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3,100 | Preconditioning modulates susceptibility to ischemia-induced arrhythmias in the rat heart: the role of alpha-adrenergic stimulation and K(ATP) channels. | A new concept of cardioprotection based on the exploitation of endogenous mechanisms is known as ischemic preconditioning (IPC). It has been hypothesized that substances released during brief ischemic stress (e.g. catecholamines) stimulate the receptors and trigger multiple cell signaling cascades. Opening of ATP-sensitive K+ channels [K(ATP)] has been suggested as a possible final step in the mechanisms of protection. In this study, the role of adrenergic activation was tested in Langendorff-perfused rat hearts subjected to test ischemia (TI; 30 min occlusion of LAD coronary artery) by: 1) mimicking IPC (5 min ischemia, 10 min reperfusion) with short-term (5 min) administration of norepinephrine (NE, 1 microM), 15 min prior to TI; 2) blockade with beta- or alpha1-receptor antagonists, propranolol (10 microM) and prazosin (2 microM), respectively, applied 15 min prior to TI during IPC. The role of K(ATP) opening was examined by perfusion with a K(ATP) blocker glibenclamide (10 microM) during IPC. Both IPC and NE-induced PC effectively reduced the incidence of ventricular tachycardia (VT) to 33% and 37%, respectively, vs 100% in the non-PC controls, whereby ventricular fibrillation (VF) was totally abolished by IPC and markedly suppressed by PC with NE (0% and 10%, respectively, vs 70% in the non-PC hearts; P < 0.05). The severity of arrhythmias (arrhythmia score, AS) was also markedly attenuated by both interventions (IPC: AS 1.7 +/- 0.4; NE-PC: AS 1.8 +/- 0.3 vs AS 4.1 +/- 0.2 in the controls; P < 0.05). Protection was not suppressed by propranolol (VT 28%; VF 14%; AS 2.2 +/- 0.6), whereas prazosin reversed the protective effect of PC (VT 83%; VF 67%; AS 4.0 +/- 0.8). Antiarrhythmic protection afforded by NE-PC was abolished by pretreatment of rats with pertussis toxin (25 microg/kg, i.p.) given 48 h prior to the experiments. Glibenclamide did not suppress the IPC-induced protection. In conclusion, the sensitivity of the rat heart to ischemic arrhythmias can be modulated by IPC. Protection is mediated via stimulation of alpha1-adrenergic receptors coupled with Gi-proteins but glibenclamide-sensitive K(ATP) channels do not appear to be involved in the mechanisms of antiarrhythmic protection in this model. |
3,101 | Differences in the activation patterns between sustained and self-terminating episodes of human ventricular fibrillation. | Experimental studies have suggested that R-R interval dynamics during ventricular fibrillation (VF) have organized features, but whether dynamic behavior of non-sustained VF differs from sustained VF is unknown.</AbstractText>The purpose of this study was to investigate whether the dynamics of R-R intervals during non-sustained VF differs from the dynamics during sustained VF.</AbstractText>A group of 67 patients undergoing routine implantable cardioverter defibrillator (ICD) testing was studied. Forty-three VF events containing mean of 38 local cardiac activation intervals before the termination by ICD shock were analyzed. From intracardiac electrogram recordings, the ratio between the short and long term variability (SD1/SD2) and fractal scaling exponent (alpha) were analyzed. After the initial analyses, data sets were randomized and reanalyzed. Local activation dynamics were then also compared in seven patients with both sustained and spontaneously terminating VF episodes.</AbstractText>Randomization caused a change in the VF dynamics from organized toward less organized dynamics (alpha) from 1.08 +/- 0.57 to 0.81 +/- 0.45, P < 0.05 and SD1/SD2 from 0.80 +/- 0.23 to 1.04 +/- 0.20, P < 0.01). Spontaneously terminating VF showed more organized dynamics than sustained VF terminated by shock (P < 0.05).</AbstractText>Local cardiac activation dynamics during initial phase of human VF shows organized dynamics. Spontaneously terminating VF episodes have more structured dynamics than sustained VF. Thus, the dynamic behavior of local cardiac activation intervals may be related to the maintenance of ventricular tachyarrhythmias.</AbstractText> |
3,102 | Intrapericardial therapeutics: a pharmacodynamic and pharmacokinetic comparison between pericardial and intravenous procainamide delivery. | Procainamide delivery into the pericardial space may produce a greater and more prolonged electrophysiologic effect, particularly in thin superficial atrial tissue, compared with intravenous delivery.</AbstractText>Swine were randomized to sequential procainamide doses delivered intravenously (n = 6) or into the pericardial space (n = 7). The cumulative pericardial doses were 0.5, 1.5, and 3.5 mg/kg, and the intravenous doses were 2, 10, and 26 mg/kg. Pericardial procainamide prolonged right atrial effective refractory period from baseline by 22% (P < 0.01) but only at the 3.5 mg/kg cumulative dose. This dose slowed interatrial conduction time by 14% (P < 0.05) and raised atrial fibrillation threshold by 70 mA (P < 0.05). Pericardial procainamide had minimal effect on ventricular electrophysiology. Similar results occurred with a single 2 mg/kg pericardial dose in a closed chest model. Intravenous 10 and 26 mg/kg cumulative doses prolonged atrial effective refractory period from baseline by 24% and 18% (P < 0.01), respectively. The 26 mg/kg cumulative intravenous dose slowed interatrial and atrial-ventricular conduction times by 27% and 17%, respectively (P < 0.05), raised atrial fibrillation threshold, and slowed ventricular conduction time by 29% (P < 0.05). Pericardial procainamide produced pericardial fluid concentrations ranging from 250 to 1,500 microg/mL, but plasma concentrations were <1 microg/mL. Intravenous procainamide doses produced pericardial fluid concentrations similar to plasma trough concentrations 0 to 12 microg/mL.</AbstractText>The single 2 mg/kg and 3.5 mg/kg cumulative pericardial procainamide doses prolonged atrial refractoriness and raised atrial fibrillation threshold similar to the 26 mg/kg cumulative intravenous dose, but the duration of effect was similar between delivery methods. Pericardial procainamide did not affect global or endocardial ventricular electrophysiology nor was it associated with ventricular proarrhythmia.</AbstractText> |
3,103 | Outcome of women versus men with ventricular tachyarrhythmias treated with the implantable cardioverter defibrillator. | Important sex differences in the incidence and outcome of patients with ischemic heart disease, the leading cause of ventricular tachyarrhythmias, have been identified. Implantable cardioverter defibrillator (ICD) therapy has become the treatment of choice for patients with ventricular tachycardia (VT) and ventricular fibrillation (VF), but little is known about gender differences in the outcome of ICD-treated patients.</AbstractText>In this retrospective study, we compared arrhythmic events and survival of 376 women and 1,654 men treated with an ICD as part of prospective evaluations of transvenous devices or lead systems. Women were younger (62+/-14 years vs 65+/-12 years, P = 0.0005), had higher left ventricular ejection fraction (0.36+/-0.15 vs 0.32+/-0.13, P < 0.0001), were more likely to present with VF (34% vs 19%, P < 0.001), and had lower implantation defibrillation threshold (11+/-6 vs 13+/-6 J, P < 0.0001). Implant complication rates were similar in men and women (2.6% vs 3.5%, P = 0.46). The 1-year and 2-year cumulative rates of appropriate ICD therapies were 31.4% and 38.4% for men and 32.6% and 40.8% for women, respectively (P = 0.63). The unadjusted 1-year and 2-year cumulative survival rates were 95.6% and 93.7% for men and 95.7% and 94.3% for women, respectively (P = 0.98). Adjusted total (P = 0.61), sudden (P = 0.82), and cardiac (P = 0.34) death-free survivals also were similar in men and women.</AbstractText>Despite clinical differences suggesting women are at lower risk than men, men and women with VT/VF who are treated with an ICD have similar arrhythmic event and survival rates. These factors should be considered when determining risk and prescription of ICD therapy for women.</AbstractText> |
3,104 | Characterization of paroxysmal and persistent atrial fibrillation in the human left atrium during initiation and sustained episodes. | Atrial fibrillation (AF) in the left atrium (LA) is poorly defined in terms of regional differences in the degree of organization, characteristics of paroxysmal and persistent variants, and electrophysiologic events that develop at the onset of episodes.</AbstractText>The study population consisted of 21 patients (15 men and 6 women; mean age 58+/-9.4 years) with paroxysmal (10 patients) or persistent (11 patients) AF. Mapping of the LA during sustained episodes and the onset of AF was performed with a 64-electrode basket catheter. At the onset of AF, repetitive beats starting with atrial premature complexes and ending with generation of the earliest fibrillatory activity were defined as intermediary rhythm. Patients with paroxysmal AF had longer AF cycle lengths and more pronounced regional differences than patients with persistent AF. In total, AF cycle lengths in the LA in patients with persistent AF were 20% shorter than in patients with paroxysmal AF. Initiation of AF was preceded by an intermediary rhythm of 5.5+/-2.5 cycles (6.3+/-2.7 cycles in paroxysmal AF vs 4.2+/-1.0 cycles in persistent AF; P = 0.026). At the onset of AF, the earliest generators of fibrillatory activity were located more frequently in the posterior wall of the LA.</AbstractText>AF in the LA displays substantial regional differences in terms of AF cycle lengths and degree of organization. Patients with persistent AF have shorter cycle lengths and a higher degree of disorganized activity than patients with paroxysmal AF. Intermediary rhythms play an important role in initiation of AF via activation of generator regions in the LA.</AbstractText> |
3,105 | [Thanatogenesis variants in drug use poisoning]. | The study of 179 autopsy cases of narcotic poisoning has distinguished four main types of tanatogenesis, the "brain death" being most frequent. The second type was tanatogenesis by type of "sudden cardiac death" with ventricular fibrillation. The third one is tanatogenesis by type of "toxic edema of the lungs" with severe respiratory failure. Rare types of tanatogenesis were acute adrenal failure, anaphylactic shock and others. Combination of several tanatogenesis types was frequent. |
3,106 | A randomised cross-over study on the haemodynamic effects of oral dofetilide compared with oral sotalol in patients with ischaemic heart disease and sustained ventricular tachycardia. | To assess the haemodynamic effects of short-term treatment with dofetilide in comparison with sotalol in patients with ischaemic heart disease.</AbstractText>Twelve patients with ischaemic heart disease and sustained ventricular tachycardia were treated with dofetilide [500 microg twice daily (b.i.d.)] or sotalol (160 mg b.i.d., randomised sequence separated by wash-out period) for 3-5 days. Right-heart catheterisation was performed at baseline and at the end of each short-term treatment phase.</AbstractText>The main findings were a significant reduction in heart rate, mean systemic pressure and cardiac index (-13%) during treatment with sotalol. Conversely, cardiac index increased significantly during dofetilide (mean percentage change 11%) with no effect on heart rate and systemic blood pressure.</AbstractText>Oral dofetilide exerts favourable haemodynamic effects in comparison with D,L-sotalol following short-term oral treatment. In view of these observations, the use of dofetilide may be proposed also in patients with ventricular tachyarrhythmias associated with impaired left-ventricular function. Whether the haemodynamic differences between dofetilide and D,L-sotalol are the basis for differences in tolerability remains to be evaluated.</AbstractText> |
3,107 | Catheter ablation for cardiac arrhythmias. | The clinical introduction of catheter ablation in 1981 revolutionized the treatment of cardiac arrhythmias. Implementation of radiofrequency as an alternative energy source, with the advantages of higher selectivity and less collateral damage, provided an expansion of catheter ablation therapy. Today the majority of arrhythmias can potentially be cured with catheter ablation therapy. The safety and efficacy of catheter ablation for treatment of AV nodal reentrant tachycardia, accessory pathway arrhythmias, focal atrial tachycardia, atrial flutter and idiopathic ventricular tachycardia, is well established. Catheter ablation for treatment of atrial fibrillation and ventricular tachycardia secondary to structural heart disease, remains an area of active research. In this article we will review the current state of knowledge about the technique, indications, and results of catheter ablation for the treatment of cardiac arrhythmias. |
3,108 | The effects of acute and chronic amiodarone on activation patterns and defibrillation threshold during ventricular fibrillation in dogs. | The goal of this study was to evaluate the effects of acute and chronic amiodarone on activation patterns during ventricular fibrillation (VF), ventricular effective refractory period (VERP) and defibrillation threshold (DFT).</AbstractText>Acute and chronic amiodarone may act through different mechanisms.</AbstractText>The VERP, VF activation patterns and DFT were determined in 24 dogs. Twelve dogs received acute intravenous amiodarone (10 mg/kg, n = 6) or saline (n = 6), and 12 dogs received chronic oral amiodarone (20 mg/kg/day, n = 6) or placebo (n = 6). Epicardial VF activation patterns were recorded with 504 electrodes. Quantitative descriptors of VF were calculated.</AbstractText>The DFT was unchanged by acute or chronic amiodarone. Although chronic amiodarone significantly extended the VERP, acute amiodarone did not. In the mapped region, acute and chronic amiodarone decreased the number of VF wavefronts by 42% and 60%. Acute amiodarone decreased conduction block by 22%, while chronic amiodarone increased block by 41% but decreased wave fractionation by 50%. Both chronic and acute amiodarone increased the size of the core of re-entrant circuits and decreased the incidence of re-entry by 44% and 57%; however, chronic amiodarone increased wavelength, while acute amiodarone did not.</AbstractText>Neither acute nor chronic amiodarone change the DFT. While both acute and chronic amiodarone decrease the number of wavefronts, decrease the incidence of re-entry and increase the size of re-entrant cores in the mapped region during VF, they achieve these antiarrhythmic effects through different electrophysiologic mechanisms. Chronic amiodarone prolonged the VF cycle length and slowed conduction velocity, indicating it increased the wavelength and/or the excitable gap.</AbstractText> |
3,109 | Do atrial tachyarrhythmias beget ventricular tachyarrhythmias in defibrillator recipients? | This study was designed to analyze the incidence of "dual tachycardia"-ventricular tachycardia (VT) or ventricular fibrillation (VF) preceded by paroxysmal atrial tachycardia (AT) or atrial fibrillation (AF)-in patients receiving dual-chamber implantable cardioverter defibrillators (ICDs).</AbstractText>Paroxysmal AT/AF occurs commonly in patients who receive ICDs for the treatment of life-threatening VT/VF. Although AF is associated with an adverse prognosis in the setting of structural heart disease, the relationship between AT/AF and VT/VF is unclear.</AbstractText>We followed 537 patients undergoing implantation of the Jewel AF ICD (Model 7250, Medtronic, Minneapolis, Minnesota) for 11.4 +/- 8.2 months. These included 398 patients with a history of at least two episodes of AT or AF during the preceding year as well as 139 patients enrolled because of VT/VF alone.</AbstractText>There were 233 dual tachycardia episodes in 45 patients during follow-up. Overall, 8.9% of episodes detected as VT/VF were dual tachycardias, and 20.3% of patients with VT/VF had at least one dual tachycardia episode. The median duration of AT/AF preceding the first VT/VF detection was 1.09 h (25% to 75% quartile 0.24 to 33.4 h). When AT/AF continued between two consecutive VT/VF detections, the median interdetection interval was 11 min. When AT/AF terminated either because of a ventricular therapy or spontaneously, the median interdetection interval was prolonged to 71 h (p < 0.001).</AbstractText>Dual tachycardia is common in ICD recipients with a history of AT/AF. The duration of AT/AF preceding the first VT/VF detection is < or =1 h about 50% of the time. Termination of the AT/AF significantly delays the time to the next VT/VF detection.</AbstractText> |
3,110 | The electrophysiologic mechanism of ST-segment elevation in Brugada syndrome. | We sought to demonstrate the electrophysiologic (EP) mechanism of the ST-T change in Brugada syndrome.</AbstractText>Brugada syndrome is characterized by various electrocardiographic manifestations (e.g., right bundle branch block, ST-segment elevation, and terminal T-wave inversion in the right precordial leads) and sudden cardiac death caused by ventricular fibrillation. Direct evidence in support of the EP mechanism underlying this intriguing syndrome has been lacking.</AbstractText>Monophasic action potentials (MAPs) were obtained from three patients with the coved-type ST-segment elevation (Brugada patients) and five control patients using the contact electrode method. Epicardial MAPs were recorded during open-chest surgery in all patients.</AbstractText>A spike-and-dome configuration was documented from epicardial sites of the right ventricular (RV) outflow tract in all Brugada patients but not in control patients. Monophasic action potential recordings from the endocardium with special focus on the RV outflow tract could not demonstrate any morphological abnormalities in three Brugada patients.</AbstractText>The presence of a deeply notched action potential in the RV epicardium, but not in endocardium, would be expected to induce a transmural current that would contribute to elevation of the ST-segment in the right precordial leads. The spike-and-dome configuration may also prolong the epicardial action potential, thus contributing to a rapid reversal of the transmural gradients and inscription of an inverted T-wave.</AbstractText> |
3,111 | The role of growth factors and ammonia in the genesis of hypokalemic nephropathy. | Hypokalemia is a common electrolyte abnormality encountered in clinical practice. It can be identified in an asymptomatic patient undergoing routine electrolyte screening or can manifest itself as part of a number of functional abnormalities in a variety of organs and systems. Among the most commonly recognized complications are profound effects on the cardiovascular and neuromuscular systems, together with abnormalities in acid-base regulation. In humans, hypokalemia contributes to the development of hypertension and predisposes patients to a variety of ventricular arrhythmias, including ventricular fibrillation. Commonly recognized neuromuscular complications include weakness, cramping, and myalgia. Hypokalemia also affects systemic acid-base homeostasis by interfering with multiple components of the renal acid-base regulation and is a frequent cause of metabolic alkalosis. Less known, however, is the role of potassium deficiency in causing progressive renal failure. In animals, potassium deficiency stimulates renal enlargement because of cellular hypertrophy and hyperplasia. If potassium deficiency persists, interstitial infiltrates appear in the renal interstitial compartment, and eventually tubulointerstitial fibrosis develops. In humans, longstanding hypokalemia is associated with the development of renal cysts, chronic interstitial nephritis, and progressive loss of renal function, the so-called hypokalemic nephropathy. This review focuses on the potential mechanisms involved in the development of the hypokalemic nephropathy with emphasis on the role of ammonia and growth factors in its pathogenesis. |
3,112 | Treatment of post resuscitation myocardial dysfunction: aortic counterpulsation versus dobutamine. | Post resuscitation myocardial stunning is well described and recognized as a significant contributor to poor long-term outcome following cardiac arrest. Optimal strategies for treatment have not been determined.</AbstractText>Ten domestic swine (49+/-3 kg) underwent 15 min of untreated ventricular fibrillation before being successfully resuscitated. Left ventricular systolic and diastolic function was measured at pre-arrest baseline, at 30 min and at 6 h post resuscitation. Five animals were treated immediately after resuscitation with intra-aortic balloon counterpulsation (IABP) and five were given dobutamine (5 mcg/kg per min).</AbstractText>No baseline differences were found. At 30 min post resuscitation pulmonary capillary wedge pressure and LVEDP were significantly higher (16+/-3 vs. 7+/-1 and 20+/-2 vs. 11+/-1 mmHg) while LV isovolumic relaxation ('Tau') was significantly longer (34+/-2 vs. 20+/-2 ms) in the IABP treated versus the dobutamine treated animals. Likewise, at 6 h post resuscitation LV ejection fraction was significantly less (21+/-6 vs. 39+/-4%), and LVEDP significantly higher (18 vs. 10 mmHg) in the IABP group. Heart rate was not different between the groups at any time post resuscitation.</AbstractText>Dobutamine was superior to IABP for treatment of post resuscitation left ventricular systolic and diastolic dysfunction. The hypothesized advantage of IABP for treatment of post resuscitation myocardial stunning without excessively raising the heart rate like dobutamine was not realized.</AbstractText> |
3,113 | Low chance of survival among patients requiring adrenaline (epinephrine) or intubation after out-of-hospital cardiac arrest in Sweden. | To relate the outcome of out-of-hospital cardiac arrest to whether medication with adrenaline (epinephrine) was given and whether patients were intubated.</AbstractText>A national survey in Sweden between 1990-1995 among patients suffering out-of-hospital cardiac arrest and in whom resuscitation was attempted. Sixty per cent of ambulance organisations in Sweden participated.</AbstractText>Prospective evaluation. Survival was defined as survival 1 month after cardiac arrest.</AbstractText>In all, 14065 patients were included in the evaluation. Of these, resuscitation was attempted in 10966 cases. Among these adrenaline (epinephrine) was given in 42.4 and 47.5% were intubated. In an univariate analysis treatment with adrenaline (epinephrine) and intubation was associated with a lower survival when all patients were evaluated. In a multivariate analysis including age, sex, place of arrest, bystander-CPR, initial arrhythmia, arrest being witnessed and aetiology, treatment with adrenaline (epinephrine) (OR 0.43, CI 0.27-0.66) and intubation (OR 0.71, CI 0.51-0.99) were both independent predictors of a lower chance of survival. When separately analysing patients with bystander witnessed cardiac arrest found in ventricular fibrillation and requiring more than 3 defibrillatory shocks neither treatment with adrenaline (epinephrine) nor intubation was associated with survival. Among patients with a non-shockable rhythm treatment with adrenaline (epinephrine) was a significant independent predictor for lower survival (OR 0.30, CI 0.07-0.82).</AbstractText>In a national survey in Sweden including 10966 cases of out-of-hospital cardiac arrest the outcome was related to whether medication with adrenaline (epinephrine) was given and whether patients were intubated. Neither in total nor in any subgroup did we find results indicating beneficial effects of any of these two interventions. Whether treatment with adrenaline (epinephrine) or intubation will increase survival after out-of-hospital cardiac arrest needs to be confirmed in prospective randomised trials.</AbstractText> |
3,114 | Prevention of deterioration of ventricular fibrillation by basic life support during out-of-hospital cardiac arrest. | Survival of cardiac arrest is improved by basic life support (BLS). This study investigated the relationship between ventricular fibrillation (VF) characteristics and survival. In a 2-year prospective study out-of-hospital witnessed non-traumatic cardiac arrests were observed. The probabilities of recording VF, asystole or other rhythms in relation to BLS and the time to the rhythm recording were analyzed with logistic regression. Amplitude and baseline crossings of VF were related to survival, using linear regression analysis. In 873 patients, the probability to record VF decreased per minute (OR 0.92, 95%CI 0.89-0.95) and of asystole increased (OR 1.13, 95%CI 1.09-1.18) as time from collapse elapsed. BLS reduced these trends significantly for VF (OR 0.97, 95%CI 0.94-0.99) and asystole (OR 1.09, 95%CI 1.05-1.13). This effect was not observed for other rhythms. The amplitude of VF decreased in time; significantly less for patients who received BLS than for those who did not (p=0.009). Survival significantly decreased with lower amplitude of VF (OR 0.23 per mV, 95%CI 0.07-0.79) and with less baseline crossings (OR 0.80 per baseline crossings per second, 95%CI 0.71-0.91). Our study demonstrated that BLS and VF as initial rhythm, considered being "baseline" predictors in survival models, were proved not independent of each other. The decrease of VF amplitude and increase in prevalence of asystole is slowed significantly by BLS. Predicting survival from VF amplitude and baseline crossings alone is limited. |
3,115 | Long-term benefits of biventricular pacing in congestive heart failure: results from the MUltisite STimulation in cardiomyopathy (MUSTIC) study. | The main objective of this study was to assess if the benefits of biventricular (BiV) pacing observed during the crossover phase were sustained over 12 months.</AbstractText>MUltisite STimulation In Cardiomyopathies (MUSTIC) is a randomized controlled study intended to evaluate the effects of BiV pacing in patients with New York Heart Association (NYHA) class III heart failure and intraventricular conduction delay.</AbstractText>Of 131 patients included, 42/67 in sinus rhythm (SR) and 33/64 in atrial fibrillation (AF) were followed up longitudinally at 9 and 12 months by 6-min walked distance, peak oxygen uptake (peak VO(2)), quality of life by the Minnesota score, NYHA class, echocardiography, and left ventricular ejection fraction by radionuclide technique.</AbstractText>At 12 months, all SR and 88% of AF patients were programmed to BiV pacing. Compared with baseline, the 6-min walked distance increased by 20% (SR) (p = 0.0001) and 17% (AF) (p = 0.004); the peak VO(2) by 11% (SR) and 9% (AF); quality of life improved by 36% (SR) (p = 0.0001) and 32% (AF) (p = 0.002); NYHA class improved by 25% (SR) (p = 0.0001) and 27% (AF) (p = 0.0001). The ejection fraction improved by 5% (SR) and 4% (AF). Mitral regurgitation decreased by 45% (SR) and 50% (AF).</AbstractText>The clinical benefits of BiV pacing appeared to be significantly maintained over a 12-month follow-up period.</AbstractText> |
3,116 | Sudden death after radiofrequency ablation of the atrioventricular node in patients with atrial fibrillation. | We evaluated the incidence and predictors of sudden death after atrioventricular (AV) node ablation and pacemaker implantation.</AbstractText>Sudden death may occur after radiofrequency catheter ablation of the AV node and pacemaker implantation in patients with atrial fibrillation (AF). Whether it is related to the procedure or to pre-existing heart disease remains unclear.</AbstractText>All patients who had radiofrequency catheter ablation of the AV node and pacemaker implantation for rate control of medically refractory AF were identified retrospectively and observed prospectively. All patients with sudden death after ablation were identified. The relationship between the procedure and sudden death was defined on the basis of the time between the two as "likely," "possibly" or "unlikely."</AbstractText>Of 334 consecutive patients with AF who underwent AV node ablation, nine had sudden death after the ablation. Four patients (1.2%) had sudden death likely related to the procedure: in 3 patients, arrest occurred within 48 h after the procedure; in one patient, arrest occurred four days after the procedure. In three other patients (0.9%), sudden death was possibly related to the procedure because the event occurred within three months afterward. The remaining two deaths were unrelated to the procedure. Diabetes, New York Heart Association functional class (>or=II), preprocedure ventricular arrhythmia, mitral or aortic stenosis, aortic regurgitation and chronic obstructive pulmonary disease were independent predictors for sudden death.</AbstractText>Sudden death likely or possibly related to catheter ablation occurred in 7 of 334 patients (2.1%). Risk of sudden death is highest within two days after the procedure.</AbstractText> |
3,117 | Successful rescue of sustained ventricular tachycardia/ventricular fibrillation after coronary artery bypass grafting by extracorporeal membrane oxygenation. | Extracorporeal membrane oxygenation (ECMO) can be set up quickly at the bedside and provides reliable temporary mechanical circulatory support for severe heart failure. We report the case of a 56-year-old female with circulatory collapse due to sustained ventricular tachycardia and ventricular fibrillation (VT/Vf) after coronary artery bypass grafting (CABG) who was successfully resuscitated using ECMO. The sustained VT/Vf might have been secondary to myocardial stunning, ischemia, infarction, or reperfusion. There were 40 cardioversions within the first 5 postoperative days. The patient improved after 8 days of ECMO in addition to use of an intraaortic balloon pump and administration of inotropic agents for profound heart failure. Left ventricular ejection fraction improved from 28% preoperatively to 54.5% on the 20th postoperative day. Cardiogenic shock due to sustained VT/Vf after CABG may be an indication for ECMO support. Immediate establishment of circulatory support using ECMO provides valuable time for spontaneous and interventional correction of reversible causes of sustained VT/Vf. |
3,118 | [Coronary bypass surgery in octogenarians]. | The age of the patients referred for coronary bypass surgery is getting older progressively. Early and late postoperative outcome of octogenarians were evaluated and compared with younger age group in this study.</AbstractText>Records of 55 patients aged 80 years or older (mean age 82.7 +/- 2.8) among 3834 patients, who had coronary bypass graft procedure, operated between 1995 and 2001 were reviewed retrospectively.</AbstractText>There were 39 men (70.9%) and 16 women (29.1%). Three patients had aortic valve replacement, 1 had left ventricular aneurysm repair, 1 had carotid endarterectomy additionally. Atrial fibrillation (21.8%), renal dysfunction (16.4%), and prolonged ventilation (10.9%) were the prominent complications. The hospital mortality rate was 7.27% (4 patients). Kaplan Meier Survival Analysis estimated that at the end of 5 years 83.1 + 5.2% of patients were still alive.</AbstractText>Coronary bypass operations can be performed in octogenarians with slightly increased but acceptable hospital mortality and longer hospital stay. Early intervention and individual modifications in cardiopulmonary bypass techniques may improve the results in this patient population.</AbstractText> |
3,119 | Atrial fibrillation, the arrhythmia of the elderly, causes and associated conditions. | Atrial fibrillation (AF) is a common clinical problem, particularly in the elderly, and in patients with organic heart disease. A small percentage of patients, have a potentially reversible cause. Atrial fibrillation is in most patients (approximately 70%) associated with chronic organic heart disease including valvular heart disease, coronary artery disease, hypertension, particularly if left ventricular hypertrophy is present, hypertrophic cardiomyopathy, dilated cardiomyopathy and congenital heart disease and most commonly in adults, atrial septal defect. As in many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (with or without mitral regurgitation), calcification of the mitral annulus, atrial myxoma, pheochomocytoma and idiopathic dilated right atrium, present a higher incidence of AF. The relationship between these findings and the arrhythmia are still unclear. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so-called "lone AF", in about 30% of cases. The term "lone AF" or "idiopathic AF" implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolf-Parkinson-White syndrome), only to mention a few of other rare causes of AF. In every instance of recently discovered AF, thyrotoxicosis should be ruled out. The autonomous nervous system may contribute to the occurrence of AF in some patients. Atrial fibrillation occurs commonly in patients with valvular heart disease, particularly when it involves the mitral valve. The occurrence of AF is unrelated to the severity of mitral stenosis but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, Af occurs predominantly in older patients, males and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. However, the relation between AF and hypertension remains unclear. The risk of the development of AF, in an individual patient, is often difficult to assess but increasing age, presence of valvular heart disease and congestive heart failure, increase the risk of AF. |
3,120 | [Do mobile telephones have adverse effects on the functions of implantable cardioverter defibrillators?]. | The aim of this study was to investigate the effects of widely used mobile telephones on the functions of implantable cardioverter-defibrillators (ICD).</AbstractText>The study included 9 patients (2 women, 7 men, mean age 65.5 +/- 6) with coronary artery disease who had underwent transvenous ICD implantation due to sustained ventricular tachycardia and/or fibrillation. First the test was performed on the basal conditions of ICD. Then, spontaneous heart rate of the patient was programmed to 10 beats/minute on VVI mode and the test was repeated. Two mobile telephones were located symmetrically 50 cm, 30 cm, 20 cm and 10 cm away from the ICD pocket in the pectoralis muscle and finally the mobile telephones antennas were touched to the pockets. On these different distances, the test was repeated during opening, standby, calling, talking and closing of the telephones. Possible ICD dysfunctions such as improper antitachycardic shock, inhibition of pacemaker functions, conversion to ventricular asynchronous mode (VOO) and development of ventricular trigger in devices with two chamber pacemaker functions were tested. The changes were observed on intracardiac and surface ECG's.</AbstractText>There were no changes in the basal and pacemaker functions of ICD's and no symptoms in any patients.</AbstractText>We have concluded that mobile telephones have no adverse effects on the functions of types of ICD assessed in the study.</AbstractText> |
3,121 | [Ultrasonic integrated backscatter analysis in patients with dilated cardiomyopathy: comparison with healthy individuals]. | Ultrasonic tissue characterization, based on the measurements of integrated backscatter (IBS) analysis, has the potential to provide quantitative information which could characterize the functional and structural state of cardiac muscle. In this study we aimed to determine whether the integrated backscatter is measurable and quantifiable in left ventricular walls in patients with dilated cardiomyopathy (DCMP) and can be used to identify changes in myocardial structure and contractility.</AbstractText>We studied 32 subjects: 16 patients with idiopathic dilated cardiomyopathy who were free of atrial fibrillation, bundle branch block and valvular heart disease (12 male, 4 female, mean age 48 +/- 18) and 16 healthy volunteers (10 male, 6 female, mean age 46 +/- 8). Left ventricular diastolic and systolic diameters, septum and posterior wall (PW) systolic and diastolic thickness were measured in the parasternal long axis view with M-mode echocardiography. Ejection fraction (EF), fractional shortening (FS), septum and posterior percent wall thickening (WT%) were calculated in the parasternal long axis view with M-mode echocardiography. Real time IBS was measured from the parasternal long axis view of the left ventricle at the level of basal posterior and septal walls. Mean IBS was expressed as averaged IBS values and cyclic variation of IBS (CVIBS) was expressed as the difference between end-diastolic (peak) and end-systolic (nadir) IBS values averaged over all cardiac cycles.</AbstractText>CVIBS values obtained from septum and PW in idiopathic DCMP group were statistically different from control group (p = 0.003, p < 0.001, respectively). Septal and PW mean IBS values in idiopathic DCMP group were greater and statistically different from control group (p < 0.05). Septum and PW CVIBS values correlated with WT%, EF and FS positively. But, septum and PW mean IBS values did not correlate with WT%, EF and FS.</AbstractText>CVIBS and mean IBS values which were obtained with IBS method may be useful to determine myocardial contractile performance and myocardial structural properties, respectively.</AbstractText> |
3,122 | Clinical and molecular characterization of patients with catecholaminergic polymorphic ventricular tachycardia. | Mutations in the cardiac ryanodine receptor gene (RyR2) underlie catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited arrhythmogenic disease occurring in the structurally intact heart. The proportion of patients with CPVT carrying RyR2 mutations is unknown, and the clinical features of RyR2-CPVT as compared with nongenotyped CPVT are undefined.</AbstractText>Patients with documented polymorphic ventricular arrhythmias occurring during physical or emotional stress with a normal heart entered the study. The clinical phenotype of the 30 probands and of 118 family members was evaluated, and mutation screening on the RyR2 gene was performed. Arrhythmias documented in probands were: 14 of 30 bidirectional ventricular tachycardia, 12 of 30 polymorphic ventricular tachycardia, and 4 of 30 catecholaminergic idiopathic ventricular fibrillation; RyR2 mutations were identified in 14 of 30 probands (36% bidirectional ventricular tachycardia, 58% polymorphic ventricular tachycardia, 50% catecholaminergic idiopathic ventricular fibrillation) and in 9 family members (4 silent gene carriers). Genotype-phenotype analysis showed that patients with RyR2 CPVT have events at a younger age than do patients with nongenotyped CPVT and that male sex is a risk factor for syncope in RyR2-CPVT (relative risk=4.2).</AbstractText>CPVT is a clinically and genetically heterogeneous disease manifesting beyond pediatric age with a spectrum of polymorphic arrhythmias. beta-Blockers reduce arrhythmias, but in 30% of patients an implantable defibrillator may be required. Genetic analysis identifies two groups of patients: Patients with nongenotyped CPVT are predominantly women and become symptomatic later in life; patients with RyR2 CPVT become symptomatic earlier, and men are at higher risk of cardiac events. These data provide a rationale for prompt evaluation and treatment of young men with RyR2 mutations.</AbstractText> |
3,123 | Long-term pharmacologic management of atrial fibrillation in the elderly. | The first decision to be made in treating atrial fibrillation in the elderly is to determine whether to pursue a treatment strategy of rate control or rhythm control. Both strategies require use of anticoagulation therapy with warfarin (target international normalized ratio, 2.5; range 2-3). If a decision is made for rhythm control, the critical therapy is almost always with an antiarrhythmic drug. Before selecting an antiarrhythmic drug for use, it is first necessary to determine the presence or absence of underlying structural heart disease, as that will affect the available options for antiarrhythmic drug use. If there is no underlying structural heart disease, any of the available antiarrhythmic drugs may be used, although a clinically reasoned approach is suggested. If there is underlying structural heart disease, not all antiarrhythmic drugs are appropriate for use. A clinically reasoned approach is suggested in the presence of coronary artery disease, left ventricular dysfunction /congestive heart failure, or hypertension based largely on the risk/benefit profile of the drugs. |
3,124 | Effects of adrenaline on electrophysiological parameters during short exposure to global ischemia. A ventricular fibrillation study in isolated heart. | The mechanisms by which adrenaline may enhance defibrillation success rate, is poorly understood.</AbstractText>To study electrophysiological effects of adrenaline during short exposure to global ischemia.</AbstractText>In isolated perfused feline hearts, coronary perfusion was eliminated repeatedly for 1 min with 10 min reperfusion intervals. Treatment included: (1) continuous perfusion alone-control, (2) global ischemia alone, (3) adrenaline (10(-7) M) during perfusion, (4) adrenaline (10(-7) M) during global ischemia (n = 10), in separate hearts, (5) control and higher adrenaline concentration (1 x 10(-6) M), (6) during perfusion, (7) during global ischemia (n = 9). Measurements during pacing included: (1) diastolic threshold of excitability; (2) refractoriness; (3) epicardial conduction time; and (4) all tissue resistivity to indirectly detect changes in passive properties of conduction. Measurements during 1 min (or 90 sec) of electrically induced ventricular fibrillation included-all tissue resistivity and, based on maximal entropy spectral analysis and normalized entropy, rate of arrhythmia and degree of arrhythmia organization.</AbstractText>Adrenaline (10(-7) M) during global ischemia vs control caused spontaneous arrhythmia termination, increased threshold significantly but reduced conduction time. Higher adrenaline concentration (1 x 10(-6) M) during global ischemia improved the passive properties of conduction and arrhythmia organization and reduced arrhythmia rate. Global ischemia alone increased conduction time but had a deleterious effect on passive properties. Adrenaline (10(-7) M) during perfusion improved conduction, but did so less than during global ischemia. Higher adrenaline concentration during perfusion (10(-6) M) improved arrhythmia organization and caused spontaneous arrhythmia termination but again less than during global ischemia.</AbstractText>During short periods of global ischemia adrenaline improved the passive properties of conduction and arrhythmia organization, reduced arrhythmia rate and increased its spontaneous termination. Such changes may be operative in improving defibrillation success.</AbstractText> |
3,125 | Management of common arrhythmias: Part II. Ventricular arrhythmias and arrhythmias in special populations. | In patients without established cardiac disease, the occurrence of premature ventricular complexes without sustained ventricular tachycardia is more an annoyance than a medical risk, and treatment is not required. In contrast, patients with established heart disease and premature ventricular complexes have a higher likelihood of developing ventricular tachycardia or fibrillation. These patients should be treated with a beta blocker or class I antiarrhythmic drug. Treatment of arrhythmias in pregnant women is rarely needed. When treatment is required, amiodarone should be avoided, and beta blockers should be used with caution, because these agents have been associated with fetal growth retardation. The most important rhythm abnormality in athletes is ventricular tachycardia associated with hypertrophic cardiomyopathy. If the presence of the disease is confirmed by echocardiography, beta-blocker therapy is necessary, and these patients should be limited to participation in nonstrenuous sports. Acute arrhythmias in children with Wolff-Parkinson-White syndrome can be treated with adenosine. Radiofrequency ablation of the accessory pathway can provide long-term control. |
3,126 | Management of common arrhythmias: Part I. Supraventricular arrhythmias. | Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option. |
3,127 | Multiple spatially distributed stimulators and timing programs for entrainment of activation during ventricular fibrillation. | Activation sequences during ventricular fibrillation (VF) display complex pattern and fast rate. Recent evidence suggests that even during VF an excitable gap may exist. Existence of excitable gap lead us to hypothesize that it should be possible to entrain activation patterns during VF by using spatially distributed and temporally phased pacing strength stimuli. We describe here the electronics hardware and software that were developed to test our hypothesis. Eight biphasic stimulators were designed and fabricated, each addressable via a TTL input and thus independently triggered. To minimize electrical interference from stimulus pulses the stimulators were optically isolated. A program written in C was used to deliver TTL inputs to time the sequence of stimulation. The parameters that could be varied were, pulse intensity, polarity, and duration, inter pulse interval and activation pattern cycle length. Restitution's of action potential duration, conduction velocity, and complex activation patterns make the timing of stimulators complex. To aid in optimal timing of these stimulators, we used a Luo-Rudy ionic model of cellular activation to simulate VF in a matrix of 400 x 400 cells. Entrainment of activation was verified using animated displays of activation sequences. Using results of simulation we verified the function of our stimulators experimentally using electrically induced VF in canines and by using electrograms recorded from 121-electrode patch. Our results show that the developed hardware and software can be used to deliver distributed stimuli in a flexible and effective pattern, which may aid in development of approaches for treatment of VF. |
3,128 | Epicardial electrogram of the right ventricular outflow tract in patients with the Brugada syndrome: using the epicardial lead. | We tried to record an epicardial electrogram directly, and we examined local electrograms before and after administration of a class IC anti-arrhythmic drug in patients with the Brugada syndrome.</AbstractText>Electrical heterogeneity of the epicardium in the right ventricular outflow tract (RVOT) has been thought to be related to the Brugada syndrome. However, an epicardial abnormality has not been demonstrated in patients with the Brugada syndrome.</AbstractText>In five patients with a Brugada-type electrocardiogram (ECG), local unipolar electrograms were recorded at the epicardium and endocardium of the RVOT. To record the epicardial electrogram directly, we introduced an electrical guidewire into the conus branch (CB) of the right coronary artery. The duration of the local electrogram after termination of the QRS complex (DP) was measured before and after class IC anti-arrhythmic drug administration. The signal-averaged electrocardiogram (SAECG) was also obtained in all patients.</AbstractText>A definite DP was observed at the epicardium, but not at the endocardium. After administration of a class IC anti-arrhythmic drug, the DP at the epicardium was prolonged from 38 +/- 10 ms to 67 +/- 24 ms. The late potential corresponding to the DP at the epicardium was observed in all patients on the SAECG.</AbstractText>An epicardial electrogram can be recorded from the CB. Recording from the CB enables identification of an epicardial abnormality in patients with the Brugada syndrome. These abnormal electrograms may be related to a myocardial abnormality in the epicardium of patients with the Brugada syndrome.</AbstractText> |
3,129 | Biphasic versus monophasic shock waveform for conversion of atrial fibrillation: the results of an international randomized, double-blind multicenter trial. | This study compared a biphasic waveform with a conventional monophasic waveform for cardioversion of atrial fibrillation (AF).</AbstractText>Biphasic shock waveforms have been demonstrated to be superior to monophasic shocks for termination of ventricular fibrillation, but data regarding biphasic shocks for conversion of AF are still emerging.</AbstractText>In an international, multicenter, randomized, double-blind clinical trial, we compared the effectiveness of damped sine wave monophasic versus impedance-compensated truncated exponential biphasic shocks for the cardioversion of AF. Patients received up to five shocks, as necessary for conversion: 100 J, 150 J, 200 J, a fourth shock at maximum output for the initial waveform (200 J biphasic, 360 J monophasic) and a final cross-over shock at maximum output of the alternate waveform.</AbstractText>Analysis included 107 monophasic and 96 biphasic patients. The success rate was higher for biphasic than for monophasic shocks at each of the three shared energy levels (100 J: 60% vs. 22%, p < 0.0001; 150 J: 77% vs. 44%, p < 0.0001; 200 J: 90% vs. 53%, p < 0.0001). Through four shocks, at a maximum of 200 J, biphasic performance was similar to monophasic performance at 360 J (91% vs. 85%, p = 0.29). Biphasic patients required fewer shocks (1.7 +/- 1.0 vs. 2.8 +/- 1.2, p < 0.0001) and lower total energy delivered (217 +/- 176 J vs. 548 +/- 331 J, p < 0.0001). The biphasic shock waveform was also associated with a lower frequency of dermal injury (17% vs. 41%, p < 0.0001).</AbstractText>For the cardioversion of AF, a biphasic shock waveform has greater efficacy, requires fewer shocks and lower delivered energy, and results in less dermal injury than a monophasic shock waveform.</AbstractText> |
3,130 | Cardioprotective effects of 9-hydroxyellipticine on ischemia and reperfusion in isolated rat heart. | We determined the effect of 9-hydroxyellipticine (9HE) on ryanodine receptor (RyR) and cardiac function after global ischemia in isolated rat hearts. The binding of [3H]-ryanodine in rabbit cardiac sarcoplasmic reticulum was displaced by 9HE in a biphasic manner corresponding to the two sites model with IC50 values of 6.1 microM and 55 mM. The increase of the intracellular Ca2+ concentration induced by caffeine in CHO cells expressing cardiac-type RyR was suppressed by 9HE in a concentration-dependent manner. Pretreatment of the heart with 9HE decreased the total duration of reperfusion-induced ventricular fibrillation (VF) and delayed the onset of VF. There was also a significant recovery of contractile force of ischemic hearts following 9HE. Unlike nifedipine, an L-type Ca2+-channel blocker, 9HE did not suppress the contraction of rat papillary muscles. Thus, 9HE exerts the cardioprotective effects against ischemia /reperfusion injury without changing hemodynamic indices. |
3,131 | 4-Aminopyridine: effects on electrical activity during ischemia and reperfusion in perfused rat hearts. | We investigated the effects of 2 and 4 mM 4-aminopyridine (4-AP,--blocker of the transient outward current I(to) on the electrophysiological response to regional ischemia and reperfusion. Spontaneously beating rat hearts were subjected to coronary occlusion (10 min) followed by reperfusion. The surface electrogram and the membrane potential from subepicardial left ventricular cells were recorded throughout. The basal effect of 4-AP was a dose dependent increase in the action potential duration (APD90) without changes in the resting potential or the heart rate. During early ischemia resting depolarization (from 87.4 +/- 1.9-70.1 +/- 2.5 mV in the controls) was enhanced by 4 mM, 4-AP (84.3 +/- 1.4 mV vs. 61.7 +/- 1.3 mV) whereas APD90 increased by 73.5%. These effects resulted in a marked reduction in the duration of diastolic intervals that led to conduction failure and aborted responses. A partial recovery was found by the end of ischemia concomitant with APD90 shortening in both, control and 4-AP treated hearts. On reperfusion, 4-AP did not influence the initial incidence of ventricular tachyarrhythmias but decreased their duration from 531.5 +/- 56.3-260.7 +/- 100 sec (2 mM) and to 75.6 +/- 10.5 sec (4 mM). These data confirm others obtained by Henry et al. in isolated cells indicating that ischemia induces sequential changes in several K+ conductances. In addition, they show that changes in action potential characteristics may exert beneficial effects on reperfusion arrhythmias by acting on the arrhythmic substrate without suppressing the trigger mechanism. |
3,132 | A selective alpha(2)-adrenergic agonist for cardiac resuscitation. | The effects of selective alpha(2)-adrenergic agonist alpha-methylnorepinephrine on the initial success of resuscitation and postresuscitation myocardial function were compared with nonselective alpha- and beta-adrenergic epinephrine in a swine model of cardiac arrest. Epinephrine, the primary pharmacological intervention in the treatment of cardiac arrest, improves immediate outcome. However, epinephrine increases the severity of myocardial dysfunction after cardiac resuscitation. Both inotropic and chronotropic actions provoke disproportionate increases in myocardial oxygen consumption by the ischemic heart, prompting this study, in which we hypothesized that a selective alpha(2)-adrenergic agonist, alpha-methylnorepinephrine (alpha-MNE), would moderate these adverse effects of epinephrine and minimize postresuscitation myocardial dysfunction. After 7 minutes of untreated ventricular fibrillation (VF) in 14 anesthetized male domestic pigs, precordial compression at a fixed rate of 80 compressions/min was begun, along with mechanical ventilation. Either alpha-MNE (100 microg/kg) or epinephrine (20 microg/kg) was administered as a bolus after 2 minutes of precordial compression. After an additional 4 minutes of precordial compression, defibrillation was attempted. Left ventricular systolic and diastolic function was quantitated with the use of transesophageal echo-Doppler imaging. Comparable increases in coronary perfusion pressure to 15 mm Hg were observed after the administration of both drugs. All animals were successfully resuscitated; epinephrine and alpha-MNE were equally quick in restoring spontaneous circulation after 7 minutes of untreated VF. Ejection fraction was reduced by 35% and 14% by epinephrine and alpha-MNE, respectively, after resuscitation. Epinephrine and alpha-MNE increased postresuscitation heart rate by 38% and 15%, respectively. Accordingly, significantly less postresuscitation impairment followed the administration of alpha-MNE. alpha-MNE, a selective alpha-adrenergic agonist, was as effective as epinephrine in restoring spontaneous circulation after 7 minutes of untreated VF in a porcine model for CPR and demonstrated lesser postresuscitation myocardial injury. |
3,133 | Routine use of the radial artery for coronary artery revascularization. | Between January 1997 and December 2000, a total of 4,000 patients underwent myocardial revascularization using the radial artery as one of the conduits. The mean age of the patients was 54 +/- 7 years, and 92.8% of them were male. Of these patients, 31% had a left ventricular ejection fraction below 40% and 22.8% underwent urgent operation. A total of 4,225 distal anastomoses were performed using the radial artery. The average number of grafts was 3.3 +/- 0.5. The hospital mortality rate was 0.8%. Low cardiac output, inotropic support, perioperative myocardial infarction, reoperation for bleeding, atrial fibrillation, and sternal infection occurred in 1.8%, 2.8%, 1.2%, 1.2%, 16.8%, and 1.2% of the patients, respectively. None of the patients had major ischemia of the hand. The incidence of local hand wound complications was 0.7% (wound infection, 0.4%; wound dehiscence without infection, 0.1%; and hematoma, 0.2%). The average length of stay in the intensive care unit was 20 +/- 7 hours and in the hospital was 6 +/- 2 days. Postoperative angiography, performed in 106 patients at a mean interval of 18 months, showed that 92.4% of radial artery, 96.2% of internal mammary artery, and 76.2% of saphenous vein grafts were patent. |
3,134 | [Coronary thrombosis on patient with the factor V Leiden mutation]. | We report a documented observation of coronary thrombosis occurring in a 25-year-old patient with no risk factor, presenting a hereditary thrombophilia (facteur V Leiden) diagnosed a few months earlier in a context of venous thrombosis. This patient had a spread out anterior myocardial infarction with cardiac arrest due to a ventricular fibrillation; although he was quickly rescued by the mobile intensive Care Unit, the patient died 48 hours later, after cerebral anoxia. The mutation called factor V Leiden is a widely spread hereditary family thrombophilia (5 to 6% of the population) and is characterized by a resistance to activated C protein provoking a hypercoagulable state. The unexpected arterial thrombosis, very rare in that case, can be extremely serious and raises the question of a preventive medication such as antiplatelet agent or low-molecular-weight heparin as soon as the genetic abnormally has been proved to be symptomatic. |
3,135 | Predictors of clinical recurrence after successful electrical cardioversion of chronic persistent atrial fibrillation: clinical and electrophysiological observations. | Recurrence of atrial fibrillation (AF) after electrical cardioversion of chronic AF is not uncommon. However, it remains unclear which parameter(s) predict clinical recurrence. To assess the potential predictors of clinical recurrence after successful electrical cardioversion, we analyzed clinical, echocardiographic and electrophysiologic parameters in 36 patients (age 63 +/- 11 years; 26 males, 10 females) with chronic persistent AF lasting more than 3 months. The dimensions of the left atrium and left ventricular end diastole and end systole were measured by echocardiography. The P wave characteristics from the surface 12-lead electrocardiogram (ECG) were studied in sinus rhythm. Atrial local activations were studied by biatrial basket electrode mapping in AF. With a mean of 7 +/- 2 months of follow-up, 17 (47%) patients had AF recurrence despite multiple antiarrhythmic drug therapy. None of the clinical or echocardiographic parameters were relevant to the recurrence. However, among the surface ECG and intraatrial electrophysiological parameters, the mean P wave duration was the only independent predictor of the risk of clinical recurrence after successful electrical cardioversion. The sensitivity and predictive accuracy of recurrence were 82 and 70%, respectively, when the mean P wave duration was more than 125 ms. |
3,136 | Brugada syndrome: an unusual cause of convulsive syncope. | A patient who presented with a new apparent seizure was found to have abnormal electrocardiographic findings, with classic features of the Brugada syndrome. He had spontaneous episodes of nonsustained ventricular tachycardia, easily inducible ventricular fibrillation at electrophysiological study in the absence of structural heart disease, and a negative neurological evaluation. These findings suggested that sustained ventricular arrhythmias known to be associated with the Brugada syndrome and resultant cerebral hypoperfusion, rather than a primary seizure disorder, were responsible for the event. Patients with the Brugada syndrome often present with sudden death or with syncope resulting from ventricular arrhythmias. In consideration of its variability in presentation sometimes mimicking other disorders, primary care physicians and internists should be aware of its often transient electrocardiographic features. |
3,137 | Determination of the target ventricular rate in patients with atrial fibrillation by evaluation of ventriculoarterial coupling. | In a pilot study, we determined the target ventricular rate of patients with atrial fibrillation by evaluating their ventriculoarterial coupling. Eleven patients with atrial fibrillation were studied. We recorded M-mode echocardiograms and radial artery blood pressure simultaneously. The left ventricular end-systolic pressure-volume ratio (Emax) and effective arterial elastance (Ea) were calculated for each beat, and the relationship of the preceding R-R interval (pRR) to Emax and Ea was evaluated. There was a significant positive correlation between pRR and Emax, and a significant negative correlation between pRR and Ea in all patients. The pRR that produced maximal stroke work was determined at the point of Emax=Ea, and the pRR that achieved maximal mechanical efficiency was determined at the point of 2Ea=Emax. By evaluating ventriculoarterial coupling in these patients who had atrial fibrillation, we were able to determine that the range between the 2 pRR intervals was the range of the optimal ventricular rate. A narrower range of the 2 pRR intervals was observed in patients with dilated cardiomyopathy than in the patients with no underlying cardiac disease. We conclude that it may be possible to determine the optimal ventricular rate in patients with atrial fibrillation by evaluating ventriculoarterial coupling. |
3,138 | Downregulation of immunodetectable atrial connexin40 in a canine model of chronic left ventricular myocardial infarction: implications to atrial fibrillation. | The substrate(s) for atrial fibrillation associated with chronic left ventricular myocardial infarction remain poorly defined. Since atrial connexin40 has a rapid turnover rate and may cause atrial fibrillation, we hypothesized that chronic left ventricular myocardial infarction downregulates atrial Connexin40 and increases atrial fibrillation vulnerability.</AbstractText>The left anterior descending coronary artery was occluded distal to the first diagonal branch in five dogs and studied 7 weeks later. Five dogs with no left anterior descending coronary artery occlusion served as control. Vulnerability to atrial fibrillation was tested by burst atrial stimulation (50 milliseconds for 3 seconds). Atrial fibrillation was induced in all myocardial infarction dogs, lasting from 20 seconds to several minutes. In contrast, only rapid repetitive activity and short-lasting atrial fibrillation (< 5 seconds) could be induced in control dogs. The mean refractory periods of epicardial RA and LA appendages were not significantly different in the two groups. Mean left ventricular myocardial infarction size was 17 +/- 4% of the left ventricle. Histologic analyses showed no signs of atrial ischemic injury or interstitial fibrosis in either group. Atrial myocyte diameter measured at the level of the nuclei of longitudinally sectioned myocytes was not significantly different in the two groups (10.1 +/- 1.2 microm vs. 10.2 +/- 1.2 microm; P = 0.3). Atrial Connexin40 (both left and right atria) in the left ventricular myocardial infarction group was highly heterogeneous and had significantly smaller total area stained than in the control (0.48 +/- 0.09% vs. 0.82 +/- 0.13%; P < 0.01).</AbstractText>Chronic left ventricular myocardial infarction downregulates immunodetectable atrial Connexin40, a property that might contribute to the increased atrial fibrillation vulnerability in this model.</AbstractText> |
3,139 | Transmyocardial laser revascularization and left ventricular reduction surgery affect ventricular arrhythmias and heart rate variability. | Transmyocardial laser revascularization (TMLR) and left ventricular reduction by endoventricular patch plasty (LVR) are 2 new surgical procedures performed in patients with endstage coronary artery disease and left ventricular dilation/aneurysms, respectively. As these are performed in patients at high risk for sudden cardiac death and may interact with arrhythmogenesis, we assessed the influence of these procedures on incidence and severity of ventricular tachyarrhythmias and time-domain heart rate variability.</AbstractText>Preoperative and one week postoperative 24-hour Holter recordings were performed in 37 patients undergoing TMLR (n = 23, CO2-laser technique) or LVR (n = 14).</AbstractText>TMLR patients received a mean of 27.2 +/- 9.2 laser channels. Postoperatively, the proportion of patients who underwent TMLR with spontaneous ventricular tachycardia (> or =4 repetitive ventricular beats) increased (0% vs 26%, P <.05), including one patient who died from documented ventricular fibrillation during monitoring. There was no correlation to the number and/or location of laser-induced channels or to perioperative CK levels. HRV parameters were not altered by TMLR. By contrast, LVR did not significantly influence ventricular tachyarrhythmia episodes but markedly depressed all major HRV parameters (SDNN 116.4 vs 61.8, RMSSD 35.2 vs 19.9, pNN50 14.5 vs 4.9, all P <.05).</AbstractText>Early after TMLR, there is evidence of an increased incidence of spontaneous ventricular tachycardia enhancing the risk for sudden cardiac death, while HRV remains unaffected. By contrast, LVR resulted in a marked reduction in HRV still present one week postoperatively, while no effect was observed on incidence and/or severity of spontaneous ventricular tachyarrhythmias.</AbstractText> |
3,140 | Baseline characteristics of patients with atrial fibrillation: the AFFIRM Study. | Although anticoagulation therapy is accepted for most patients with atrial fibrillation, 2 different strategies exist for management of the cardiac rhythm: atrial fibrillation is allowed to persist while the ventricular rate is controlled; and atrial fibrillation is converted, and an attempt is made to maintain sinus rhythm.</AbstractText>The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Study was a randomized clinical trial that compared these 2 strategies. We report the baseline characteristics of the patients enrolled in the AFFIRM Study.</AbstractText>More than 7400 patients at more than 200 North American hospitals and clinics qualified for enrollment in the AFFIRM Study. A total of 4060 patients were enrolled in the AFFIRM Study. The average age of patients enrolled was 70 years, with 39% female and 89% white. Hypertension was present in 71%. Coronary artery disease was present in 38%. Echocardiography was performed in 3311 patients, and results showed normal ventricular function in 68% and normal left atrial size in 33%. Most patients with recurrent episodes had symptoms with atrial fibrillation. Approximately one third of patients were enrolled with a first episode of atrial fibrillation.</AbstractText>The AFFIRM Study enrolled 4060 predominantly elderly patients with atrial fibrillation to compare ventricular rate control with rhythm control. The patients in the AFFIRM Study were representative of patients at high risk for complications from atrial fibrillation, which indicates that the results of this large clinical trial will be relevant to patient care.</AbstractText> |
3,141 | Quality of life improves with treatment in the Canadian Trial of Atrial Fibrillation. | The impact of atrial fibrillation (AF) and its treatment on health-related quality of life (QOL) is not well understood. We assessed QOL in patients with symptomatic AF participating in the Canadian Trial of Atrial Fibrillation.</AbstractText>Self-report QOL questionnaires including the Short-Form-36 (SF-36), symptom checklist (SCL) and AF Severity Scale (AFSS) were completed at baseline and 3, and 12 months after randomization.</AbstractText>The study group was aged 65 +/- 10 years and 59% were male. By design, 50% of patients were randomized to amiodarone (n = 132), 25% to sotalol (n = 66), and 25% to propafenone (n = 66). Most patients had normal left ventricular function (89%). Physical (41.9 +/- 9.3 to 43.7 +/- 9.2, P =.001) and mental health (47.5 +/- 10.5 to 49.0 +/- 9.8, P =.023) summary measures from the SF-36 improved significantly from baseline to 3 months. Arrhythmia symptom frequency and severity (SCL) also improved markedly from baseline to 3 months (symptom frequency 20.4 +/- 9.4 to 16.2 +/- 9.5 and symptom severity 16.7 +/- 8.2 to 12.9 +/- 7.4, both P <.001). QOL improvements were not significantly different among the groups randomized to amiodarone, sotalol, or propafenone. However, patients with no symptomatic recurrences of AF had higher scores at 3 months on measures of global well-being than those with recurrences in the first 3 months (7.4 +/- 1.8 vs 6.9 +/- 1.8, P <.05). There were no significant QOL changes from the 3 to 12 month assessment.</AbstractText>In patients with symptomatic AF, QOL improves after treatment, independent of the specific drug used for treatment. This is especially true for patients in whom treatment prevents AF recurrence.</AbstractText> |
3,142 | Effect of low-dose amiodarone on atrial fibrillation or flutter in Japanese patients with heart failure. | The efficacy and safety of amiodarone in the management of atrial fibrillation (AF) or flutter in 108 Japanese patients with heart failure was retrospectively examined. Thirty-four (41%) of the 82 patients who were in sinus rhythm after 1 month of amiodarone administration had their first recurrence, 70% of cases occurring within 1 year of initiation. The cumulative rates of maintenance of sinus rhythm were 0.68, 0.55, and 0.47 at 1, 3, and 5 years, respectively. Amiodarone was more effective in maintaining sinus rhythm in patients with paroxysmal AF or flutter than in those with the persistent form (p<0.05). The cumulative rates for cases that remained in permanent AF were 0.04, 0.11, and 0.14 at 1, 3, and 5 years, respectively. Apart from suppressing AF, the mean heart rate during Holter monitoring was significantly decreased with amiodarone therapy in cases of permanent AF. Adverse effects requiring the discontinuation of amiodarone therapy occurred in 16% of patients. Low-dose amiodarone therapy may prevent AF or flutter in Japanese patients with heart failure. |
3,143 | Long-term prognosis of patients with mildly dilated cardiomyopathy. | The long-term prognosis of patients with mildly dilated cardiomyopathy (MDCM) was investigated in 21 patients. MDCM was defined as left ventricular ejection fraction < or = 40% and left ventricular end-diastolic volume < or = 120 ml/m2 by left ventriculography. During a follow-up period of 6.8+/-3.7 years, there were 9 cardiac events (5 heart failure deaths, 2 sudden deaths, and 2 re-hospitalizations for heart failure). Only in the patients without cardiac events was there a significant decrease in left ventricular size (end-diastolic dimension decreased from 58+/-6 mm to 50+/-8 mm, p<0.001) and an improvement in systolic function (fractional shortening increased from 17+/-5% to 26+/-11%, p=0.007). However, left atrial dilation was observed in the patients with an event (from 39+/-5 mm to 43+/-5 mm, p=0.02). Based on proportional hazard analysis, left ventricular end-diastolic pressure and mean pulmonary artery pressure at diagnosis and left atrial dimension at the time of follow-up were significant predictors of poor outcome. A subset of patients with MDCM has impaired hemodynamics at diagnosis, left atrial dilation at follow-up and a poor prognosis, and must be followed carefully even if the left ventricular dilatation is mild. |
3,144 | Clinical significance of the dispersion of the activation--recovery interval and recovery time as markers for ventricular fibrillation susceptibility in patients with Brugada syndrome. | Brugada syndrome (BS) is associated with sudden cardiac death and the markers for ventricular fibrillation (VF) remain unclear, so the activation-recovery interval (ARI) dispersion and recovery time (RT) dispersion were investigated as possible markers in 20 subjects with BS (BS group) and 22 healthy individuals (H group). The 20 BS subjects were divided into 8 cases with documented VF (BS-VF group), 3 of which had recurrences, and 12 without (BS-N group). The corrected dispersion measurements from the standard 12-lead ECG of the QT interval (QTcd), ARI (ARIcd) and RT (RTcd) were compared among the groups. There were significant differences noted between the BS-VF and BS-N groups for the ARIcd and the RTcd, but not for the QTcd. Further, there were critical differences, 150 ms(1/2), observed for the ARIcd and RTcd, and these were associated with a prolongation of the maximum ARI or RT, shortening of the minimum ARI or RT, and prolongation only of the maximum QT for the QTcd. Susceptibility to VF may be predicted by the ARIcd or RTcd in BS. |
3,145 | Effects of physiological and pharmacological concentrations of melatonin on ischemia-reperfusion arrhythmias in rats: can the incidence of sudden cardiac death be reduced? | Cardiac arrhythmias during ischemia-reperfusion (I/R) are believed to be related to free radicals generated in the heart especially during the period of reperfusion. The pineal secretory product, melatonin, is known to be a potent free radical scavenger and its pharmacological concentrations have been shown to reduce the I/R-induced arrhythmias in isolated rat hearts. However, the physiological role of melatonin in the prevention of these arrhythmias is unknown. Rats were pinealectomized (Px) or sham-operated (non-Px) (control) 2 months before the I/R studies. To produce arrhythmias, left main coronary artery was occluded for 7 min, followed by 7 min reperfusion, in anesthetized rats. The incidence of mortality resulted from irreversible ventricular fibrillation (VF) was found significantly higher in the Px rats (63%) than in the control group (25%). Melatonin administration (0.4 mg/kg, either before ischemia or reperfusion) to Px rats significantly reduced the incidence of total (irreversible plus reversible) and irreversible VF and returned them to control values. On the other hand, melatonin administration (0.4 and 4 mg/kg) to non-Px rats failed to attenuate the I/R arrhythmias, significantly. These results suggest that physiological melatonin concentrations are important to reduce the I/R-induced VF and mortality, while pharmacological concentrations of melatonin did not increase its beneficial effect on these arrhythmias. As melatonin levels have been reported to decrease with age, melatonin replacement therapy may attenuate the incidence of sudden cardiac death especially in older patients. |
3,146 | Vasopressin improves survival in a pig model of hypothermic cardiopulmonary resuscitation. | During hypothermic cardiopulmonary resuscitation with a body core temperature <30 degrees C administration of a vasopressor to support coronary perfusion pressure is controversial. The purpose of the current study was to assess the effects of a single 0.4-unit/kg dose of vasopressin on coronary perfusion pressure, defibrillation success, and 1-hr survival in a pig model of hypothermic closed-chest cardiopulmonary resuscitation combined with rewarming.</AbstractText>Prospective, randomized study in an established pig model.</AbstractText>University hospital research laboratory.</AbstractText>Fifteen 12- to 16-wk-old domestic pigs.</AbstractText>Pigs were surface cooled to a body core temperature of 26 degrees C and ventricular fibrillation was induced. After 15 mins of untreated cardiac arrest, manual closed-chest cardiopulmonary resuscitation and thoracic lavage with 40 degrees C warmed tap water were started. After 3 mins of external chest compression, animals were assigned randomly to receive vasopressin (0.4 units/kg, n = 8; or saline placebo, n = 7). Defibrillation was attempted 10 mins after drug administration.</AbstractText>Compared with saline placebo treated-animals, coronary perfusion pressure in vasopressin-treated pigs was significantly higher 90 secs (36 +/- 5 mm Hg vs. 7 +/- 4 mm Hg, p =.000) to 10 mins (24 +/- 4 mm Hg vs. 8 +/- 4 mm Hg, p =.000) after drug administration. Restoration of spontaneous circulation and 1 hr survival were significantly higher in vasopressin animals compared with saline placebo (8 of 8 vasopressin pigs vs. 0 of 7 placebo pigs, p <.001).</AbstractText>A single 0.4-unit/kg dose of vasopressin administered at a body core temperature <30 degrees C significantly improved defibrillation success and 1-hr survival in a pig model of hypothermic cardiopulmonary resuscitation.</AbstractText> |
3,147 | Myocardial function and effect of serum in isolated heart from hypertriglyceridemic and hypertensive rats. | We evaluated the myocardial function of rats with sugar-induced hypertriglyceridemia (HTG) and hypertension, and the effect of serum on myocardial performance in the isolated heart preparation. Also, the response to reperfusion after 30 minutes of global ischemia was investigated. Hearts from HTG rats developed lower ventricular pressure (VP) and the conduction rate was higher than in hearts from control rats (CR). The recovery of VP after ischemia was significantly lower in HTG than in CR hearts (p < 0.05). The HTG sera produced a higher increase in the VP and in the perfusion pressure. During reperfusion, the incidence of premature beats, ventricular fibrillation and tachycardia in HTG hearts was increased so hypertriglyceridemia caused alterations in the mechanical and electrical conduction of the myocardium and exacerbated the injury produced by ischemia-reperfusion. Also a circulating factor in the HTG serum induced a vasoactive response of the heart which was reflected in its mechanical performance. |
3,148 | Dynamics and interaction of filaments in a computational model of re-entrant ventricular fibrillation. | Ventricular fibrillation (VF) is a lethal cardiac arrhythmia. Re-entry, in which action potential wavefronts rotate around filaments, is believed to sustain VF. In this study we used a computational model of multiple wavelet fibrillation in the thin-walled right ventricle (10 mm thick) and the thicker walled left ventricle (16 mm thick) to investigate the effect of tissue thickness and initiation protocol on re-entry, and to examine whether filament dynamics and interaction in the model could explain why re-entry is both rarely observed and short-lived in experimental studies that map electrical activation on the heart surface. We found (i) that the density of filaments, the proportion of transmural filaments and the proportion of filaments visible on the model surface were all higher in the 10 mm simulation, (ii) that the initiation protocol influences the rate of filament breakdown but not the number of filaments present after 1 s, and (iii) that although many filaments are visible on the surface of the model, the majority are visible for less than one rotation. This study shows that tissue thickness, geometry and initiation protocol influence electrical activation during VF, and that the rapid motion and interaction of filaments result in transient appearance of surface re-entry. |
3,149 | Protein kinase Calpha mediates the effect of antiarrhythmic peptide on gap junction conductance. | We investigated the effects of the antiarrhythmic peptide AAP10 (GAG-4Hyp-PY-CONH2, 50 nM) on pairs of adult guinea pig cardiomyocytes and on pairs of HeLa-cells transfected with rat connexin43 (Cx43). Using double cell voltage clamp technique in cardiomyocytes under control conditions, gap junction conductance (Gj) steadily decreased (by -0.3 to -0.4 nS/min). In contrast, 50 nM AAP10 significantly enhanced Gj (by +0.22 to +0.29 nS/min). This effect of AAP10 could be significantly antagonized by bisindolylmaleimide I (BIM), and by the protein kinase C (PKC) subtype-specific inhibitors HBDDE (PKCgamma and -alpha) and CGP 54345 (PKCalpha). In HeLa-Cx43 cells we found similar electrophysiological effects of AAP10. For further analysis, we incubated HeLa-Cx43 cells with [32P]orthophosphate (0.05 mCi/ml) for 4 h at 37 degrees C followed by addition of 50 nM AAP10 for 15 min. We found that incorporation of 32P into Cx43 was significantly enhanced in the presence of AAP10, which was completely inhibited in presence of BIM. PKC enzyme-linked immunosorbent assay (ELISA) revealed significant activation of PKC by AAP10 in HeLa-Cx43 cells, which could be inhibited by HBDDE and CGP 54345. Finally, a binding study using [14C]-AAP10 as radioligand was performed. We found a saturable binding of [14C]-AAP10 with a KD of 0.88 nM to cardiac membrane preparations. For assessment of the antiarrhythmic activity in anesthetized rats, we infused aconitine until the occurrence of ventricular fibrillation (VF). The aconitine dose required for initiation of VF was significantly enhanced in the presence of AAP10. In conclusion; AAP10 increases Gj in both adult cardiomyocytes and transfected HeLa-Cx43 cells. AAP10 leads to enhanced phosphorylation of Cx43 via activation of PKCalpha. A membrane receptor exists for antiarrhythmic peptides. |
3,150 | Ventricular pacing or dual-chamber pacing for sinus-node dysfunction. | Dual-chamber (atrioventricular) and single-chamber (ventricular) pacing are alternative treatment approaches for sinus-node dysfunction that causes clinically significant bradycardia. However, it is unknown which type of pacing results in the better outcome.</AbstractText>We randomly assigned a total of 2010 patients with sinus-node dysfunction to dual-chamber pacing (1014 patients) or ventricular pacing (996 patients) and followed them for a median of 33.1 months. The primary end point was death from any cause or nonfatal stroke. Secondary end points included the composite of death, stroke, or hospitalization for heart failure; atrial fibrillation; heart-failure score; the pacemaker syndrome; and the quality of life.</AbstractText>The incidence of the primary end point did not differ significantly between the dual-chamber group (21.5 percent) and the ventricular-paced group (23.0 percent, P=0.48). In patients assigned to dual-chamber pacing, the risk of atrial fibrillation was lower (hazard ratio, 0.79; 95 percent confidence interval, 0.66 to 0.94; P=0.008), and heart-failure scores were better (P<0.001). The differences in the rates of hospitalization for heart failure and of death, stroke, or hospitalization for heart failure were not significant in unadjusted analyses but became marginally significant in adjusted analyses. Dual-chamber pacing resulted in a small but measurable increase in the quality of life, as compared with ventricular pacing.</AbstractText>In sinus-node dysfunction, dual-chamber pacing does not improve stroke-free survival, as compared with ventricular pacing. However, dual-chamber pacing reduces the risk of atrial fibrillation, reduces signs and symptoms of heart failure, and slightly improves the quality of life. Overall, dual-chamber pacing offers significant improvement as compared with ventricular pacing.</AbstractText> |
3,151 | Electrical refractory period restitution and spiral wave reentry in simulated cardiac tissue. | Theoretical and experimental studies have shown that restitution of the cardiac action potential (AP) duration (APD) plays a major role in predisposing ventricular tachycardia to degenerate to ventricular fibrillation, whereas its role in atrial fibrillation is unclear. We used the Courtemanche human atrial cell model and the Luo-Rudy guinea pig ventricular model to compare the roles of electrical restitution in destabilizing spiral wave reentry in simulated two-dimensional homogeneous atrial and ventricular tissue. Because atrial AP morphology is complex, we also validated the usefulness of effective refractory period (ERP) restitution. ERP restitution correlated best with APD restitution at transmembrane potentials greater than or equal to -62 mV, and its steepness was a reliable predictor of spiral wave phenotype (stable, meandering, hypermeandering, and breakup) in both atrial and ventricular tissue. Spiral breakup or single hypermeandering spirals occurred when the slope of ERP restitution exceeded 1 at short diastolic intervals. Thus ERP restitution, which is easier to measure clinically than APD restitution, is a reliable determinant of spiral wave stability in simulated atrial and ventricular tissue. |
3,152 | Effect of the cardioselective ATP-sensitive potassium channel inhibitor HMR 1883 in a porcine model of cardiopulmonary resuscitation. | HMR 1883 (the free acid form of HMR 1098) selectively inactivates myocardial ATP sensitive potassium channels, which may be a potential important therapeutic approach to prevent life-threatening arrhythmias. This study was designed to assess the effects of HMR 1883 combined with adrenaline on haemodynamic variables, blood gases, and cardiac arrhythmias in a porcine cardiac arrest model.</AbstractText>After 8 min of untreated cardiac arrest, followed by 1 min of cardiopulmonary resuscitation (CPR), 12 pigs weighing 30-40 kg were assigned randomly to receive either 45 microg/kg adrenaline alone (n=6), or 45 microg/kg adrenaline combined with 3 mg/kg HMR 1883 (n=6), followed by up to three defibrillation attempts 2 min later. Five minutes after return of spontaneous circulation, cardiac arrest was induced for 1 min, with the CPR protocol following as described above. All animals subsequently underwent four cardiac arrest intervals of 1, 2, 3, and 4 min duration which were separated by four episodes of 5 min of return of spontaneous circulation.</AbstractText>Haemodynamic variables, cardiac arrhythmias in the acute resuscitation phase between termination of chest compressions and return of spontaneous circulation, and after return of spontaneous circulation in both groups were comparable throughout the experiment. Survival rates throughout the experiment were comparable between groups. Arterial blood gases, electrolyte, glucose, and lactate levels in both groups during the experiment indicated comparable severe metabolic acidosis, with increasing levels after each episode of simulated refibrillation, and subsequent return of spontaneous circulation.</AbstractText>Combining HMR 1883 with adrenaline during CPR resulted in comparable haemodynamic variables, return of spontaneous circulation rates, cardiac arrhythmias, lactate and glucose levels compared with adrenaline alone. This indicates that injection of HMR 1883 was safe under these conditions.</AbstractText> |
3,153 | Noradrenaline, infused locally, reduces arrhythmia severity during coronary artery occlusion in anaesthetised dogs. | To contribute to the debate, discussed in an earlier issue, regarding the role of adrenoceptors in the genesis of early, coronary artery occlusion-induced ventricular arrhythmias.</AbstractText>Mongrel dogs anaesthetised with chloralose and urethane were given either noradrenaline (NA, 100 ng kg(-1) min(-1)), phenylephrine (PHE, 200 ng kg(-1) min(-1)) or isoprenaline (ISO 12.5 ng kg(-1) min(-1)) by intracoronary infusion into a side branch of the left anterior descending coronary artery (LAD), commencing 10 min prior to the occlusion and then throughout the 25-min occlusion period. Control dogs were infused for the same period with saline. In another group of dogs noradrenaline was infused intravenously in a dose of 1 and then 2 microg kg(-1) min(-1) over a period of 60 min, 24 h prior to coronary artery occlusion. Haemodynamic and coronary blood flow changes, as well as changes in the epicardial ST-segment and in the degree of inhomogeneity were continuously recorded. Ventricular arrhythmias were evaluated as ventricular premature beats (VPBs), tachycardiac (VT) episodes and the incidences of VT and ventricular fibrillation (VF) during occlusion and following reperfusion.</AbstractText>Compared to the controls, NA markedly reduced the severity of ventricular arrhythmias resulted from coronary artery occlusion and increased survival (to 40%) following reperfusion; there were no survivors in the control group. Noradrenaline released endogenously following guanethidine administration was also protective. Protection was also seen, although to a lesser extent with intracoronary PHE (occlusion VF 20% cp 80% in controls; survival 42%). In contrast, ISO enhanced arrhythmia severity; five out of seven dogs infused with ISO fibrillated within 10 min of the commencement of occlusion and no dog survived reperfusion. Other indices of ischaemia severity (epicardial ST-segment and inhomogeneity) were also reduced by NA and by PHE. NA, infused 24 h prior to occlusion was also protective against ischaemia and reperfusion-induced arrhythmias and ischaemia-induced changes in inhomogeneity.</AbstractText>We conclude that exogenously administered NA, or released endogenously by chemical means, reduces the severity of ischaemia and reperfusion-induced ventricular arrhythmias and that this is mediated by alpha-adrenoceptors, perhaps through presynaptic inhibition of local NA release or by a 'preconditioning' effect presumably mediated by PKC.</AbstractText> |
3,154 | Dedifferentiation of atrial myocytes during atrial fibrillation: role of fibroblast proliferation in vitro. | Severe myocyte alterations, characterized by enlarged myocytes and myolysis, is observed in fibrillating and dilated atria and contributes to atrial fibrillation. The aim of this study was to determine the nature of this cellular remodeling process and factors involved in its regulation.</AbstractText>In vivo, contractile proteins were studied in 24 human right atrial specimens by means of immunohistochemical techniques. In an attempt to reproduce in vitro the myocyte remodeling and to study its regulation, human atrial myocytes were cultured (n=27) and analyzed immunocytochemically; intracellular Ca(2+) transients (Ca(i)-tr) in response to electrical stimulation were monitored using Fura-2/AM.</AbstractText>In diseased specimens, sarcomeres, seen at the periphery of myolytic myocytes, stained positively with antibodies against sarcomeric proteins of the Z-band (alpha-actinin and titin epitope T12) but not with antibodies against titin epitope T11 (I-band) or desmin (intermediate filament). beta-myosin heavy chain (MHC) and smooth muscle alpha-actin, two proteins of the fetal program, were re-expressed. In culture, diseased myocytes also showed myolysis and glycogen accumulation; their sarcomeres stained positively with anti-alpha-actinin, anti-T12, anti-beta-MHC and anti-smooth muscle alpha-actin but not with anti-titin T11 or anti-desmin antibodies. At confluence, myocytes regained a normal sarcomeric apparatus and were excitable, as shown by electrical Ca(i)-tr triggering. This redifferentiation process was inhibited by fibroblast proliferation.</AbstractText>In diseased atria, myolytic myocytes are in a dedifferentiated state resembling that of immature muscle cells. In vitro, fibroblast proliferation prevents the reversibility of this cellular alteration.</AbstractText> |
3,155 | Body surface potential mapping in patients with Brugada syndrome: right precordial ST segment variations and reverse changes in left precordial leads. | The aim of this study was to perform quantitative signal analysis of high-resolution body surface potential mapping (BSPM) recordings to assess its usefulness for the electrocardiographic characterization of patients with Brugada syndrome. The diagnostic value of the QRS integral and of the gradient of the ST segment have not been elucidated in Brugada syndrome.</AbstractText>In 27 subjects (16 with Brugada syndrome and 11 healthy subjects), 120-lead BSPMs were recorded at baseline and after pharmacological provocation with intravenous administration of ajmaline (1 mg/kg). The recordings were analyzed for two regions outside the positions of the standard ECG leads: the right precordial leads (RPL) on the second and third intercostal space (high RPL) and the left precordial leads (LPL) between the fifth and seventh intercostal space (low LPL).</AbstractText>At baseline, in high RPL regions, patients with Brugada syndrome showed more positive QRS integrals (-5+/-8 vs. -16+/-8 mV ms) and a steeper negative ST segment gradient (-0.62+/-0.41 vs. -0.29+/-0.40 mV/s) compared to healthy subjects, P<0.001. In contrast, in low LPL regions, reduced QRS integrals and positive ST segment gradients were observed. These ECG signs were even more pronounced after intravenous ajmaline and showed a better discrimination for patients with Brugada syndrome than differences in RPL or LPL during baseline, respectively.</AbstractText>In the left precordial leads, patients with Brugada syndrome showed ECG changes which were reversed in relation to the ECG changes observed in right precordial leads. BSPM measurement is a useful tool to improve the understanding of the electrocardiographic changes in the Brugada syndrome.</AbstractText> |
3,156 | Enalapril effects on atrial remodeling and atrial fibrillation in experimental congestive heart failure. | Atrial remodeling contributes to the maintenance of atrial fibrillation (AF) in several cardiac disorders. There is evidence that angiotensin-converting enzyme (ACE) inhibitors reduce the prevalence of AF in patients with congestive heart failure (CHF). There have been no studies performed to assess the effects of ACE inhibitors on atrial dimensions and emptying function in relationship to vulnerability to AF in the setting of experimental CHF.</AbstractText>CHF was produced in 20 dogs by rapid right ventricular pacing during 5 weeks. The dogs were randomized to enalapril (EN) therapy (2 mg/kg/day, n=10) or to a control group (n=10). Echocardiography was performed at baseline and weekly thereafter. At the 5-week electrophysiological study, AF was induced by burst pacing and AF duration was measured.</AbstractText>Atrial areas increased significantly with CHF. Left atrial (LA) fractional area shortening (FAS) decreased by 42% (P=0.0001) in controls but by 9% (P=NS) in the EN group (P=0.01, EN vs. controls). Similar findings were observed for right atrial (RA) changes (P=0.02). Atrial fibrosis was highly correlated with the decrease in LA FAS (r=0.85, P<0.01) and was reduced by EN (from 11.2+/-1.6 to 8.3+/-0.7%, P=0.008). AF duration was 720+/-461 s for controls and 138+/-83 s for EN (P=0.001). LA and RA areas and FAS at 5 weeks correlated with AF duration (P< or =0.001 for all). FAS decrease in both atria also correlated with AF duration at follow-up (r=0.78 and 0.77 for LA and RA, P< or =0.001 for both).</AbstractText>Experimental CHF causes structural and functional abnormalities in both atria, which are correlated with AF duration. ACE inhibition attenuates CHF-induced atrial fibrosis and remodeling and reduces associated AF promotion. These results indicate a role for the renin-angiotensin system in arrhythmogenic atrial structural remodeling in CHF.</AbstractText> |
3,157 | Adenoviral gene transfer to the heart during cardiopulmonary bypass: effect of myocardial protection technique on transgene expression. | Adenoviral gene transfer to the arrested heart during cardiopulmonary bypass (CPB) is a novel method of allowing prolonged vector contact with the myocardium. In this model we investigated the importance of temperature, duration of arrest and cardioplegia on transgene expression.</AbstractText>First-generation adenoviral vector (1 x 10(12) total viral particles) containing the transgene for the human beta2-adrenoceptor (Adeno-beta(2)AR) or beta-galactosidase (Adeno-beta(gal)) was delivered to neonatal piglets via the proximal aorta, during simulated cardiac surgery, and allowed to dwell for the cross-clamp duration. Four treatment groups received Adeno-beta(2)AR. Groups A (n=4) and B (n=6) underwent cold crystalloid cardioplegia arrest for 10 and 30 min, respectively, Group C (n=5) underwent warm crystalloid cardioplegia arrest for 10 min, and Group D (n=5) underwent warm fibrillatory arrest for 10 min. Group E (n=6) received Adeno-beta(gal) and underwent cold crystalloid cardioplegia arrest (30 min). Animals were weaned off CPB and recovered for 2 days. Receptor density was assessed in membrane fractions using radioligand binding and compared using the Mann-Whitney U-test.</AbstractText>Left ventricular transgene overexpression, as evidenced by elevated betaAR density, following Adeno-beta(2)AR treatment was greatest with cold cardioplegia (Group A 588+/-288.8 fmol/mg; P=0.002 and Group B 520+/-250.9 fmol/mg; P=0.01) versus control (Group E 109+/-8.4 fmol/mg). Overexpression also occurred with warm cardioplegia (Group C 274+/-69.5 fmol/mg; P=0.05) and ventricular fibrillation (Group D 215+/-48.4 fmol/mg; P=0.02) versus control. Comparison of the combined cold cardioplegia groups versus those treated with warm conditions showed a trend towards increased expression with cold conditions (P=0.1). Receptor density was also significantly increased in the right ventricle of animals in Group B (165+/-18.1 fmol/mg; P=0.03) and Group D (181+/-23.4 fmol/mg; P=0.02) versus control (Group E 118+/-5.8 fmol/mg).</AbstractText>Cold crystalloid cardioplegia is not detrimental to gene transfer in vivo. In fact, there was a trend towards increased left ventricular transgene expression when the adenoviral vector was delivered following cold versus warm cardioplegia. Shorter periods of contact with the vector may reduce transgene overexpression. Therefore, gene transfer is possible during cardiac surgery with clinically used myocardial protection techniques.</AbstractText> |
3,158 | [Effect of estrogens on the coronary circulation, cardiac contractile function, and development of reperfusion arrhythmia]. | 17-beta-estradiolsulfate (17-ES) was shown to exert a distinct vasoconstrictory effect on coronary vessels resulting in a decrease of the force contraction as well indexes of contractility. The distinct antiarrhythmic effect suggests that 17-ES possesses some properties of calcium antagonist. |
3,159 | Mechanism of syncope in patients with heart disease and negative electrophysiologic test. | In patients with syncope and structural heart disease, syncope is suspected to be attributable to a primary cardiac arrhythmia, but little is known of its mechanism when electrophysiologic study is unremarkable.</AbstractText>We applied an implantable loop recorder in 35 patients with overt heart disease at risk of ventricular arrhythmia, because these were patients with previous myocardial infarction or cardiomyopathy with depressed ejection fraction or nonsustained ventricular tachycardia in whom an electrophysiologic study was unremarkable. During a follow-up of 3 to 15 months, syncope recurred in 6 patients (17%) after a mean of 6+/-5 months; in 3 patients, the mechanism of syncope was bradycardia with long pauses (sudden-onset AV block in 2 cases and sinus arrest in 1 case); in 1 patient, there was stable sinus tachycardia; and in 2 patients, who had chronic atrial fibrillation, there was an increase in ventricular rate. A total of 23 episodes of presyncope were documented in 8 patients (23%): no rhythm variation or mild tachycardia in 12 cases, paroxysmal atrial fibrillation or atrial tachycardia in 10 cases, and sustained ventricular tachycardia in 1 case. No patient died during the study period nor suffered from injury attributable to syncopal relapse.</AbstractText>The patients with unexplained syncope, structural heart disease, and negative electrophysiologic study had a favorable medium-term outcome with no case of death and a low recurrence rate of syncope without related injury. The mechanism of syncope was heterogeneous, and ventricular tachyarrhythmia was unlikely.</AbstractText> |
3,160 | Analysis of factors associated with successful cardiopulmonary resuscitation in non-traumatic dead-on-arrival patients in emergency department. | Out-of-hospital cardiopulmonary arrest has a dismal prognosis. Successful resuscitation of these patients depends on the "chain of survival". In Taiwan, the emergency medical services (EMS) system is under development and the links of "chain of survival" are weak and frequently broken. A 2-year retrospective study was conducted from January, 1999, to December, 2000 to evaluate the factors of successful cardiopulmonary resuscitation (CPR) in non-traumatic DOA patients in ED. Of 175 studied patients, 51 patients (29.1%) were successfully resuscitated with return of spontaneous circulation (ROSC), but only 7 patients (4%) survived to hospital discharge. Most successfully resuscitated patients (84.3%) regained their vital signs within 30 minutes. There were no significant differences in age, sex, vehicle of transportation, administration of prehospital CPR or not, EMS response interval, on-scene duration, and scene-to-hospital interval between patients with ROSC and without ROSC. Compared with asystole cardiac rhythm, patients with pulseless electrical activity (PEA) had a higher successful resuscitation rate (p = 0.001), but no significant differences existed between patients with ventricular fibrillation/ventricular tachycardia (VF/VT) and PEA or VF/VT and asystole. However, there were no significant differences in the survival discharge rate among patients with different initial cardiac rhythms in ED. |
3,161 | [Open heart radio frequency left atrial compartmentation during mitral valve surgery: an alternative to the labyrinth procedure?]. | The authors report their experience of radiofrequency left atrial compartimentation during open heart mitral valve surgery on 37 patients with a 42 +/- 12 months history of atrial fibrillation. The preoperative left ventricular ejection fraction was 62 +/- 8%; the left atrial diameter was 59 +/- 11 mm. The mean operative time was 245 +/- 60 minutes, which included 19 +/- 5 minutes for the ablation procedure. There were 2 early postoperative deaths and 2 deaths from non-cardiac causes at 3 and 6 months. The left ventricular ejection fraction and left atrial dimension were significantly decreased at the time of hospital discharge (54 +/- 12% and 51 +/- 7 mm respectively) (p < 0.01). After an average follow-up of 1 year, 81% of patients were free of atrial fibrillation: 6 patients had undergone DC cardioversion and 1 had a dual-chamber pacemaker. Patients in sinus rhythm after the ablation were associated with shorter periods of atrial fibrillation and smaller left atrial dimensions postoperatively than those who remained in fibrillation. The authors conclude that radiofrequency compartimentation of the left atrium associated with antiarrhythmic therapy can interrupt atrial fibrillation in 81% of patients at 1 year: the ablation procedure takes only 8% of the operation time. Predictive factors of success of ablation should be defined to determine which patients benefit most from this technique. |
3,162 | [Role of antiarrhythmics in the treatment of paroxysmal atrial fibrillation]. | Atrial fibrillation is not a homogenous entity. Numerous parameters affect its cause, its continuation, and the arrest of an attack. The presence or absence of cardiopathy and left ventricular dysfunction play a major role via the electrophysiological and haemodynamic consequences and the repercussions on the state of the autonomic nervous system, and finally on the effect of anti-arrhythmics themselves. This shows the importance of taking into account all of these parameters together in order to adapt the therapeutic approach. Equally, this underlines the difficulty in interpreting clinical studies comparing pharmacological treatments when the populations treated are poorly defined or very heterogenous. Most often, one drug is not more or less effective than another, it is more or less suited to the patients treated. The frequency of recurrences of AF despite anti-arrhythmic treatment (on average 50% to 60% at one year) means that in paroxysmal AF the goal of anti-arrhythmic treatment is relatively modest: essentially reducing the frequency, duration and severity of AF attacks, allowing an improvement in the quality of life. The consequences in daily practice are clear: one must ensure good patient compliance and minimise the risks of treatment: side effects of and pro-arrhythmic effects of anti-arrhythmics. |
3,163 | [Monophasic action potentials: considerations and limits]. | Monophasic action potentials are currents recorded in vivo in the extracellular milieu which can reproduce the repolarisation signal of intracellular action potentials. For a long time unstable and complex to record, they now require simply a firm myocardial contact with a bipolar electrophysiological catheter and modification with recording filters, without a high-pass filter (DC). They have been widely used in recent years to study in vivo modifications of the action potential durations with frequency, epi-, endo-, or intramyocardial cellular topography, endocavity pressure modifications, or antiarrhythmic medication. They allow a unique means of continuous analysis in animals or in patients of the action potentials during polymorphic arrhythmias such as atrial fibrillation, ventricular fibrillation and torsades de pointes, although in these cases the refractory periods can not be measured precisely and continuously, beat after beat. In contrast, their clinical or experimental use in the study of arrhythmias dependent on premature post-depolarisations has without doubt been excessive and disputable, because it appears improbable that authentic premature post-depolarisations could ever be obtained on a monophasic action potential, which always represents the summation of the action potentials of dozens of cells. |
3,164 | [Endocavitary ablation for arrhythmias. New modalities of radiofrequency applications. New energy types]. | Radiofrequency remains the reference energy type for catheter ablation of rhythm disorders. In the classic indications, which are atrial flutter or tachycardia, nodal re-entry and Wolff-Parkinson-White syndrome, this energy source has the best cost-efficiency-safety ratio, subject to strict conditions of use. Some new modalities of application have further improved performance, especially active irrigation of the electrode which allows induction of deeper lesions which is very useful for the ablation of difficult atrial flutters, epicardial fascicles of Kent and ischaemic ventricular tachycardias. The only emerging alternative energy type, in the framework of classical ablation, is cold, for which the principal advantages are the homogenous and slightly thrombogenic character for the lesion involved, and the possibility of reversible applications tests which are especially useful in the ablation of structures at risk. The situation is more open-ended concerning research on ablation for atrial fibrillation or the so-called new energy types, such as ultrasound and laser, whilst recognising a renewal in interest, especially for circumferential ablation of the pulmonary veins to isolate the ectopic venous foci. Mechanical energy such as luminous energy is emitted across a catheter balloon deployed at the orifice of the vein, perpendicular to its axis, aiming to reach a continuous circumferential lesion with a minimum of applications. Equally radiofrequency has been undergoing significant evolution for this application, such as by the development of porous catheter balloons with a liquid electrode, as well as by the development of deployable circumferential catheters. Ablation is use for atrial fibrillation, by endocavity atrial segmentation remains a field of research in which radiofrequency retains an important place. It is delivered via multi-electrode catheters according to the new application modalities, either pulsed or by phase interval, which secure better efficacy by better continuity of the line of block. Research is equally underway on the use of microwaves and cold in this application. |
3,165 | [Role of atrial stimulation in the treatment of paroxysmal atrial fibrillation]. | Preventive treatments for atrial fibrillation by stimulation have been developed for several years now, mainly due to the relative failure of anti-arrhythmic treatments. They are based on the hypothetical effects of stimulation by controlling cardiac frequency, abolishing bradycardia-dependent extrasystoles, by the inhibition of atrial automatic foci with "overdrive", and by the modification of intra- or inter-atrial conduction delays as well as by remodelling the arrhythmogenic substrate. It is clear that an undeniable effect exists for the prevention of atrial fibrillation, even for the risk of cerebral vascular accident, by physiological stimulation (DDD/DDDR) compared to pure ventricular stimulation (VVI/VVIR) in a heterogenous global population of stimulated patients. For the moment, there is not sufficient proof of a positive effect for the emerging sites of cardiac stimulation, either atrial mono-site or double site in the populations at high risk of atrial fibrillation, with or without associated bradycardia. Some new prevention algorithms by "overdrive" are under development but for the moment only a few preliminary studies seem to show a slight benefit. It is clear that at present stimulation should be reserved only for cases of atrial fibrillation associated with a classic indication for implantation. In these patients it is recommended to position the probes in an optimal manner in order to counteract conduction disorders, choosing an adapted double chamber stimulator with prevention algorithms. That said, the patient should be clearly warned that the long term success rate is no more than 50%. |
3,166 | CVT-510 (CV Therapeutics). | CVT-510, the lead compound from a series of selective adenosine A1 receptor agonists, is being developed by CV Therapeutics for the potential treatment of supraventricular tachycardias and atrial arrhythmias [224364], [299365]. Phase II trialsfor atrial fibrillation commenced in December 1999 [349469], while a phase III trial for paroxysmal supraventricular tachycardia (PSVT) began in June 2001; this multicenter, randomized, double-blind, placebo-controlled trial, was to determine the safety and efficacy of CVT-510 in the conversion of PS VT to normal sinus rhythm [414190]. Analysts at Morgan Stanley predicted in December 2001, that the product would befiled with the FDA in 2004 and be launched onto the US market in 2005, with revenues of US $25 million, rising to US $83 million in 2006 [435233]. |
3,167 | Novel mutations in domain I of SCN5A cause Brugada syndrome. | Brugada syndrome, an autosomal dominantly inherited form of ventricular fibrillation characterized by ST-segment elevation in leads V1-V3 and right bundle-branch block on surface electrocardiogram, is caused by mutations in the cardiac sodium channel gene SCN5A. Patients with Brugada syndrome were studied using single-strand conformation polymorphism analysis, denaturing high-performance liquid chromatography, and DNA sequencing of SCN5A. Mutations were identified in SCN5A in two families and one sporadic case. In one family, a missense mutation leading to a glycine to valine substitution (G351V) in the pore region between the DIS5 and DIS6 transmembrane segments was detected. Biophysical analysis demonstrated that this mutation caused significant current reduction. In the other family, a 20-bp deletion of the exon 5 splice acceptor site was identified; as exon 5 encodes part of the intracellular loop between DIS2 and DIS3, this portion of the channel is disrupted. In the sporadic patient, a missense mutation resulting in the substitution of lysine by glutamic acid (K126E) in the intracellular loop at the boundary with DIS1 was identified. These three new SCN5A mutations in Brugada syndrome patients are all located within domain I of SCN5A, a region not previously considered important in the development of ventricular arrhythmias. |
3,168 | Method for ventricular fibrillation detection in the external electrocardiogram using nonlinear prediction. | The automatic external defibrillator is a lifesaving device which processes and analyses the electrocardiogram (ECG) and delivers defibrillation shock when necessary. The accuracy of the built-in algorithm for ECG analysis must be very high, with sensitivity and specificity aimed to approach the maximum values of 100%. An algorithm based on nonlinear prediction of the external ECG signal is proposed. It extracts seven parameters characterizing the prediction possibility of the assessed ECG signal. By means of the K-nearest neighbours rule the diagnostic accuracy of different combinations of these parameters was evaluated. Thus the accuracy obtained was higher than 95% with sensitivity and specificity values depending on the combination of parameters. The method was tested with ECG records from the widely recognized databases of the American Heart Association (AHA) and Massachusetts Institute of Technology (MIT). |
3,169 | A novel ultrasound technique to estimate right ventricular geometry during fibrillation. | Finite element modelling of the heart for the purpose of studying the electric fields of defibrillation shocks requires knowledge of the geometry of the heart during fibrillation. However, the standard method of measuring this geometry, MRI. cannot be used during fibrillation because the heart geometry changes rapidly and perhaps unpredictably. We present a new ultrasound approach to measuring the right ventricular geometry during fibrillation and preliminary data using this technique. In six anaesthetized pigs, we find that a short axis cross-sectional area of the right ventricle increases by 38% during a 30 s episode of ventricular fibrillation. A long axis cross-sectional area increases by 19% during this same time. By fitting parameters of a simple geometric model to the experimental data, we estimate that the volume of blood in the right ventricular cavity increases by approximately 30% during the episode of ventricular fibrillation. We present the first study of the RV area during-fibrillation with the estimated volume. Our data suggest changes in defibrillation threshold may be linked to current shunting through the increased blood volume. |
3,170 | Randomized study of early intravenous esmolol versus oral beta-blockers in preventing post-CABG atrial fibrillation in high risk patients identified by signal-averaged ECG: results of a pilot study. | Patients with prolonged signal-averaged ECG have four times higher risk for development of atrial fibrillation (AF) after coronary artery bypass surgery (CABG). Incidence of AF is reduced, but not eliminated by prophylaxis with beta-blockers. The limitations of prophylaxis with oral beta-blockers may be related to the delayed effect of oral therapy. We performed a pilot study of the efficacy of early intravenous esmolol and an oral beta-blocker regimen for prevention of postoperative AF.</AbstractText>Fifty patients referred for CABG and considered to be at high risk for postoperative AF on the basis of prolonged signal-averaged ECG P wave duration > 140 ms were randomized to receive either a 24-hour infusion of esmolol 6-18 hours after CABG, at an average dose 67 +/- 7 microg/kg/min, followed by oral beta-blockers versus oral beta-blockers only beginning on postoperative day 1.</AbstractText>Seven of 27 patients (26%) in the esmolol group and 6 of 23 patients (26%) in the oral beta-blocker group developed postoperative AF, P = NS. The mean time of onset of AF (2.7 +/- 0.5 vs 2.7 +/- 0.3 postoperative day, P = NS) and the median duration of AF (10 [2192] vs 7 [1.16] hours, P = NS) were similar between the two groups. Eleven (41%) patients treated with esmolol developed adverse events (hypotension: 8, bradycardia requiring temporary pacing: 2, left ventricular failure:1 patient) as compared to only one patient (4%) in the beta-blocker group who developed hypotension, P = 0.006.</AbstractText>This randomized controlled pilot study suggests that intravenous esmolol is less well tolerated and offers no advantages to standard beta-blocker in preventing AF after CABG.</AbstractText> |
3,171 | Documentation of acute rise in ventricular capture thresholds associated with flecainide acetate. | Treatment of paroxysmal atrial fibrillation with flecainide acetate resulted in a 4-fold increase in ventricular capture thresholds. The detailed time course of the threshold increase and decrease was documented using the AutoCapture algorithm and graphic summary. |
3,172 | Minimal principle for rotor filaments. | Three-dimensional rotors, or scroll waves, provide essential insight into the activity of excitable media. They also are a suspected cause in the formation and maintenance of ventricular fibrillation, whose lethality is well known. It is therefore of considerable interest to find out what configurations can be adopted by such pathologies. A scroll's behavior is embodied in its organizing center or filament, a largely quiescent tube about which the scroll rotates. Predicting filament shape has normally required computer-intensive simulations of the whole scroll in time. We have found a fast and robust principle that yields the prediction for stationary filaments on a purely geometrical basis, blind to the reaction parameters of the medium. The procedure is to calculate the filament shape as a minimal path. We work in singly diffusive media whose diffusivity tensor--and no other feature--varies spatially. Mathematical and numerical evidence is presented for the proposition that a stable filament is a geodesic in a three-dimensional space whose metric is given by the inverse diffusivity tensor of the medium. Away from the boundaries, a stable filament is unaffected by the reaction parameters. The algorithmic aspects of this work are subsidiary to our main purpose of drawing attention to the universal and unexpectedly exact fit of an elementary geodesic principle within reaction-diffusion theories. |
3,173 | Frequency distribution, variance, and moving average of left ventricular rhythm and contractility during atrial fibrillation in dog. | Mean levels of left ventricular rhythm and contractility averaged over arrhythmic beats would characterize the average cardiac performance during atrial fibrillation (AF). However, no consensus exists on the minimal number of beats for their reliable mean values. We analyzed their basic statistics to find out such a minimal beat number in canine hearts. We produced AF by electrically stimulating the atrium and measured left ventricular arrhythmic beat interval (RR) and peak isovolumic pressure (LVP). From these, we calculated instantaneous heart rate (HR = 60,000/RR), contractility (E(max) = LVP/isovolumic volume above unstressed volume), and beat interval ratio (RR1/RR2). We found that all their frequency distributions during AF were variably nonnormal with skewness and kurtosis. Their means +/- standard deviations alone cannot represent their nonnormal distributions. A 90% reduction of variances of E(max) and RR1/RR2 required a moving average of 15 and 24, respectively, arrhythmic beats on the average, whereas that of RR and HR required 60 beats on the average. These results indicate that a statistical characterization of arrhythmic cardiodynamic variables facilitates better understanding of cardiac performance during AF. |
3,174 | Improvement in resuscitation knowledge after a one-day paediatric life-support course. | To assess the effect of a one-day paediatric life-support course on the knowledge of paediatric trainees.</AbstractText>A telephone survey was performed prior to and at set intervals following the course. Responses to individual questions before and after the course were analysed and an overall test score was calculated. The acquisition and retention of knowledge was measured by comparing test scores for the same group of trainees at time intervals after the course.</AbstractText>All candidates were surveyed. The median duration of paediatric training prior to the course was 3 years. Eighteen candidates (78%) had previously intubated a child and 13 (57%) had previously used an intraosseous needle. Prior to the course, few of the 23 candidates had adequate knowledge of either the management of the cervical spine in the seriously injured child (17%), fluid resuscitation in meningococcal septicemia (52%), shock dose in ventricular fibrillation (61%), or the management of anaphylactic shock (35%). There was a significant improvement in the knowledge of the group after the course, with median test scores increasing from 19 to a maximum of 22 (P < 0.001). This knowledge was retained at 4 months after the course.</AbstractText>Despite a high level of experience and previous training in paediatric resuscitation, many candidates lacked the basic knowledge necessary for the resuscitation of seriously ill or injured children. There was a significant improvement in this knowledge after the course, and this was maintained for 4 months. The paediatric life-support course is an important means of resuscitation training for junior doctors.</AbstractText> |
3,175 | Dynamic nature of atrial fibrillation substrate during development and reversal of heart failure in dogs. | Clinical atrial fibrillation (AF) often results from pathologies that cause atrial structural remodeling. The reversibility of arrhythmogenic structural remodeling on removal of the underlying stimulus has not been studied systematically.</AbstractText>Chronically instrumented dogs were subjected to 4 to 6 weeks of ventricular tachypacing (VTP; 220 to 240 bpm) to induce congestive heart failure (CHF), followed by a 5-week recovery period leading to hemodynamic normalization at 5-week recovery (Wk5(rec)). The duration of burst pacing-induced AF under ketamine/diazepam/isoflurane anesthesia increased progressively during VTP and recovered toward baseline during the recovery period, paralleling changes in atrial dimensions. However, even at full recovery, sustained AF could still be induced under relatively vagotonic morphine/chloralose anesthesia. Wk5(rec) dogs showed no recovery of CHF-induced atrial fibrosis (3.1+/-0.3% for controls versus 10.7+/-1.0% for CHF and 12.0+/-0.8% for Wk5(rec) dogs) or local conduction abnormalities (conduction heterogeneity index 1.8+/-0.1 in controls versus 2.3+/-0.1 in CHF and 2.2+/-0.2 in Wk5(rec) dogs). One week of atrial tachypacing failed to affect the right atrial effective refractory period significantly in CHF dogs but caused highly significant effective refractory period reductions and atrial vulnerability increases in Wk5(rec) dogs.</AbstractText>Reversal of CHF is followed by normalized atrial function and decreased duration of AF; however, fibrosis and conduction abnormalities are not reversible, and a substrate that can support prolonged AF remains. Early intervention to prevent fixed structural abnormalities may be important in patients with conditions that predispose to the arrhythmia.</AbstractText> |
3,176 | A comparison between ischemic preconditioning, intermittent cross-clamp fibrillation and cold crystalloid cardioplegia for myocardial protection during coronary artery bypass graft surgery. | The aim of this study was to compare ischemic preconditioning (IPC) with two established methods of myocardial protection, namely cold crystalloid cardioplegia and intermittent cross-clamp fibrillation (ICCF), in coronary artery bypass graft (CABG) surgery. This was a prospective randomised study. Thirty CABG patients were randomised to receive: (a) St Thomas' cardioplegia solution no. 2; (b) ICCF; or (c) IPC (two 3-min periods of ischemia with 2-min of reperfusion). Surgery was performed under standardised conditions by one surgeon (WBP). The primary endpoint was cardiac troponin T release during the first 72 h after surgery. Mean troponin T at 72 h was significantly lower in the IPC group (0.5 microg/l; p=0.05, ANOVA) compared with the cardioplegia and ICCF groups (2.1 and 1.3 microg/l respectively). This suggests that ischemic preconditioning is superior at limiting myocardial necrosis during CABG, but there is no difference between cold crystalloid cardioplegia and intermittent cross-clamp fibrillation. |
3,177 | Non-invasive Wedensky modulation within the QRS complex. | To investigate non-invasively induced Wedensky modulation, 2ms pulses of 5, 20 and 40mA were delivered between precordial and subscapular patches synchronously with the ORS complex. Wavelet vector magnitude was obtained for averaged modulated and non-modulated complexes. The surface area of a 3D-envelope of their difference (WSR) was compared in 59 patients with an uncomplicated follow-up after myocardial infarction (MI) (42 men, 64.3+/-9.1 years), in 30 patients with ischaemic heart disease and a history of ventricular tachycardia/fibrillation (VT/VF) (29 men, 63.1+/-9.8 years), and in 53 healthy subjects (control) (22 men, 56.6+/-10.1 years). Reproducibility of the assessment was tested by computing relative errors in a sub-population of 30 VT/VF patients and 47 controls. Wedensky modulation parameters differed significantly between control, MI and VT/VF subjects. In 10 ms post-modulation windows, the following WSR values were obtained: controls: 1184+/-496 (5mA), 1553+/-838 (20 mA) and 2092+/-1488 (40 mA); VT/VF: 861+/-412 (5mA), 1134+/-636 (20 mA) and 1320+/-1036 (40 mA); MI: 1305+/-885 (5mA) and 1779+/-1169 (20 mA). With all modulating energies used, the VT/VF patients differed significantly from both the controls and MI patients; control patients against VT/VF patients: p<0.004 (5 mA), p<0.01 (20 mA) and p<0.001 (40 mA); VT/VF patients against MI patients: p<0.02 (5mA), p<0.01 (20 mA); control patients against MI patients: all p=NS. The reproducibility assessment showed an acceptable stability of Wedensky modulation parameters. This study demonstrated that wavelet decomposition detects non-invasive Wedensky modulation within the QRS complex, and VT/VF patients are less sensitive to Wedensky modulation than control and MI patients. |
3,178 | Low recurrence of syncope in patients with inducible sustained ventricular tachyarrhythmias treated with an implantable cardioverter-defibrillator. | To determine the effectiveness of the implantable cardioverter defibrillator (ICD) in preventing recurrence of syncope in patients with structural heart disease, previously unexplained syncope and inducible ventricular arrhythmias.</AbstractText>Thirty-eight patients with syncope, structural heart disease and inducible arrhythmias had an ICD implanted. All ICDs delivered antitachycardia pacing and shocks of adjusted energy. Detection and therapy were programmed according to uniform criteria.</AbstractText>The mean age of the patients was 63+/-11 years and most of them were male (36/38). After a mean follow-up of 28+/-15 (4-61) months, six patients died and one underwent heart transplantation. Syncope recurred in three patients, but in none of them was it caused by an arrhythmic event. In 18 patients, 113 episodes of ventricular tachycardia/ventricular fibrillation were detected and appropriately treated by the ICD. The mean time from implant until first appropriate therapy was 18+/-14 months. The actuarial probability of receiving appropriate therapy was 20% and 42% at 12 and 24 months, respectively.</AbstractText>In patients with unexplained syncope, structural heart disease and inducible arrhythmias, ICD prevents syncope associated with arrhythmic events. Frequent effective use of antitachycardia pacing and shocks of adjusted energy seem essential to this aim.</AbstractText>Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.</CopyrightInformation> |
3,179 | J wave and ST segment elevation in the inferior leads: a latent type of variant Brugada syndrome? | In a patient referred for the evaluation of non-sustained monomorphic ventricular tachycardia on Holter recordings, ventricular fibrillation was electrically induced during electrophysiologic study. Despite the absence of structural heart diseases, his ECG revealed J wave and ST segment elevation in the inferior leads, which showed circadian variation and were augmented by the sodium channel blocker, pilsicainide. This case might lead us to notice a new concept, a 'latent' type of variant Brugada syndrome, and these ECG findings and changes might serve as its diagnostic sign. |
3,180 | [The amiodarone-beta blockers combination could represent an alternative treatment in patients at risk for sudden death in which a benefit from implantable defibrillators has not been clearly demonstrated]. | The combination of amiodarone and beta-blockers appears superior to amiodarone alone in the prevention of sudden death. At present this combination can be proposed to patients at risk of sudden death in whom a beneficial effect of the implantable defibrillator has not been clearly demonstrated. Therefore, the patients who can be treated with this combination appear the following ones: patients with sustained ventricular tachycardia (VT) causing severe hemodynamic compromise and ejection fraction > 35%; patients with hemodynamically well-tolerated sustained VT; patients with ischemic heart disease, syncope of unknown cause and induction of VT or ventricular fibrillation (VF) during electrophysiologic study; patients with sustained VT or VF and age > 80 years; patients with left ventricular dysfunction, without history of sustained VT or VF, but with "symptomatic ventricular arrhythmias". |
3,181 | Left ventricular function in atrial fibrillation during overdrive pacing. | Our purpose was to measure the effect of ventricular pacing in patients with atrial fibrillation (AF) on stroke volume and cardiac output.</AbstractText>Unceasing variation in cycle length in AF decreases stroke volume and cardiac output. Because ventricular-inhibited pacing after atrioventricular node ablation has been reported to improve left ventricular performance, we tested the hypothesis that overdrive pacing would produce a similar benefit by regularizing cycle length.</AbstractText>We studied 18 patients with chronic AF and permanent pacemakers. The aortic time velocity integral (TVI) was measured with continuous-wave Doppler and was used as a surrogate measure of stroke volume (stroke volume = TVI x aortic valve area, and aortic valve area is constant whether in AF or during pacing). For each patient, the linear relation between preceding cycle length and TVI in AF was used to estimate relative stroke volume (TVI compared within each patient) at a preceding cycle length of 666 ms in AF, and a similar comparison between AF and pacing was made at the minimum allowable pacing rate. Relative stroke volume in AF was then compared with relative stroke volume at both the fixed cycle (666 ms) and the minimum allowable rate. During pacing at 666 ms, relative stroke volume increased significantly by 18% (t = 2.8, P =.048), but there was no difference in cardiac output during pacing at the minimum possible rate and the corresponding preceding cycle length in AF.</AbstractText>Our data suggest that regularization of ventricular rhythm by overdrive pacing in patients with AF only improves stroke volume (and by extension, cardiac output) at pacing rates at the outer limit of and above the normal physiologic range.</AbstractText> |
3,182 | Effect of surgical revascularization in patients with coronary artery disease and ventricular tachycardia or fibrillation in the Antiarrhythmics Versus Implantable Defibrillators (AVID) Registry. | Patients who undergo resuscitation from near-fatal ventricular arrhythmias often have significant coronary artery disease, and revascularization has been shown to reduce myocardial ischemia and cardiac arrest episodes in this patient population. The magnitude of benefit attributed to revascularization has varied by study, and the use of adjunct implantable cardioverter defibrillator (ICD) therapy has not been well-characterized.</AbstractText>The Antiarrhythmics Versus Implantable Defibrillators (AVID) registry included 3117 patients with life-threatening ventricular arrhythmias, of whom 2321 (77%) had documented coronary artery disease and 281 (17%) underwent a coronary artery bypass grafting revascularization procedure after the index event. Patients who underwent a revascularization procedure were younger, had a lower incidence rate of prior myocardial infarction and ventricular arrhythmia, had a higher left ventricular ejection fraction, had less congestive heart failure, and were more likely to have had ventricular fibrillation as the presenting arrhythmia. Patients who underwent revascularization had a better survival rate than did those who did not undergo such a procedure after the index event, and adjustment for differing baseline patient covariates did not alter the relative survival rate benefit. Further, ICD implantation offered a similar survival rate advantage to those patients in the AVID registry with coronary artery disease independent of revascularization.</AbstractText>Coronary revascularization in the AVID registry patients with coronary artery disease effected a survival rate benefit that was not attributable to differences in baseline patient characteristics. The benefit of ICD on patient survival rate was not attenuated by a revascularization procedure.</AbstractText> |
3,183 | Electrophysiologic characteristics and implications of induced ventricular fibrillation in symptomatic patients with Brugada syndrome. | The study examined the electrocardiographic and electrophysiologic characteristics in relation to programmed ventricular stimulation (PVS)-induced ventricular fibrillation (VF), as well as the implications of PVS-induced VF on the recurrence of cardiac events in symptomatic Brugada syndrome.</AbstractText>Brugada syndrome is characterized by ST-segment elevation in the right precordial leads (V(1)-V(3)) and an episode of VF.</AbstractText>Thirty-four symptomatic patients with Brugada syndrome (33 men and 1 woman; 44 +/- 12 years old) were classified into two groups according to the inducibility of VF with PVS: 22 patients with induced VF requiring direct cardioversion for termination (Induced VF group) and 12 patients without induced VF (Noninduced VF group).</AbstractText>The induced VF group showed a longer QRS duration, a higher incidence of right bundle branch block and late potentials detected on the signal-averaged electrocardiogram, longer His-ventricular intervals and a longer conduction time from the RVOT to the left ventricle at extrastimulation than those in the non-induced VF group. However, there was no significant difference in the recurrence of cardiac events (VF documented by an implantable cardioverter-defibrillator and sudden cardiac death) between the two groups (8 [36%] of 22 patients vs. 7 [58%] of 12 patients) during long-term follow-up (range 1 to 149 months; mean 38).</AbstractText>Our data suggest that induction of VF by PVS depends on the severity of depolarization abnormalities but does not predict the recurrence of cardiac events in symptomatic Brugada syndrome, indicating that both depolarization and repolarization abnormalities are important in the development of VF.</AbstractText> |
3,184 | Quality of care for patients hospitalized with heart failure: assessing the impact of hospitalists. | The quality of care provided to patients hospitalized for heart failure has been shown to vary by physician, hospital, and region. Hospitalists appear to reduce costs and length of stay, yet their impact on quality of care is less certain.</AbstractText>To compare quality of care and resource utilization among patients with heart failure treated by hospitalists and nonhospitalist general internists.</AbstractText>We reviewed the medical records of patients with a principal diagnosis of heart failure between April 1, 1999, and March 30, 2000, at a 550-bed community-based teaching hospital in Massachusetts. We evaluated quality of care by measuring adherence to a set of commonly used process measures and compared resource utilization using severity-adjusted length of stay and costs.</AbstractText>The analysis included 280 patients, accounting for 326 heart failure admissions: 20 hospitalists cared for 137 (42%) cases, while 65 nonhospitalists cared for 189 (58%). Of 137 hospitalist cases, 129 (94%) had new or prior left ventricular ejection fraction testing results documented during the hospitalization compared with 165 (87%) of 189 nonhospitalist cases (P =.04). In cohorts of ideal candidates, performance rates for hospitalist and nonhospitalist cases were similar for prescriptions of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers for patients with ejection fractions lower than 40% (97% vs 96%; P>.99) and warfarin for patients with atrial fibrillation (60% vs 55%; P =.64). Rates of comprehensive discharge counseling was similar in the 2 groups. Multivariable modeling did not substantially alter these findings. After adjusting for differences in severity, patients treated by hospitalists had a shorter length of stay but similar overall costs when compared with those treated by nonhospitalists.</AbstractText>Compared with nonhospitalists, hospitalists were more likely to document assessment of left ventricular function and their patients had a shorter length of stay.</AbstractText> |
3,185 | [Ventricular fibrillation after surgical revascularization]. | Ventricular fibrillation (VF) presents a complete disintegrated myocardial activity associated with hemodynamic collapse and loss of consciousness requiring urgent reanimation. VF mostly occurs following myocardial infarction and endstage of ischemic heart disease in patients with ejection fraction less than 30%.</AbstractText>This paper analyzes occurrence of VF following coronary artery revascularization in patients undergoing surgery at the Institute of Cardiovascular Diseases in Sremska Kamenica. During the period 1994-1998, 3.186 patients underwent coronary artery revascularization procedure, whereas following it VF occurred in 20 patients (0.63%).</AbstractText>In all patients VF presented in the first postoperative week, while in 16 patients it occurred in the first 3 days following surgery. Nine patients with VF underwent left coronary artery revascularization with endarterectomy, 9 patients underwent right coronary artery revascularization with endarterectomy. One patient had a left-ventricular aneurysmectomy and 80% of patients had low ejection fraction rate--20-35%. After VF in 75% of patients urgent reoperation was performed, and only one suffered from thrombotic occlusion, that is perioerative infarction. After defibrillation patients were treated with xylocaine, amiodarone and beta-blockers. During the 30-day period following surgery, there were no lethal outcomes, whereas in the 24-month period after surgery 3 patients died. Cardiac-related death occurred in one patient, while two died due to cerebral insult.</AbstractText>VF was not a frequent complication in our patients. Effective antiarrhythmic drugs prevent repeated VF. Beta-blockers, xy-locaine and amiodarone are drugs of choice for the treatment of malignant cardiac rhythm disturbances.</AbstractText> |
3,186 | Impact of myocardial ischemia and reperfusion on ventricular defibrillation patterns, energy requirements, and detection of recovery. | Shocks that have defibrillated spontaneous ventricular fibrillation (VF) during acute ischemia or reperfusion may seem to have failed if VF recurs before the ECG amplifier recovers after shock. This could explain why the defibrillation threshold (DFT) for spontaneous VF appears markedly higher than for electrically induced VF.</AbstractText>The DFT for electrically induced VF (E-DFT) was determined in 15 pigs before ischemia, followed by left anterior ascending or left circumflex artery occlusion. VF was electrically induced 20 minutes after occlusion, followed 5 minutes later by reperfusion. Whether spontaneous or electrically induced, VF during occlusion or reperfusion was treated with up to 3 shocks at 1.5xE-DFT. If all 3 shocks failed, shock strength was increased. Thirty minutes after reperfusion, the other artery was occluded and the protocol was repeated. Defibrillation was considered successful if postshock sinus/idioventricular rhythm was present for > or = 30 seconds. VF recurring within 30 seconds after the shock was considered immediate or delayed if the first postshock activation complex in a rapidly restored ECG recording was VF or sinus/idioventricular rhythm, respectively. Defibrillation efficacy at 1.5xE-DFT was significantly higher for electrically induced ischemic VF (76%) than for spontaneous VF (31%). The incidence of delayed recurrence after electrically induced nonischemic (3%) or ischemic (20%) VF was significantly lower than after spontaneous VF (75%). Mean VF recurrence time after spontaneous VF was 4.6+/-5.3 seconds.</AbstractText>Spontaneous VF can be halted by a shock but then quickly restart before a standard ECG amplifier has recovered from postshock saturation, making it appear that the shock failed.</AbstractText> |
3,187 | Short-term effects of sinus rhythm restoration in patients with lone atrial fibrillation: a hormonal study. | It is well known that atrial fibrillation can lead to heart failure, and is attributed to rapid ventricular rate (tachycardia-induced cardiomyopathy). Some recent studies suggest the possible existence of an intrinsic left-ventricular factor related to atrial fibrillation, irrespective of other elements. In order to demonstrate the implication of this factor, we measured B-type Natriuretic Peptide, known as a functional marker of left-ventricular dysfunction, in 40 consecutive patients with chronic non-valvular atrial fibrillation, with low ventricular rate and absence of clinical heart failure or echocardiographic left-ventricular dysfunction. In all patients, Brain Natriuretic Peptide (BNP) plasma level was high and dramatically decreased 24 h after external electrical cardioversion (61.4 pg/ml before cardioversion, 23.5 pg/ml 1 day after cardioversion, P<0.002). Our study demonstrates that atrial fibrillation, in absence of high ventricular rate, induces an asymptomatic cardiac alteration that is not detectable by echocardiography. |
3,188 | Longstanding atrial fibrillation causes depletion of atrial natriuretic peptide in patients with advanced congestive heart failure. | Congestive heart failure (CHF) is characterized by neurohormonal activation, including increased plasma concentrations of atrial natriuretic peptide (ANP) and N-terminal ANP (N-ANP). Onset of atrial fibrillation (AF) further increases these peptides, but it may be hypothesized that concentrations decrease during longstanding AF due to inherent atrial degeneration.</AbstractText>We sought to investigate the relation between neurohormonal activation in patients with CHF and the duration of concomitant AF.</AbstractText>The study group comprised 60 patients (age 70 +/- 8 years) with advanced CHF due to left ventricular systolic dysfunction (left ventricular ejection fraction (LVEF) < 0.35) and chronic AF (duration 21 (1-340) months). Plasma neurohormone concentrations were measured, and multiple regression analysis was performed to identify their clinical predictors.</AbstractText>Median plasma neurohormone concentrations were: ANP 113 pmol/l, N-ANP 1187 pmol/l, norepinephrine 496 pg/ml, renin 127 micro units/l, aldosterone 128 pg/ml and endothelin 8.1 pg/ml. Norepinephrine, renin, aldosterone and endothelin were not significantly related to the duration of AF. In contrast, ANP decreased along with the duration of AF (P = 0.03), while the same trend was observed for N-ANP (P = 0.10). However, for these peptides a first order interaction with LVEF was present, which was not observed in the other neurohormones. In patients with LVEF > 0.25 ANP and N-ANP increased along with the duration of AF, whereas in patients with LVEF < or = 0.25 an inverse relation between ANP (P = 0.02) and N-ANP (P = 0.04) and the duration of AF was present, longer-standing AF being associated with lower concentrations.</AbstractText>In patients with advanced CHF with low LVEF plasma ANP and N-ANP concentrations decrease during longstanding AF. This finding agrees with the concept that longstanding AF leads to impaired ability of the atria to produce these neurohormones due to inherent degenerative changes.</AbstractText> |
3,189 | Large sample test of defibrillation waveform sensitivity. | An unknown mechanism causes defibrillation efficacy to be sensitive to the temporal pattern (waveform) of the delivered energy. Using a guinea pig model, we tested hypotheses in 140 defibrillation waveforms.</AbstractText>Two hundred seven male guinea pigs (950 +/- 100 g) were instrumented to continuously monitor the ECG and an optical plethysmographic signal from a forepaw. Two amplifiers served as a voltage-based defibrillator with a maximum output of 400 V at 2 A. Defibrillation electrodes (12-mm diameter) were placed 40 mm apart on the thorax. Thirty ventricular fibrillation episodes were induced where the first 10 episodes were used to estimate ED50 for a biphasic pulse (7/2 msec) and the remaining episodes were defibrillated with 18 test waveforms and two control waveforms all at the ED50 energy. Seven groups of 20 waveforms were tested. We directly tested hypotheses based on charge banking/burping, frequency concentration, and stimulus strength/duration. Of the hypotheses tested, nine are able to predict at least a 10% change in efficacy (P < 0.05): parabolic fit to duration; maximum, minimum, and remaining delivered charge; power at peak frequency; stimulus charge; and maximum, minimum, and maximum of the absolute value of stimulus strength. However, of these, only three are independent predictors of waveform efficacy (P < 0.05, near-minimum residual variance): power at peak frequency; parabolic fit to the stimulus duration; and minimum stimulus strength.</AbstractText>Stimulus strength and duration are the main determinants of the efficacy of a defibrillation waveform.</AbstractText> |
3,190 | Prognostic significance of nonsustained ventricular tachycardia after revascularization. | Two randomized trials (Multicenter Automatic Defibrillator Implantation Trial [MADIT] and Multicenter Unsustained Tachycardia Trial [MUSTT]) suggest that implantable cardioverter defibrillator (ICD) placement is associated with improved survival in patients with coronary artery disease, depressed left ventricular function, and nonsustained ventricular tachycardia (VT) who also have inducible sustained VT. However, neither study directly addresses the management of such patients who develop nonsustained VT early after revascularization.</AbstractText>We evaluated 109 consecutive patients who underwent electrophysiologic testing to evaluate nonsustained VT, which occurred 5 +/- 4 days following revascularization. Sustained monomorphic VT was inducible in 46 (42%) patients; these patients received an ICD. The remaining 63 (58%) noninducible patients received neither antiarrhythmic drug therapy nor an ICD. During 27 +/- 12 months of follow-up, 15 (33%) of 45 patients with an implanted ICD received at least one appropriate therapy from the device and 26 (24%) of the 109 study patients died. The 1- and 2-year freedom from ventricular tachycardia/fibrillation or sudden death in noninducible patients (97% and 93%) was significantly greater than that of inducible patients (84% and 71%; P = 0.001). However, no difference was observed in total mortality.</AbstractText>Patients with nonsustained VT during the early postrevascularization period who have inducible VT have a high incidence of arrhythmic events. Although this study was not designed to assess the impact of ICD placement on the total mortality of inducible patients, the finding that one third of these patients received appropriate ICD therapy suggests that the device may have a protective effect in these patients.</AbstractText> |
3,191 | Lack of benefit of an active pectoral pulse generator on atrial defibrillation thresholds. | Atrial defibrillation can be achieved with standard implantable cardioverter defibrillator leads, which has led to the development of combined atrial and ventricular devices. For ventricular defibrillation, use of an active pectoral electrode (active can) in the shocking pathway markedly reduces defibrillation thresholds (DFTs). However, the effect of an active pectoral can on atrial defibrillation is unknown.</AbstractText>This study was a prospective, randomized, paired comparison of two shock configurations on atrial DFTs in 33 patients. The lead system evaluated was a dual-coil transvenous defibrillation lead with a left pectoral pulse generator emulator. Shocks were delivered either between the right ventricular coil and proximal atrial coil (lead) or between the right ventricular coil and an active can in common with the atrial coil (active can). Delivered energy at DFT was 4.2 +/- 4.1 J in the lead configuration and 5.0 +/- 3.7 J in the active can configuration (P = NS). Peak current was 32% higher with an active can (P < 0.01), whereas shock impedance was 18% lower (P < 0.001). Moreover, a low threshold (< or = 3 J) was observed in 61% of subjects in the lead configuration but in only 36% in the active can configuration (P < 0.05). There were no clinical predictors of the atrial DFT.</AbstractText>These results indicate that low atrial DFTs can be achieved using a transvenous ventricular defibrillation lead. Because no benefit was observed with the use of an active pectoral electrode for atrial defibrillation, programmable shock vectors may be useful for dual-chamber implantable cardioverter defibrillators.</AbstractText> |
3,192 | Impaired detection of ventricular tachyarrhythmias by a rate-smoothing algorithm in dual-chamber implantable defibrillators: intradevice interactions. | Rate smoothing is an algorithm initially designed to prevent rapid changes in pacemaker rates. In this study, we sought to determine the potential of the rate-smoothing mechanism in preventing detection of ventricular tachyarrhythmias.</AbstractText>Clinical testing of rate smoothing was performed at the time of defibrillator arrhythmia induction in 16 patients with implantable defibrillators during 65 episodes of ventricular tachyarrhythmias. We also performed simulator-based testing to assess detection of ventricular tachycardia between 170 and 220 beats/min with systematic sequential change of rate-smoothing percent, AV delay, and maximal rate. During clinical testing of 54 ventricular fibrillation/polymorphic ventricular tachyarrhythmia episodes, there were no cases of nondetection and 3 episodes (5%) of minimally delayed detection. Of 10 monomorphic ventricular tachyarrhythmias, 6 had either delayed (2 cases) or absent (4 cases) detection. During simulator testing, complex interrelationships were demonstrated in AV delay, upper rate, and rate-smoothing percent in determining the severity of the effect on detection. Generally, long AV delay, higher upper rate, and smaller (more aggressive) rate smoothing were associated with increased risk of ventricular tachyarrhythmia underdetection. Importantly, use of parameters that impaired detection was always accompanied by a programmer warning message.</AbstractText>Rate smoothing may result in delay or failure of ventricular tachycardia detection. It is important to consider warning messages when programming rate smoothing and to test for appropriate detection when rate smoothing is used despite warning messages.</AbstractText> |
3,193 | Temporal patterns of atrial arrhythmia recurrences in patients with implantable defibrillators: implications for assessing antiarrhythmic therapies. | The statistical measures commonly used to assess therapies for recurrent atrial arrhythmias (such as time to first recurrence) often assume a uniformly random pattern of arrhythmic events over time. However, the true temporal pattern of atrial arrhythmia recurrences is unknown. The aim of this study was to use linear and nonlinear analyses to characterize the temporal pattern of atrial arrhythmia recurrences in patients with implantable cardioverter defibrillators.</AbstractText>The time and date of atrial tachyarrhythmias recorded in 65 patients with combined atrial and ventricular defibrillators were used to construct a probability density function (PDF) and a model of a Poisson distribution of arrhythmic events for each patient. Average patient age was 66 +/- 10 years and follow-up was 7.8 +/- 4.8 months. A total of 10,759 episodes of atrial tachyarrhythmias were analyzed (range 43 to 618 episodes per patient). The PDF fit a power law distribution for all 65 patients, with an average r2 = 0.89 +/- 0.08. The PDF distribution differed significantly from the model Poisson distribution in 47 of 65 patients (P = 0.0002). Differences from the Poisson distribution were noted for patients both taking (30/43 patients; P < or = 0.015) and not taking (17/22 patients; P < or = 0.017) antiarrhythmic drugs. Median time between atrial arrhythmia detections for all 65 patients was 10.8 minutes.</AbstractText>In implantable cardioverter defibrillator patients, the temporal pattern of frequent recurrences of atrial tachyarrhythmias usually is characterized by a power law distribution. The unique statistical properties of this type of distribution should be considered in designing outcome measures for treatment of atrial tachyarrhythmias.</AbstractText> |
3,194 | [Women and cardiovascular diseases]. | The authors draw attention to the important role played by menopause in the onset of arterial hypertension, enhanced coronary risk and dyslipidemia, for which a particularly useful association has been found to be estrogens, only if administered by mouth (alone or with progestins), and statins. The authors review numerous studies for or against the use of estrogens as a means of reducing arterial hypertension and the incidence of myocardial ischemia in menopausal women. In order to ensure therapeutic efficacy, replacement estrogen therapy should not be started at not too late an age, but instead as young as possible (the first 5 years after the start of menopause are optimal), namely before levels of endothelial estrogen receptors start to fall. Moreover, therapy should not be continued for more than 5 years in order to avoid the risk of breast cancer and endometrial carcinoma. With regard to myocardial infarction, it is worth noting that women show a higher frequency of silent and atypical infarction leading to a late diagnosis and therefore the arrival in the coronary unit half an hour or an hour later than men. Together with the onset of myocardial infarction at an older age in women compared to men (5-10 years), and the fact that diagnosis is less accurate in women and treatment less sophisticated, this accounts for the higher immediate and medium-term mortality figures in women following myocardial infarction. However, at least in America studies have shown that the less aggressive diagnostic and therapeutic management of myocardial infarction in women compared to men is not sufficient to cause a significant difference in mortality between men and women 30 days after the event. Turning to arrhythmia, it is worth recalling that supraventricular tachycardia with close rapid complexes, caused by return in the atrioventricular node is more frequent in females and in the second lutein or progestin phase of the menstrual cycle, thus demonstrating the protective role of estrogens against the onset of arrhythmia. The authors also point out the frequent association between ischemic ictus and chronic non-valvular atrial fibrillation in women aged over 75 since they present a very high risk (94%) of death by ischemic ictus. On the one hand, the guidelines recommend the use of anticoagulating therapy in these patients, but on the other there is a very high risk of hemorrhage which acts as a major constraint. Lastly, pregnancy is mentioned as a condition that facilitates the onset of arrhythmia; for example, orthodromic supraventricular tachycardia in Wolf Parkinson White and ventricular tachycardia which usually regresses post-partum. |
3,195 | Small aortic root as a cause of sudden death in a young adult: a controversial topic revisited. | Sudden cardiac death over the age of 35 years is mostly due to coronary atherosclerosis, whereas under the age of 35 years, a variety of mainly congenital malformations prevail. However, hypoplasia of the aortic root in adults, first introduced by Laurie in 1968 as a cause of sudden cardiac death in adults, is never included.</AbstractText>We present a case of a 29-year-old female who suddenly and unexpectedly collapsed during recreational bicycling. Ventricular fibrillation was recorded, but resuscitation attempts failed, and the patient was declared dead about 1 h after the event. Autopsy revealed cardiac hypertrophy with extensive scarring and a small aortic root (calculated inlet/outlet diameters=14.9/14.3 mm), without obstructive coronary artery disease or any other plausible cause for sudden cardiac death.</AbstractText>The observations strongly suggest that small aortic root (less than 2 cm in diameter) provided the background for cardiac hypertrophy and, eventually, myocardial ischemia and ventricular fibrillation. Pathologists should be aware of this possibility while evaluating cases of sudden cardiac death without an obvious pathologic substrate.</AbstractText> |
3,196 | Effects of captopril and losartan on myocardial ischemia-reperfusion induced arrhythmias and necrosis in rats. | Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II type 1 (AT (1)) receptor blockers improve ischemia-reperfusion induced arrhythmias and infarct size in several animal models. However, the effects of pretreatment with ACEIs or AT (1) receptor blockers on acute myocardial infarct size and arrhythmias are controversial. Thus, we sought to assess the comparative effects of pretreatment with ACEI captopril and AT (1)-receptor blocker losartan on myocardial infarct size and arrhythmias in a rat model of ischemia-reperfusion. We randomly assigned 92 male Wistar rats for arrhythmias ( n= 60) and necrosis ( n= 32) experiments. To produce arrhythmia, the left main coronary artery was occluded for 7 min, followed by 7 min of reperfusion and to produce necrosis, the the left main coronary artery was occluded for 30 min, followed by 120 min of reperfusion. Captopril (3 mg kg (-1)) and losartan (0.2 and 2 mg kg (-1)) were given intravenously 10 min before occlusion. Captopril reduced the incidences of ventricular fibrillation (VF) and mortality associated with irreversible VF, whereas the studied doses of losartan did not. Captopril also decreased the number of ventricular beats on reperfusion. Losartan 2 mg kg (-1) reduced both the number of ventricular premature beats and the incidence of ventricular tachycardia (VT) on reperfusion, while losartan at dose of 0.2 mg kg (-1) had no effect on these arrhythmias. Compared to the control group, both captopril and losartan reduced myocardial infarct size in the rat model of ischemia-reperfusion, but this was statistically significant for captopril only. In this experimental model, although captopril did not reduce the incidence of reperfusion-induced VT, it was more effective than the AT (1)-receptor blocker losartan at preventing mortality associated with irreversible VF and to reduce myocardial infarct size in rat model of ischemia-reperfusion. |
3,197 | Osborn waves associated with ventricular fibrillation in a patient with vasospastic angina. | A 52-year-old man with a history of vasospastic angina experienced a severe ischemic episode accompanied by a non-Q wave myocardial infarction. Two episodes of ventricular fibrillation (VF) occurred during the acute phase of the event. Osborn waves were observed on the ECG preceding each episode of VF. In the second episode, the gradual development of Osborn waves until VF occurred was confirmed on ECG. The Osborn waves appeared to be related to the occurrence of VF. This case may provide clinical evidence that a prominent I(to) participates in the development of VF during myocardial ischemia. |
3,198 | Afterdepolarizations promote the transition from ventricular tachycardia to fibrillation in a three-dimensional model of cardiac tissue. | Recent experimental results regarding the action potential duration restitution curve have explained the transition from ventricular tachycardia (VT) to fibrillation (VF) in terms of spiral wave (SW) meandering and breakup. However, it remains unclear whether VF always has a steep restitution curve. The present study was designed to test the hypothesis that afterdepolarizations occur at excitable gaps during VF and affect the SW dynamics, even if the restitution curve is gentle. Homogeneous and isotropic 3-dimensional tissue was simulated with a LRd model. Because of the gentle restitution curve, it was not expected that SW instabilities would occur in this condition. In the tissue, a stationary SW reentry was initially observed; however, afterdepolarizations erupted from the excitable gap near the SW tip, and the SW then meandered widely. Following that, afterdepolarizations erupted far from the SW tip, resulting in SW breakup. In this manner, the wave dynamics degenerated into a chaotic state within a few seconds. Furthermore, not only triggered activity but also subthreshold afterdepolarizations were found to cause SW instabilities. These results suggest that afterdepolarizations may play an important role in the transition to VF and that the mechanism is independent of restitution properties. |
3,199 | Mitral valve surgery under perfused ventricular fibrillation with moderate hypothermia. | The safety and myocardial protective effect of perfused ventricular fibrillation (VF) under moderate hypothermia were investigated. Through a midline sternotomy and opening the left atrium from the right side, isolated mitral valve surgery was performed under aortic cross-clamping (ACC) and cardioplegic arrest using Bretschneider HTK solution in 96 patients, and under perfused VF in 20 patients (VF Group). Patient characteristics, clinical outcomes, and perioperative variables were compared. A satisfactory surgical view was obtained in all VF Group patients. Patient characteristics in the 2 groups were similar, and both groups had comparable results for mortality and morbidity, operation time, cardiopulmonary bypass time, peak levels of creatine kinase (CK) and its myocardial fraction, hours of mechanical ventilation, intensive care unit stay, and postoperative left ventricular ejection fraction. Even in VF Group patients with preoperative critical hemodynamic compromise, inotropes could be discontinued within 3 days. Thus, no detrimental effect of perfused VF was observed. On the other hand, in patients who underwent ACC and cardioplegic arrest of 120min or longer, peak levels of CK and its myocardial fraction were significantly higher than those of the rest of C group patients and VF Group patients. Perfused VF under moderate hypothermia can be a good alternative myocardial protection strategy during mitral valve surgery, particularly in patients in whom ACC is unsuitable or the duration of ACC is expected to be long. |
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