Occurrence Of Malignant Ventricular Arrhythmias Research Articles

Incidence, time course, and predictors of early malignant ventricular arrhythmias after non-ST-segment elevation myocardial infarction in patients with early invasive treatment

The incidence of non-ST-segment elevation myocardial infarction (NSTEMI) is increasing. With the limited intensive care facilities, knowledge of the total risk and predictors of acute life-threatening arrhythmias is of major interest to guide the decision on the intensity of care at the time of admission. We continuously monitored 588 consecutive patients with NSTEMI admitted to the coronary care unit of a primary and tertiary care centre for malignant ventricular arrhythmias requiring defibrillation. Ninety-seven per cent of the patients underwent coronary angiography during the index hospital admission. Total rate of malignant ventricular arrhythmias and mortality was 2.6% (n=15) and 3.6% (n=21), respectively. More than two-thirds of arrhythmias occurred within the first 12 h after onset of symptoms. In a bootstrapped multivariable regression analysis, the only factor associated with the occurrence of malignant ventricular arrhythmia was higher white blood cell count on admission. Popular risk assessment tools such as Thrombolysis in Myocardial Infarction, Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy, and Predicting Risk of Death in Cardiac disease Tool were predictive of mortality but not of early arrhythmia. Patients with NSTEMI treated aggressively with early revascularization are at low risk for developing life-threatening arrhythmias. The occurrence of such events remains difficult to predict. The role of baseline inflammatory status as a determinant merits further investigations.

Safety And Feasibility Of Stress Testing In Patients With Implantable Cardioverter Defibrillators

Stress testing is integral to evaluate patients with heart disease. However, few data are available regarding safety of stress testing in patients with implantable cardioverter defibrillators (ICDs). Some exercise laboratories consider maximal exercise stress testing and pharmacologic stress testing with dobutamine contraindications in patients with ICDs and some laboratories inactivate ICDs prior to stress testing. PURPOSE The aim of this retrospective study was to assess the safety and feasibility of exercise and pharmacologic stress testing (PST) in patients with ICDs. METHODS Patients with ICD implantation and subsequent stress testing were included in this analysis. Chart review was performed. Primary end-points were occurrence of malignant ventricular arrhythmias (MVAs), onset of burst pacing or ICD firing, cardiopulmonary resuscitation (CPR) or death during stress testing. Secondary end-points were need for urgent coronary revascularization based on stress testing results and hospital readmissions for MVAs. RESULTS From January 1999 to December 2003, 1734 patients underwent ICD implantation or generator replacement. A total of 84 patients subsequently underwent 107 stress tests at William Beaumont Hospital, Royal Oak. Mean age was 67±12 years and 76% were men. Indications for ICD implantation were dilated cardiomyopathy (51%), sustained ventricular tachycardia (39%), sudden cardiac death (8%) and long QT syndrome (1%). 41% underwent exercise stress testing and 59% underwent PST utilizing dobutamine (21%) or dipyridamole (38%). Left ventricular ejection fraction was 32±20. 71% had fixed defects and 22% had reversible perfusion defects as determined by myocardial perfusion imaging. None of the ICDs were inactivated prior to stress testing. Heart rate at peak stress averaged 92±27 beats per minute. 83% were on beta-receptor antagonists. Although 4% of patients had self-terminating, non-sustained ventricular tachycardia at peak stress, none had sustained ventricular tachycardia precipitating burst pacing, ICD shock, CPR or death. One patient underwent urgent coronary angiography, but was found to have non-critical coronary disease. There were no hospital readmissions for MVAs. CONCLUSIONS These preliminary findings suggest that stress testing can be performed safely in patients with ICDs. MVAs requiring emergent treatment are rare occurrences during stress testing. Knowledge of programmed ventricular tachycardia and ventricular fibrillation zones may help predetermine maximal heart rates on stress testing and preclude routine inactivation of ICDs prior to testing.

Lipid-lowering therapy reduces the prevalence of atrial fibrillation

Recent studies have implicated oxidative stress in the genesis of atrial fibrillation (AF). Statins have antioxidant properties, and have been shown to reduce the occurrence of malignant ventricular arrhythmias. We hypothesized that lipid-lowering therapy is associated with reduced occurrence of AF. Data from AdvancentSM, a large multicenter registry of patients with reduced left ventricular ejection fraction (LVEF), was used to explore the relationship between lipid-lowering therapy and AF. A total of 25,268 patients were included in the analysis. The mean age was 66±13 years and 72% were men. The LVEF was 31±10%, and 72% had ischemic cardiomyopathy. β-blockade was used in 79% of patients and 82% were treated with either angiotensin converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB). 26% of the patients had a history of AF. There was no difference in the prevalence of AF between patients without a history of hyperlipidemia and those with hyperlipidemia who were not treated (32.8 vs 32.6%, p=ns). Patients on lipid-lowering therapy had a 25.1% prevalence of AF, representing a 23% reduction compared to those not treated (p<.001). To determine the influence of other known risk factors for AF, multivariate logistic regression was performed. After adjusting for age, gender, diabetes, etiology of heart disease, heart failure class, and concomitant therapy with β-blockers, ACEI, and ARB, lipid-lowering therapy remained strongly associated with freedom from AF (OR 0.66, 95% CI 0.61-0.71). Results were comparable for subsets of patients with paroxysmal and permanent patterns of AF. In conclusion, results from this very large multicenter registry suggest that lipid-lowering therapy is strongly protective against the development of AF in patients with impaired LV function. This benefit appears to be independent of the lipid profile and additive to the protective effects of β-blockade and ACEI/ARB.

Preconditioning attenuates the shortening of recovery during coronary occlusion in isolated rabbit hearts with D-sotalol-induced long QT intervals.

The effects of 20-min ligations of the anterior branch of the left coronary artery were studied in Langendorff-perfused rabbit hearts with 92 microM D-sotalol added to the perfusate to induce long QT intervals and triggered arrhythmias. Epicardial electrograms, a left ventricular endocardial monophasic action potential, and simulated X and Y lead electrocardiograms were used to characterize ventricular conduction and recovery. In contrast to previous work showing that global ischemia eliminated triggered activity, coronary occlusion did not alter its mean incidence. Although the anatomic distribution of earliest sites of epicardial activation by triggered beats was altered, triggered beats still appeared on the epicardial surface in the nonperfused regions. Coronary occlusion had a small and variable effect on epicardial conduction velocity but caused a significantly greater percent shortening of epicardial activation-recovery intervals in the nonperfused region of hearts given D-sotalol than in control hearts. In hearts given D-sotalol, preconditioning significantly attenuated the shortening of epicardial activation-recovery intervals in response to coronary occlusion. However, preconditioning had no effect on the mean incidence of triggered activity during coronary occlusion. Thus, the persistence of triggered activity and the shortened myocardial recovery time associated with coronary occlusion could contribute to increasing the likelihood of occurrence of malignant ventricular arrhythmias. Preconditioning by attenuating the shortening of recovery would be anti-arrhythmic.

Pharmacological and device approach to therapy of inherited cardiac diseases associated with cardiac arrhythmias and sudden death

A genetic origin in diseases like the long QT syndrome, the Brugada syndrome, or hypertrophic cardiomyopathy have been identified over the past years. These diseases have in common that they may result in sudden cardiac death of the patient. Recognition of patients based on their phenotype and application in clinical practice of the knowledge acquired on the genetic basis may have a major impact on how we approach them. In the long QT syndrome several mutations have been identified both in the sodium and in the potassium channels. The different electrophysiological effects of the mutations lead to a common phenotype: prolongation of the QT interval; but also to a common clinical impact: occurrence of malignant ventricular arrhythmias. Genetics should help us in treating in a more rational way our patients depending on the type of mutation. In the Brugada syndrome, mutations affecting the sodium channel have been so far identified. The results are electrophysiologically opposite to the ones observed in the long QT syndrome. Thus different mutations in the same gene lead to different functional consequences. Again, identification and study of the right mutation may lead to a more rational treatment directed to correct the malfunction of the channel.

QT Dispersion as a Noninvasive Arrhythmiogenic Marker in Acute Myocardial Infarction

Backround: Prolongation of QT dispersion (QTD), defined as the difference between maximum and minimum QT intervals on surface ECG, has been proposed as a noninvasive arrythmogenic marker. The aim of this study was to estimate the value of QTD in identifing patients susceptible to ventricular fibrillation or ventricular tachycardia (VF/VT) after an acute myocardial infarction (AMI) and to evaluate the behavior of QTD in relation to the thrombolytic therapy.Methods: We studied 108 consecutive patients with AMI. All patients had a 12‐lead surface ECG recorded upon admission and a second ECG 24 hours later. QT interval was measured from the onset of Q to the end of T in each of 12 standard ECG leads. QTD was the difference between the longest and shortest values of QT. All QTD measurements were corrected for heart rate (QTcD) using QTc values according to Bazzet formula.Results: Fifteen patients (13.8%) developed VF/VT in the first week after AMI (group 1A) and 93 patients (86.2%) did not have VF/NT (group 1B). QTD and QTcD values were significantly greater in group 1A in comparison to group 1B on admission and 24 hours later. Sixty‐five patients (60%) received intravenous thrombolysis in the acute phase of AMI (group 2A) and 43 patients (40%) did not (group 2B). No significant difference in QTD and QTcD was observed in the first ECG on admission between the two groups. Conversely, QTD and QTcD were lower in group 2A patients in the second ECG 24 hours after admission.Conclusions: These results provide evidence that increased values of QTD are correlated well with occurrence of malignant ventricular arrhythmias after acute myocardial infarction while lower values associated with the thrombolytic therapy. A.N.E. 1999;4(1):35–38

Prognostic Value of Thrombolysis, Coronary Artery Patency, Signal-Averaged Electrocardiography, Left Ventricular Ejection Fraction, and Holter Electrocardiographic Monitoring for Life-Threatening Ventricular Arrhythmias After a First Acute Myocardial Infarction

Prognostic studies after acute myocardial infarction (AMI) have mainly been performed in the prethrombolytic era. Despite the fact that modern management of AMI has reduced mortality rates, the occurrence of malignant ventricular arrhythmias in the late phase of AMI remains an important issue. We prospectively studied 244 consecutive patients (97 treated with thrombolytics) who survived a first AMI. All patients underwent time domain signal-averaged electrocardiography (vector magnitude: measurements of total QRS duration, terminal low [<40 μV] amplitude signal duration, and root-mean-square voltage of the last 40 ms of the QRS complex), Holter electrocardiographic monitoring, and cardiac catheterization. Late life-threatening ventricular arrhythmias were recorded. Eighteen arrhythmic events occurred during a mean follow-up period of 57 ± 18 months. Three independent factors were associated with a higher risk of arrhythmic events: (1) left ventricular ejection fraction (odds ratio 1.9/0.10 decrease), (2) terminal low-amplitude signal duration (odds ratio 1.5/5 ms increase), and (3) absence of thrombolytic therapy (odds ratio 3.9). Low-amplitude signal duration sensitivity for sudden cardiac death was low (30%). Left ventricular ejection fraction had the highest positive predictive value for sudden cardiac death (10%). Thus, thrombolysis decreases both the incidence of ventricular tachycardia and sudden cardiac death with a higher reopening rate of the infarct-related vessel. Signal averaging predicts the occurrence of ventricular tachycardia and an impaired left ventricular ejection fraction predicts the occurrence of sudden cardiac death.

Immediate and long-term pathophysiologic mechanisms underlying the genesis of sudden cardiac death in patients with congestive heart failure

Congestive heart failure is the most important predisposing factor to the occurrence of sudden death in patients with cardiovascular disease. As left ventricular dysfunction deteriorates and symptoms of heart failure become evident, ambulatory ventricular arrhythmias become increasingly frequent and complex, and sudden cardiac death becomes an increasingly common occurrence. When the left ventricular ejection fraction has declined to less than 30 percent and symptoms of heart failure become refractory to treatment with digitalis and diuretics, 35 to 50 percent of patients will die of a lethal cardiac arrhythmia within three years. A number of factors interact to determine the occurrence of malignant ventricular arrhythmias in patients with congestive heart failure. Myocardial fibrosis and enhanced left ventricular wall stress may alter the electrophysiologic properties of the myocardium, but these factors may not be sufficient to explain the development of lethal rhythm disturbances. Neurohormonal activation may exacerbate the frequency and complexity of ambulatory arrhythmias in these patients, but such activation can persist for long periods without fatal electrophysiologic sequelae. Recent investigations suggest that electrolyte depletion may provide an important immediate precipitating cause for the occurrence of fatal ventricular tachyarrhythmias in the patient with severe left ventricular dysfunction whose susceptibility is markedly heightened by preexisting structural, hemodynamic, or neurohormonal factors. Further work is needed to determine if prophylactic therapy directed at preventing electrolyte depletion can favorably modify the long-term outcome of these severely ill patients.

Mapping of activation changes within the acutely ischaemic canine specialised conduction system.

Ligation of the anterior septal artery was used to produce acute ischaemia of the specialised conduction system in ten dogs. Activation times at selected positions within the specialised conduction system were recorded. Marked delays of activation occurred between several discrete anatomic sites within the specialised conduction system. This study demonstrates that extremely slow conduction is common in localised areas of the acutely ischaemic infra-nodal conduction system. Heterogeneity of myocardial activation secondary to changes of speed of the conduction during acute septal ischaemia is postulated as a mechanism facilitating the occurrence of malignant ventricular arrhythmias.

実験的心筋こうそくにおける急性期心室性不整脈に対するＣａｒｔｅｏｌｏｌ Ｈｙｄｒｏｃｈｌｏｒｉｄｅの抑制効果の検討

The effects of carteolol, a β-blocking agent, on the incidence of ventricular arrhythmias and ventricular automaticity were studied in a canine acute myocardial infarction model. Carteolol (10 μ g/kg) was given intravenously 5∼ 30 minutes before balloon occlusion of the left anterior descending coronary artery in anesthetized, closed chest dogs (Group I). The total incidence of ventricular arrhythmias during the first 30 minutes of coronary occlusion was 91% (10/11) in group I, similar to control dogs without pretreatment of carteolol (Group II; 92%, 12/13, NS).However, ventricular fibrillation or sustained ventricular tachycardia was not observed in Group I, compared to 2 cases in the Group II dogs.Ventricular escape interval (VET), used as an index of ventricular automaticity, progressively shortened in the periods between 1 and 4 hours post-occlusion in both groups. However, the mean value of VET at 4 hours after coronary occlusion in Group I was significantly longer than.that of the Group II dogs (1549 ± 1259 msec vs 610 ± 224 msec, P<0.05).It was suggested that carteolol prevented the occurrence of malignant ventricular arrhythmia in the acute phase (within 30 minutes) and suppressed the enhancement of ventricular automaticity in the delayed phase (4 hours) of myocardial infarction.

Increased R-wave amplitude induced by acute myocardial ischemia in the dog: A predictor of malignant ventricular arrhythmias

The ability of an increase of 25 % or greater in the sum of R-wave amplitudes in leads X, Y, Z, L 2, and V 5 to predict the occurrence of malignant ventricular arrhythmias (10 or more ventricular premature beats/min, ventricular tachycardia [5 or more consecutive premature beats], and/or fibrillation) was evaluated in 17 dogs during experimental acute myocardial ischemia. Each dog underwent a 15 minute ligation of the left anterior descending coronary artery followed by reperfusion and after recovery, 2 hours later, a 15 minute ligation of the circumflex coronary artery. During ligation of the left anterior descending coronary artery, 12 of 17 dogs (71%) showed no R-wave increase and no arrhythmias (true-negative response). In 5 (29%) of 17 dogs malignant ventricular arrhythmias developed: 2 of 5 (40%) dogs with arrhythmias had a concomitant R-wave increase (true-positive response), and 3 of 5 (60%) with arrhythmias had a less than 25% increase in R-wave amplitude (false-negative results). During circumflex coronary artery ligation, 13 of 17 (76%) dogs showed both R-wave increases and arrhythmias (true-positive response). Four (24%) of 17 dogs had no arrhythmias: 3 of 4 (75%) with no arrhythmias also had a less than 25% increase in R-wave amplitude (true-negative response), whereas 1 of 4 (25%) dogs with no arrhythmias had an increase in R-wave amplitude (false-positive response). In dogs with both arrhythmias and R-wave increases, R-wave changes preceded the onset of arrhythmias by a mean (± standard deviation) of 1 minute 27 seconds (± 43 seconds). Overall, R-wave increases were highly sensitive (83%), specific (94%), and predictive (94%) for the occurrence of malignant ventricular arrhythmias during experimental acute myocardial ischemia.