +/- 11 years; 76% male; New York Heart Association functional class, 3.1 +/- 0.8; ejection fraction 0.28 +/- 0.06; ischemic heart failure, 43%; QRS interval duration, 153 +/- 11 msec) treated at our cardiac pacing unit between January 1999 and April 2001. In the first year (control phase), BVP alone was implanted. After that, BVP with ICD backup was used (prophylactic phase). Follow-up data were obtained by outpatient visits with electrocardiographic and echocardiographic examinations done at 3-month intervals. For patients who died, we examined hospital records, death certificates, and autopsy reports. Follow-up time averaged 840 days. The first 47 patients received BVP alone. During follow-up study, 19% of these patients died suddenly, and 11% died of worsening heart failure. None of the patients who died suddenly had hemodynamic deterioration or BVP malfunction before the event. The BVP-ICD group comprised 88 patients (18% with VT/VF inducibility on electrophysiologic testing). During follow-up study, 32% of these patients (18% with positive electrophysiologic testing) had VT/VF episodes successfully treated by ICD; 5% received inappropriate discharges on atrial fibrillation; and 6% died of heart failure with 1 sudden cardiac death. Cox proportional hazards model in the BVP-ICD group compared with BVP alone revealed hazard ratios for all-cause mortality and sudden cardiac death of 0.76 (95% confidence interval [CI], 0.58 to 0.96; p = 0.01) and 0.08 (95% CI, 0.05 to 0.42; p <0.01), respectively, adjusting for baseline characteristics and follow-up duration. Mortality in patients with heart failure remains high after BVP implantation, mainly because of sudden cardiac death. Although there are limitations with an observational study, our experience suggests that ICD backup grants increased security in BVP patients without conventional class I ICD indications. |
2,482 | Prevention and management of chronic heart failure with electrical therapy. | Sudden cardiac death is responsible for >40% of patients with heart failure losing their lives. Thus, the prevention of life-threatening cardiac arrhythmias is a major goal in the management of heart failure. In several randomized clinical trials, electrical therapy with the implantable cardioverter defibrillator (ICD) has proved superior to medical antiarrhythmic therapy in both the secondary and primary prevention of sudden cardiac death in patients with reduced left ventricular function. In addition to the severity of left ventricular dysfunction, the etiology of the cardiomyopathy appears to be a determinant in the benefit derived from this form of electrical therapy. Whereas patients with ischemic cardiomyopathy clearly show improved survival with ICD therapy, outcome data in patients with nonischemic cardiomyopathy are less convincing. The major challenge lies in the risk stratification of patients with heart failure for arrhythmic death. Catheter ablation is another form of electrical therapy that can help in the treatment of patients with heart failure. In patients with a tachycardia-mediated cardiomyopathy because of drug-refractory atrial fibrillation with rapid ventricular response, catheter ablation of the atrioventricular node and pacemaker implantation can effectively restore a physiologic heart rate, often with dramatic regression of left ventricular dysfunction. In patients with frequent ICD therapies because of frequent recurrences of ventricular tachyarrhythmias, catheter ablation of ventricular tachycardia can be an effective adjunctive therapy. New catheter ablation techniques and new atrial pacing algorithms can also significantly reduce the atrial fibrillation burden in patients with heart failure who are particularly susceptible to decompensation because of atrial fibrillation. Pacing for hemodynamic benefit in heart failure has evolved from dual-chamber pacing modes with optimized atrioventricular delay to biventricular pacing resulting in cardiac resynchronization. This new treatment modality for advanced heart failure has been shown to result in significant symptomatic and hemodynamic improvement. |
2,483 | Pharmacologic therapy for patients with chronic heart failure and reduced systolic function: review of trials and practical considerations. | Heart failure (HF) is a complex clinical syndrome resulting from any structural or functional cardiac disorder impairing the ability of the ventricles to fill with or eject blood. The approach to pharmacologic treatment has become a combined preventive and symptomatic management strategy. Ideally, treatment should be initiated in patients at risk, preventing disease progression. In patients who have progressed to symptomatic left ventricular dysfunction, certain therapies have been demonstrated to improve survival, decrease hospitalizations, and reduce symptoms. The mainstay therapies are angiotensin-converting enzyme (ACE) inhibitors and beta-blockers (bisoprolol, carvedilol, and metoprolol XL/CR), with diuretics to control fluid balance. In patients who cannot tolerate ACE inhibitors because of angioedema or severe cough, valsartan can be substituted. Valsartan should not be added in patients already taking an ACE inhibitor and a beta-blocker. Spironolactone is recommended in patients who have New York Heart Association (NYHA) class III to IV symptoms despite maximal therapies with ACE inhibitors, beta-blockers, diuretics, and digoxin. Low-dose digoxin, yielding a serum concentration <1 ng/mL can be added to improve symptoms and, possibly, mortality. The combination of hydralazine and isosorbide dinitrate might be useful in patients (especially in African Americans) who cannot tolerate ACE inhibitors or valsartan because of hypotension or renal dysfunction. Calcium antagonists, with the exception of amlodipine, oral or intravenous inotropes, and vasodilators, should be avoided in HF with reduced systolic function. Amiodarone should be used only if patients have a history of sudden death, or a history of ventricular fibrillation or sustained ventricular tachycardia, and should be used in conjunction with an implantable defibrillator [corrected]. Finally, anticoagulation is recommended only in patients who have concomitant atrial fibrillation or a previous history of cerebral or systemic emboli. |
2,484 | Echocardiographic changes and predictors of arrhythmia recurrence after long-term use of the atrial defibrillator. | The patient-activated atrial defibrillator allows patients to cardiovert themselves from atrial fibrillation soon after the onset of symptoms. The long-term effects of early cardioversion from persistent atrial fibrillation on left ventricular performance and left atrial size are unknown.</AbstractText>Eighteen patients, mean age 63.4, 83% male, had the Jewel((R)) AF atrial defibrillator implanted for persistent atrial fibrillation only. Transthoracic echocardiography was performed 3-monthly following implant. Parasternal long axis measurements were taken using conventional M-mode techniques.</AbstractText>Over follow-up of 28.0+/-9 months, 377 episodes of persistent atrial fibrillation were terminated by patient-activated cardioversion (median 15 per patient). Echocardiographic measurements at implant were; left atrium 44+/-6 mm, left ventricular end-diastolic diameter 49+/-7 mm, left ventricular end-systolic diameter 34+/-7 mm, fractional shortening 33+/-10% and ejection fraction 65+/-17%. After 1 year there had been a significant decrease in mean left atrial size to 41+/-6 mm (P=0.02) and an increase in mean ejection fraction to 73+/-8% (P=0.04). At long-term follow-up however, all parameters reverted to pre-implant levels. Baseline echocardiographic variables did not predict which patients would demonstrate serial increases in sinus rhythm duration between shocks during long-term follow-up. Patients on antiarrhythmic drug therapy however were more likely to demonstrate "sinus rhythm begetting sinus rhythm".</AbstractText>Use of the atrial defibrillator for spontaneous persistent atrial fibrillation is associated with a medium-term (1 year) reduction in left atrial size and an increase in ejection fraction. These changes were not maintained in the long-term. Synergistic therapy with antiarrhythmic drugs may prolong periods of sinus rhythm between arrhythmia recurrences.</AbstractText> |
2,485 | Diagnosis and treatment of sick sinus syndrome. | Sick sinus syndrome comprises a variety of conditions involving sinus node dysfunction and commonly affects elderly persons. While the syndrome can have many causes, it usually is idiopathic. Patients may experience syncope, pre-syncope, palpitations, or dizziness; however, they often are asymptomatic or have subtle or nonspecific symptoms. Sick sinus syndrome has multiple manifestations on electrocardiogram, including sinus bradycardia, sinus arrest, sinoatrial block, and alternating patterns of bradycardia and tachycardia (bradycardia-tachycardia syndrome). Diagnosis of sick sinus syndrome can be difficult because of its nonspecific symptoms and elusive findings on electrocardiogram or Holter monitor. The mainstay of treatment is atrial or dual-chamber pacemaker placement, which generally provides effective relief of symptoms and lowers the incidence of atrial fibrillation, thromboembolic events, heart failure, and mortality, compared with ventricular pacemakers. |
2,486 | Electron microscopic study of intrinsic cardiac ganglia in the adult human. | The aim of the present study was to describe in detail the ultrastructure of intrinsic cardiac ganglionic cells in the healthy human as these cells appear to be directly involved in the development of tachycardia, atrioventricular block, ventricular fibrillation, and sudden cardiac death. Tissues examined in this study were obtained from hearts of 10 adult humans of either sex aged 22-80 years at autopsy performed no more than 8 h after death. The examined human intrinsic cardiac nerve cells were in most respects typical autonomic neurons surrounded by a sheath of satellite cells that was either uni- or multilayered. In addition to regular unmyelinated axons, prominent large axon terminals containing lamellated dense bodies, mitochondria and vesicles in the cytoplasm were observed in the ganglion neuropil. Synaptic profiles were more common in the ganglion neuropil than on neuronal somata. According to axon terminal contents, synaptic profiles were of three types. The most common Type 1 synaptic profiles contained a predominance of small clear, with a few larger dense-cored vesicles and mitochondria. Type 2 synaptic profiles, in addition to the same components as in Type 1, had glycogen-like particles. Type 3 vesicle-containing profiles clearly differed from both the previous ones as they were the largest in diameter and included plentifiul large clear pleomorphic or dense-cored vesicles together with small clear and larger dense-cored vesicles, mitochondria, dense and multivesicular bodies. Independently of age of the human, the most frequent neuronal abnormality was an abundant accumulation of inclusions inside of somata and dendrites that, in profile, appeared like circular membranous or fine granular bodies variable in electron density. In addition to inclusions, some neuronal somata and dendrites had strongly swollen mitochondria filled up with granular material in spite of their close association with normal looking ganglionic neurons. Structures resembling an axon growth cone in profile were revealed inside of cardiac ganglia derived from an 80 year old man. In conclusion, the present results provide baseline information on the normal ultrastructure of intracardiac ganglia in healthy humans which may be useful for assessing and interpreting the degree of damage of ganglionic cells both in autonomic and sensory neuropathies of the human heart. |
2,487 | Correlation of the Tei index with invasive measurements of ventricular function in a porcine model. | The Doppler myocardial performance (Tei) index has been reported to be clinically useful in assessing left ventricular systolic and diastolic function in both adults and children. However, there are limited data to compare the Tei index with invasive measurements of ventricular function. We used a porcine model to directly correlate the Tei index with invasive indices of systolic and diastolic function.</AbstractText>Pressure volume loops were obtained from 10 pigs (32-45 kg). A micromanometer and a conductance catheter were placed in the left ventricle to record pressure and volume, respectively. A flow probe was placed around the ascending aorta to record cardiac output. Baseline pressure volume loops were generated during preload reduction through caval occlusion. Epicardial echocardiograms were performed just before the caval occlusion. Invasive indices including preload recruitable stroke work, ventricular stiffness constant, and cardiac output were assessed, as were noninvasive echocardiographic indices including Tei index and ejection fraction. An ischemic insult, ventricular fibrillation, was induced to alter ventricular function. After cardioversion and 40 minutes of reperfusion, echocardiographic and invasive measurements were repeated.</AbstractText>There was a statistically significant inverse relationship between the percent change in Tei and the percent change in preload recruitable stroke work after ventricular fibrillation (r = -0.70, P =.02), although the correlation between the actual values of Tei and preload recruitable stroke work were not statistically significant. There was a statistically significant inverse relationship between the percent change in Tei and the percent change in cardiac output (r = -0.65, P =.03). There was a direct correlation between the value of Tei and the ventricular stiffness constant at baseline (r = 0.63, P <.05). As anticipated, the value of Tei was inversely related to ejection fraction by epicardial echocardiogram at baseline (r = -0.85, P <.001). The percent change in Tei was inversely related to the percent change in ejection fraction as well (r = -0.69, P <.05).</AbstractText>This animal model is one of the first studies to demonstrate a direct correlation between the Tei index and systolic and diastolic invasive measurements of ventricular function. This supports the clinical use of this index as a measure of global ventricular function.</AbstractText> |
2,488 | [Risk of ventricular fibrillation in patients with Wolff-Parkinson White syndrome]. | A 16-year-old boy suddenly fell off his stool, a 26-year-old man had persistent palpitations and a 29-year-old man was reanimated without an incriminating anamnesis. The diagnosis 'Wolff-Parkinson-White(WPW)-syndrome' was made in all three cases. The boy died as a result of postanoxic neurological injury; in the two men, further cardiac rhythm disturbances were prevented by interrupting the accessory atrioventricular connection via radiofrequency catheter ablation. In ECG databases, a WPW-pattern is encountered in 1-3 of 1000 electrocardiograms. Atrial fibrillation with 1:1 conduction via the accessory pathway, leading to ventricular fibrillation, is the most common cause of sudden death in WPW-patients. In some cases, atrial fibrillation with a rapid ventricular response is the first sign of the syndrome. The risk of sudden death in these patients is estimated to be 0.0-0.6% per patient per year and cannot be predicted easily. Curative treatment is possible in the form of radiofrequency catheter ablation. |
2,489 | Implications of the LIFE trial. | The recent Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study was conducted in patients with essential hypertension with electrocardiogram evidence of left ventricular hypertrophy. This showed that losartan compared to atenolol resulted in a significant reduction in the primary endpoint of cardiovascular morbidity and mortality, as well as a greater reduction in electrocardiographically-defined left ventricular hypertrophy. Importantly, this was despite a mean blood pressure reduction which was similar in both groups. Furthermore, the atenolol arm was associated with higher incidence of newly diagnosed diabetics. The LIFE study has firmly confirmed a place for losartan (and other angiotensin receptor blockers) in the management of hypertension. Losartan has also been shown to be effective in diabetics and in patients with atrial fibrillation, as well as in left ventricular hypertrophy regression. This trial also raises the possibility that beta-blockers should perhaps not be used as first-line monotherapy. |
2,490 | Electrophysiological effects of a single intravenous administration of ivabradine (S 16257) in adult patients with normal baseline electrophysiology. | Ivabradine is a heart rate-lowering agent that selectively inhibits the pacemaker current, I(f), in the sinoatrial node. The objective of this study was to evaluate the effects of a single intravenous administration of ivabradine on cardiac electrophysiological parameters in patients with normal baseline electrophysiology. The safety profile of ivabradine was also investigated.</AbstractText>This was an open-label, single-dose, non-controlled study conducted at one centre. Patients received a single dose of ivabradine (0.2 mg/kg) intravenously as a slow bolus over 15 seconds. Electrophysiological investigations, after catheter ablation for cardiac dysrhythmia, were performed at baseline and 30 minutes and 1 hour after drug administration. Electrode catheters were introduced and advanced to the right atrium, the bundle of His and the right ventricular apex of the heart. Electrophysiological parameters assessed included heart rate, QT interval, corrected QT interval (QTc), PR interval, sinoatrial conduction time, sinus node recovery time, and right atrial and ventricle refractory periods. Changes in electrophysiological parameters over time were assessed using one-way analysis of variance. In the case of a significant time effect, the Newman-Keuls procedure was used for comparison.</AbstractText>A total of 14 patients, 12 male and 2 female, aged 18-75 years were included in the study. The arrhythmia requiring catheter ablation was atrioventricular (AV) excitation in seven patients, paroxysmal supraventricular tachycardia in five patients, atrial fibrillation and flutter in one patient, and cardiac dysrhythmia in one patient. All patients had normal electrophysiology at baseline.</AbstractText>Mean heart rate decreased significantly with ivabradine by 12.9 beats/min at 30 minutes and 14.1 beats/min at 1 hour. The mean QT interval increased but QTc showed no significant change from baseline. The PR and QRS intervals were unchanged. The right atrial and right ventricle refractory periods showed no significant change from baseline. The measured QT interval and the sinus node recovery time were increased. There were no clinically relevant changes in any other major electrophysiological parameters. Ivabradine was well tolerated and no serious adverse events occurred.</AbstractText>A single intravenous dose of ivabradine had a significant heart rate-lowering effect, observed at 30 minutes and 1 hour after administration. Ivabradine did not prolong QTc or modify conductivity and refractoriness of the atrium, AV node, His-Purkinje system and ventricles, or repolarisation duration. These results confirm the action of ivabradine as a specific heart rate-lowering agent.</AbstractText> |
2,491 | Atrial fibrillation in the pacemaker clinic. | Electrocardiographic (ECG) recognition of the underlying rhythm in patients with ventricular pacing can be difficult. Atrial fibrillation (AF) in particular may go unreported.</AbstractText>To compare the underlying atrial rhythm determined in the pacemaker clinic with the 12-lead ECG interpretation of the atrial rhythm in those who were continuously paced in the ventricle. It was intended to determine whether long term anticoagulation therapy was related to whether AF was diagnosed before or after pacemaker implantation.</AbstractText>Pacemaker clinic patients were enrolled if they had a 100% paced ventricular rhythm. The underlying rhythm was determined using pacemaker programming manoeuvres. A 12-lead ECG was recorded on all patients within 10 min of their pacemaker assessment and interpreted by one of the several geographic full-time cardiologists at the centre. All cardiologists were blinded to the results of pacemaker assessment and to the clinical history.</AbstractText>Fifty-six patients were enrolled. At the pacemaker clinic, 37 were determined to be in AF and three were in atrial flutter (AFL). Of these 40 patients with AF/AFL, 28 were correctly identified as such on the 12-lead ECG interpretation. Twelve of the 40 were interpreted only as having an 'electronic ventricular pacemaker' (EVP). Sixteen of the 40 patients (40.0%) with AF or AFL were not taking warfarin. Twenty-two of 25 patients with an AF/AFL diagnosis before pacemaker implantation were taking warfarin, compared with two of 15 patients with AF/AFL diagnosis after pacemaker implantation (P<0.0001).</AbstractText>These results show that the underlying rhythm in patients with ventricular pacing is frequently unrecognized by routine ECG interpretation. This may be of particular importance in the AF/AFL population as a potential contributor to the underuse of warfarin, especially when AF develops after pacemaker implantation. The pacemaker clinic may be in a position to play an important role in the identification of these patients.</AbstractText> |
2,492 | Biphasic shocks compared with monophasic damped sine wave shocks for direct ventricular defibrillation during open heart surgery. | Biphasic waveform shocks are more effective than monophasic shocks for transchest ventricular defibrillation, atrial cardioversion, and defibrillation with implantable defibrillators but have not been studied for open chest, intraoperative defibrillation. This prospective, blinded, randomized clinical study compares biphasic and monophasic shock effectiveness and establishes intraoperative energy dose-response curves.</AbstractText>Patients undergoing cardiothoracic surgery with bypass cardioplegia were randomly assigned to the monophasic or biphasic shock group. Ventricular fibrillation occurring after aortic clamp removal was treated with escalating energies of 2, 5, 7, 10, and 20 J until defibrillation occurred. If ventricular fibrillation persisted, a 20-J crossover shock of the other waveform was used.</AbstractText>Cumulative defibrillation success at 5 J, the primary end point of the study, was higher in the biphasic group than in the monophasic group (25 of 50 vs. 9 of 41 defibrillated; P = 0.011). In addition, the biphasic group required lower threshold energy (6.8 vs. 11.0 J; P = 0.003), less cumulative energy (12.6 vs. 23.4 J; P = 0.002), and fewer shocks (2.5 vs. 3.5; P = 0.002). Crossover-shock effectiveness did not differ between groups. Dose-response curves show biphasic shocks to have higher cumulative success rates at all energies tested.</AbstractText>Biphasic shocks are substantially more effective than monophasic shocks for direct defibrillation. The dose-response curve guides selection of first-shock energy for traditional step-up protocols. Starting at 5 J optimizes for lowest threshold and cumulative energy, whereas 10 or 20 J optimizes for more rapid defibrillation and fewer shocks.</AbstractText> |
2,493 | Electrical heterogeneity and arrhythmogenesis: importance of conduction velocity dispersion. | An experimental model of conduction velocity (CV) and refractory period dispersion was established to determine which variable is a determinant of myocardial vulnerability. Anesthetized swine were instrumented with a left anterior descending coronary artery catheter for regional infusion of lidocaine (n = 6), low-dose d-sotalol (n = 4), high-dose d-sotalol (n = 6), or saline (n = 6), to create dispersion in CV (lidocaine), refractoriness (d-sotalol), or neither (saline). Ventricular fibrillation thresholds (VFTs) and refractory periods were determined at five sites (one drug perfused, four non-drug perfused). CV was determined in one drug-perfused area (left ventricular epicardial apex) and one non-drug perfused area (right ventricular epicardial base). Lidocaine and low- and high-dose d-sotalol increased VFT when stimuli were delivered in the drug-perfused area. However, lidocaine decreased VFT when stimuli were delivered at non-drug perfused areas by an average of 52%. Neither d-sotalol dose affected VFT when stimuli were delivered in non-drug perfused areas. Lidocaine increased CV dispersion by 18-26 cm/s but did not alter refractoriness. Both d-sotalol doses increased dispersion in refractoriness by 15-27 ms but did not alter CV. Saline did not affect either variable. Regional lidocaine had profibrillatory effects when stimuli were delivered in non-drug perfused areas, whereas regional d-sotalol did not. Hence, CV dispersion is a more likely determinant of myocardial vulnerability than refractoriness. |
2,494 | SNC-80-induced preconditioning: selective activation of the mitochondrial adenosine triphosphate-gated potassium channel. | Pharmacologic preconditioning by delta-opioid agonists occurs via activation of an adenosine triphosphate (ATP)-gated potassium channel (I(KATP)). Opening of mitochondrial I(KATP) confers pharmacologic preconditioning whereas opening the sarcolemmal I(KATP) shortens action potential duration and is proarrhythmic. This study investigated whether SNC-80, a selective delta-opioid agonist, is associated with development of ventricular arrhythmia due to activation of I(KATP). Rabbit isolated hearts were subjected to 12 min of hypoxia and 40 min of reoxygenation after pretreatment with SNC-80 (1 microM, n = 6), pinacidil (1.25 microM, n = 12), or BMS-191095 (6.0 microM, n = 4). Nine additional hearts served as controls. The cytoprotective effects of SNC-80 at a concentration of 1 microM were confirmed using 30 min of regional ischemia followed by 120 min of reperfusion. Ventricular fibrillation (VF) developed in 11 of 12 pinacidil-treated hearts whereas none of the SNC-80-treated (zero of six) hearts developed VF (P < 0.001 compared with pinacidil pretreatment) and zero of four BMS-191095-pretreated hearts developed VF. Similarly, zero of nine control hearts developed VF. SNC-80 reduced infarct size expressed as a percentage of the area at risk from 33 +/- 4% to 14 +/- 3% (P = 0.004) compared with control. SNC-80, which selectively activates the delta-opioid receptor, provided cytoprotection but did not induce VF after hypoxia reoxygenation. The results indicate that pinacidil-induced nonselective activation of I(KATP) results in proarrhythmia that is dependent on activation of the sarcolemmal I(KATP). Selectivity for the mitochondrial I(KATP) is necessary to prevent induction of a proarrhythmic state. |
2,495 | Combined sodium and calcium channel blockade in prevention of lethal arrhythmias. | Anti-arrhythmic compounds with multiple actions reduce arrhythmic death risk in post-myocardial infarction (MI) patients. Sudden death prevention, however, may rely more on implantable defibrillators than anti-arrhythmic drugs due to ineffective pharmacologic intervention. Widespread use of implantable defibrillators should not obscure the need for development of new anti-arrhythmic drugs. This study tested the hypothesis that combined blockade of I(Na) and I(Ca(L)) prevents ischemia-dependent ventricular fibrillation (VF) in conscious dogs after MI. I(Na) and I(Ca(L)) blockade was accomplished with levosemotiadil in 11 dogs known to be at high risk for VF during 2 min of coronary occlusion during submaximal treadmill exercise 30 days after MI. Negative chronotropic effect of levosemotiadil was examined using the heart rate response to isoproterenol and comparing it with response to propranolol. Levosemotiadil prevented VF in 64% (7 of 11) of the high-risk animals. Heart rate responses to myocardial ischemia and to graded doses of isoproterenol were blunted by the high dose of levosemotiadil. Propranolol prevented VF in 73% (8 of 11) of the dogs. Levosemotiadil had approximately one half the beta-blocking activity of propranolol. The combination of I(Na) and I(Ca(L)) channel blockade coupled with partial beta-adrenergic blockade was equally effective in preventing VF as propranolol. |
2,496 | Deleterious effects of acute treatment with a peroxisome proliferator-activated receptor-gamma activator in myocardial ischemia and reperfusion in pigs. | Thiazolidinediones exert electrophysiologic effects in noncardiac cells in vitro, but to date there have been no reports of effects on cardiac rhythm. We previously demonstrated that chronic pretreatment with a thiazolidinedione peroxisome proliferator-activated receptor (PPAR)-gamma activator, troglitazone, improves recovery of left ventricular (LV) function and substrate metabolism after ischemia and reperfusion, without causing arrhythmias. In this study, we determined whether similar salutary effects are achieved with acute treatment with troglitazone. Anesthetized pigs underwent 90 min of regional LV ischemia and 90 min of reperfusion. Fifteen pigs were treated with troglitazone (10 mg/kg load, 5 mg. kg(-1). h(-1) infusion i.v.) beginning 1 h before ischemia. Seven pigs received corresponding vehicle. Plasma troglitazone concentration (mean 5 microg/ml) was similar to that achieved in clinical use of this agent. Before ischemia, acute troglitazone treatment had no effect on LV function, electrocardiogram, or substrate utilization. During ischemia or reperfusion, eight pigs in the troglitazone group died of ventricular fibrillation, compared with no pigs in the vehicle group (P < 0.05). Pigs that developed ventricular fibrillation had shorter QT intervals than survivors of either group. Among survivors, neither LV function nor substrate utilization differed between groups. Acute treatment with troglitazone increases susceptibility to ventricular fibrillation during myocardial ischemia and reperfusion. Whether thiazolidinediones have proarrhythmic potential in clinical use requires further investigation. |
2,497 | Atrial infarction: a neglected electrocardiographic sign with important clinical implications. | A case of atrial infarction in the setting of an acute infero-posterolateral and right ventricular myocardial infarction is reported. Although often only a subtle ECG sign, this finding must make the physician aware of possible complications, such as arrhythmias (atrial fibrillation, sinus bradycardia, and AV conduction disturbances), pump failure of the right and left ventricle, atrial wall rupture, and thromboembolization. |
2,498 | Detection of proarrhythmia in the female rabbit heart: blinded validation. | Reliable detection of drug-induced proarrhythmia, especially the potential for polymorphic ventricular tachycardia, is of great importance in the development of new compounds that are safe for the heart and was evaluated in a blinded study.</AbstractText>In 142 female rabbits, the monophasic action potential was used to determine intraventricular conduction, action potential duration (APD), triangulation (APD30 to APD90), reverse use-dependence, instability and presence of chaotic behavior, early afterdepolarizations, torsades de pointes (TdP), and ventricular fibrillation. In addition, 31 coded drugs were tested in a blinded fashion in another 150 hearts. Prototype cardiovascular agents [quinidine (IA), lidocaine (IB), flecainide (IC), propranolol (II), sotalol (IIIB), amiodarone (IIIAB) and verapamil (IV)] were correctly characterized in terms of their effects upon conduction and APD. Agents documented in clinical practice to have proarrhythmic potential (droperidol, sotalol, mibefradil, bepridil, lidoflazine, ketanserin, sertindole, terfenadine, haloperidol, astemizole, cisapride, ziprasidone, lubeluzole, dofetilide, quinidine, ibutilide) were identified as such. Pimozide is reported to rarely produce TdP and was also found to elicit Class III action with few adverse effects. Equally important, agents believed not to be proarrhythmic (two solvents, atenolol, propranolol, fenoximone, cetirizine, verapamil, sildenafil, lidocaine, diltiazem) were identified as having no proarrhythmic activity.</AbstractText>The SCREENIT method properly characterized and quantified prototype cardiovascular drugs and correctly identified proarrhythmic noncardiovascular agents of various mechanisms, but it did not produce false-positive results.</AbstractText> |
2,499 | Effects of glucose-induced insulin secretion on ST segment elevation in the Brugada syndrome. | ST segment elevation in patients with Brugada syndrome is known to fluctuate occasionally, influenced by multiple factors. Insulin has been shown to affect QT dispersion in healthy volunteers, as well as result in abnormality of ventricular repolarization in patients with congenital long QT syndrome.</AbstractText>To assess a possible role of insulin in ST segment elevation in patients with Brugada syndrome, an oral glucose tolerance test (OGTT) was administered to 20 patients with Brugada syndrome and 20 normal patients without ST-T changes as a control group. Plasma glucose and potassium levels, immunoreactive insulin concentration (IRI), and ST segment elevation and ST-T wave changes on 12-lead ECG during OGTT were analyzed. Augmentation (>1 mm) of ST elevation or morphologic changes in ST-T waves were observed frequently in response to increased IRI during OGTT [15/20 cases (75%)] in patients with Brugada syndrome but in none of the patients in the control group [0/20 cases (0%), P < 0.01]. The changes returned to baseline 180 minutes after the glucose load in 9 of 15 patients. Patients who showed coved-type ST elevation before the glucose load exhibited positive ECG changes more frequently than patients with saddleback-type elevation or transiently normalized ST segment [8/8 cases (100%) vs 7/12 (58%), P < 0.05]. There was no significant difference between the two groups in terms of glucose, IRI, and potassium levels during OGTT.</AbstractText>The findings suggest that glucose-induced insulin secretion is one of the contributing factors to fluctuation of ST segment elevation in patients with Brugada syndrome.</AbstractText> |
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