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Sudden cardiac death in well-trained athletes is most often superimposed on the presence of structural heart disease. However, some athletes die suddenly in the absence of overt heart disease. To improve identification of athletes at high risk for ventricular tachycardia (VT), ventricular repolarization, the signal-averaged electro-cardiogram (ECG), and the echocardiogram from 13 male athletes with symptomatic VT and without evidence of manifest cardiac disease were compared with data obtained in 3 matched control groups (15 apparently healthy professional road cyclists, 10 professional basketball players, and 15 normal control subjects without any sports activity). All patients had apparently normal QRS duration on the routine ECG, and none were taking antiarrhythmic drugs. Echocardiography and signal-averaged electrocardiography were useful in distinguishing the group of athletes with tachyarrhythmias from the group of normal nonsporting controls, but not from both groups of normal athletes. The QT interval ([V.sup.4]) and the QT interval corrected with the cubic root were shorter for the nonsporting controls. Three parameters for QT dispersion showed significant differences (p (Am J Cardiol 1994; 74:1124--1128)

The hypothesis that non-right-handedness is associated with sudden cardiac death was tested based on evidence that sympathetic imbalance may contribute to ventricular arrhythmogenesis and evidence that left-handers may have a shorter lifespan than right-handers. The study included 26 patients with coronary artery disease (CAD), a history of ventricular tachycardia-ventricular fibrillation (VT-VF), and implanted defibrillators, and 26 patients with CAD and no history of serious arrlhythmias who were match for age, sex, and New York Heart Association functional class. Patients with any history of neurololoc disorders were excluded. Left-handers either wrote with the left hand or were convert from left- to right-handedness in childhood. Non-right-handers used the left hand for writing, drawing, or throwing. Handedness rates in patients with VT-VF and case-control subjects were compared with published norms in the general population to take expected rates into account. The rates of left-handedness (6 of 26 or 23.1%) and non-right-handedness (9 of 26 or 34.6%) in patients with VT-VF were significantly higher (p

Ventricular premature complexes (VPCs) after acute myocardial infarction (AMI) remain important determinants of survival in the post-thrombolytic era. The role of thrombolysis, left ventricular function, and Holter ST-segment depression in modulating VPC frequency is unclear. In a placebo-controlled, randomized study of tissue-type plasminogen activator (t-PA) in 103 patients with AMI (Tissue Plasminogen Activator: Toronto study), VPC frequency and ST depression on Holter monitoring (day 7), ejection fraction by radionuclide scan (day 9), and infarct artery patency and cross-sectional area on day 1 (n 42) were assessed. After administering t-PA, VPC frequency was 10 [+ or -] 58/hour (mean [+ or -] SD), similar to that after placebo (23.5 [+ or -] 91.7, p = NS). However, patients with ST depression had greater VPC frequency (56 [+ or -] 140/hour) than those without it (1.3 2.6/hour, p = 0.05). Ejection fraction was negatively correlated with VPC frequency (r = -0.33, p

This study was undertaken to examine whether clinical factors predict reinfarction within 1 year of a first acute myocardial infarction (AMI) and to quantity the subsequent influence of reinfarction on long-term mortality. Data from 3,695 patients with a first AMI included in the Secondary Prevention Reinfarction Israeli Nifedipine Trial Registry were analyzed. The 1-year reinfarction incidence was 6.0% (220 of 3,695) and in-hospital mortality during reinfarction was 31%. Patients with reinfarction were older (63.0 vs 60.8 years) at entry. The independent clinical prodictors for 1-year reinfarction were (adjusted relative odds): peripheral vascular disease (2.12), anterior location of the first AMI (1.62), angina before the first AMI (1.53), congestive heart failure on admission (1.34), diabetes (1.33), systemic hypertension (1.28) and age increment (1.13). One-year reinfarction rate increased from 4.0% in patients with 0 or 1 risk factor to 23.3% in patients with 5 to 6 risk factors (p

One hundred twenty-two patients treated chronically with amiodarone for sustained ventricular tachyrardia or ventricular fibrillation after failing conventional antiarrythmic therapy were analyzed to determine which factors were predictive of sudden cardiac death during follow-up. The mean left ventricular ejection fraction in the study group was 0.32, and 87% of the patients had coronary artery disease with a prior myocardial infarction. During a median follow-up of 19.5 months, 30 patients died suddenly. The only variable that was predictive of sudden death was left ventricular ejection fraction. Twenty-nine of the 84 patients with ejection fractions (Am J Cardiol 1993;71:823-826)

Programmed stimulation n patients with nonsustained ventricular tachycardia (VT) and coronary artery disease (CAD) induces sustained VT in 30 to 50% of patients at high risk for sudden death. This study sought to determine whether patients with nonsustained VT who have inducible, sustained VT would have differences of left ventricular endocardial activation and conduction compared with those of patients without inducible, sustained VT would have differences of left ventricular endocardial activation and conduction compared with those of patients without inducible sustained VT. Thirty-six patients with CAD referred for evaluation of nonsustained VT underwent programmed ventricular endocardial activation. Using previously validated methods, electrograms were classified as normal abnormal or fractionated based on measurement of local eletrogram duration and amplituted. Programmed stimulation induced sustatined, uniform VT in 16 of 36 patients (44%). Patients with inducible, sustained, uniform RV had significantly more sites with abnormal (48%) and fractionated (5.5%) electrograms than did those without inducible VT (35T abnormal and 0.4% fractionated; p = 0.05 and 0.01, respectively). Patients with inducible VT had a mean of 15% of mapped sites displaying late electrograms versus only 3% in those without inducible VT (p

Reduced heart rate (HR) variability is associated with increased risk of cardiac arrest in patients with coronary artery disease. In this study, the power spectral components of HR variability and their circadian pattern in 22 survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction were compared with those of 22 control patients matched with respect to age, sex, previous myocardial infarction, ejection fraction and number of diseased coronary arteries. Survivors of cardiac arrest had significantly lower 24-hour average standard deviation of RR intervals than control patients (29 [+ or -] 10 vs 51 [+ or -] 15 ms, p

This randomized study evaluates survivors of out-of-hospital ventricular fibrillation (VF) not associated with a Q-wave acute myocardial infarction who are deemed to be at a high risk of recurrence of VF. it compares the outcome of treatment with empirically administered amiodarone with the outcome of treatment with other antiarrhythmic agents guided by electrophysiologic testing or Holter recording, or both. The goal of therapy guided by electrophysiologic testing is to suppress inducible ventricular tachycardia (VT) or VF. Holter recording is used as the primary means of adjusting therapy only if patients are noninducible at the baseline electrophysiologic study. Patients are stratified according to cardiac diagnosis, ejection fraction, and whether they had previously received an antiarrhythmic agent that failed to suppress their arrhythmias. The primary end point of the study is total cardiac mortality. The first patient was enrolled in a pilot study on April 26, 1984. By October 1988, 142 patients had been enrolled in the full study and, as of May 1990, 199 patients have been enrolled. Compliance with therapy has been good, with no patients lost to follow-up and 8% of patients, equal in both drug groups, crossing over to alternate therapy. Baseline clinical characteristics remain similar in amiodarone and conventional drug groups. Pulmonary toxicity with amiodarone is 7% at 1 year, with no patients dying of pulmonary toxicity. in the first 142 patients, the overall 1-year cardiac mortality was 19%, with a 17% arrhythmic mortality (either VF or presumed arrhythmic death). Because of this relatively high mortality, even with aggressive evaluation, treatment and follow-up, the investigators concluded that all patients who were participants in the study should also have an automatic defibrillator implanted when possible. Enrollment will continue until March 31, 1991, with follow-up for an additional year thereafter. This study should provide data about the relative efficacy of empirically administered amiodarone compared with other antiarrhythmic agents guided by electrophysiologic study and Holter monitoring. (Am J Cardiol 1991;67:578-584), Under normal circumstances, the heart muscle has synchronized, rhythmic contractions while pumping blood to the body. Under a variety of conditions, this contractile pattern is disrupted; the resulting cessation of pumping is known as cardiac arrest, and is fatal if not reversed immediately. Patients who recover from an out-of-hospital episode of cardiac arrest are at high risk for recurrence of this condition. Frequently the episode of cardiac arrest results from an occurrence of ventricular fibrillation (VF; desynchronized, ineffectual contraction of individual heart muscle fibers), and recurrence of VF is common as well. It is assumed, but not proven, that administration of antiarrhythmic drugs will prevent another episode of VF. Because antiarrhythmic medication is almost universally administered to patients following VF, it has not been possible to compare drug therapy with placebo control. Amiodarone is a commonly prescribed, long-acting antiarrhythmic; the high rate of side effects makes it desirable to know if amiodarone is superior to other drugs of this class. To evaluate its usefulness, 199 patients have enrolled to date in the Cardiac Arrest in Seattle: Conventional Versus Amiodarone Drug Evaluation (CASCADE) study after suffering an episode of out-of-hospital VF. The goal of this ongoing study is to assess the outcome of treatment with amiodarone and the outcome of treatment with other antiarrhythmic drugs (conventional therapy). Drug dosages are titrated to prevent either physician-inducible bouts of VF, or in cases where VF can not be experimentally induced, spontaneous bouts of arrythmia as determined by ambulatory electrocardiographic monitoring. Thus far, baseline clinical data remain similar in amiodarone and conventional therapy groups. Pulmonary toxicity has occurred in about seven percent of the amiodarone patients; no patients have died of this complication. In the first 142 patients, overall one-year cardiac mortality was 19 percent, with 17 percent dying from VF or presumed arrythmia. Because of the high mortality rate even with closely monitored drug therapy, the investigators recommend that all participants in the study have an automatic defibrillator implanted when possible. (Consumer Summary produced by Reliance Medical Information, Inc.)

A prospective study correlated the effect of quinidine or procainamide versus no antiarrhythmic drug on sudden cardiac death, total cardiac death and total death in 406 elderly patients with heart disease and asymptomatic complex ventricular arrhythmias detected by 24-hour ambulatory electrocardiograms. Of 397 patients treated with quinidine, 184 (46%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Of 9 patients treated with procainamide, 2 (22%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Adverse effects developed during long-term therapy in 6 patients 2%) receiving quinidine and in 3 patients (33%) receiving procainamide. Mean follow-up was 24 [+ or -] 15 months in both groups. Sudden cardiac death, total cardiac death and total death occurred in 21, 43 and 65% of patients receiving quinidine or procainamide, respectively, and in 23, 44 and 63% of patients receiving no antiarrhythmic drug, respectively (difference not significant). Survival by Kaplan-Meier analysis showed no significant difference between the 2 groups for sudden cardiac death, total cardiac death or total death through 4 years. Patients with abnormal left ventricular ejection fraction had a 3.4 times higher incidence of sudden cardiac death, a 2.4 times higher incidence of total cardiac death and a 1.4 times higher incidence of total death than patients with normal left ventricular election fraction. These data showed no significant difference in sudden cardiac death, total cardiac death or total death between patients treated with quinidine or procainamide or with no antiarrhythmic therapy. The presence or absence of antiarrhythmic therapy did not affect the event risk regardless of left ventricular ejection fraction [is greater than or equal to] 50% versus (Am J Cardiol 1990;66:423-428), The effects of the cardiovascular drugs quinidine and procainamide on sudden cardiac death, total cardiac death, and total death were assessed in 406 elderly patients with heart disease and ventricular arrhythmias (abnormal heart rhythms). Within the first two weeks of treatment, 184 of 397 patients treated with quinidine and 2 of 9 patients treated with procainamide developed adverse reactions and discontinued drug therapy. During long-term therapy, toxic effects developed in six patients treated with quinidine and three patients treated with procainamide. Patients were assessed over a 24-month period. The incidence of sudden cardiac death, total cardiac death, and total death was 21, 43, and 65 percent, respectively, in patients treated with antiarrhythmic agents and 23, 44, and 65 percent, respectively, in patients not receiving these agents. At four years there was no difference in survival between the two groups of patients. However, abnormal left ventricular ejection fraction (the proportion of blood emptied from the left heart ventricle at the end of a contraction) was associated with higher incidences of sudden cardiac death, total cardiac death, or total death through four years. The incidences of sudden cardiac death, total cardiac death, or total death were similar among patients who were and were not treated with these antiarrhythmic agents. These findings confirm that treatment with quinidine or procainamide did not alter the risks of sudden and total cardiac death and total death. In addition, the lack of effect of these antiarrhythmic agents on the risks of cardiac and total death was not influenced by abnormal left ventricular ejection fraction, ventricular arrhythmias, or ischemic heart disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

Although there is an overall increased risk of cardiac death associated with physical exertion, the risk is small. Yet it warrants consideration by physicians and their adult patients who pursue exercise because, in any individual patient, the risk may be high. To advise patients properly on the risks and benefits of exercise, physicians should have an understanding of the risks of exercise, a strategy for patient evaluation that effectively identifies patients at risk, and a knowledge of appropriate exercise procedures that minimize risk. Patients should also know proper exercise procedures, be aware that there is some degree of risk in exercise, know their exercise tolerance, understand self-monitoring procedures, and be sensitive to prodromal symptoms. The essential feature of prudent exercise is a gradual progression during which an individual remains well within the limits of his/her exercise tolerance. (Am J Cardiol 1990;66:183-188), Physical exertion may be associated with a small, but increased, risk of sudden cardiac death, the irreversible cessation of heart beat. The risk of cardiac death associated with exercise must be taken into consideration by physicians and cardiac patients interested in exercise. To advise patients on the risks and benefits of exercise, physicians must have an understanding of the risks of exercise, a plan for evaluating and identifying patients at risk, and knowledge about the exercise procedures that reduce the risk of sudden cardiac death. Patients should be informed of suitable exercise procedures, the degree of risk associated with exercise, and their ability to tolerate exercise. In addition, patients should understand methods of monitoring themselves and be aware of symptoms that precede and are associated with sudden cardiac death. Essentially, exercise should be performed with gradually increasing intensity and within the limits of a patient's ability to withstand physical exertion. (Consumer Summary produced by Reliance Medical Information, Inc.)

Certain factors increase the risk of death in the year after an acute myocardial infarction (heart attack). These include ventricular premature complexes, which are abnormal heart rhythms arising in the ventricles of the heart, and impaired left ventricular ejection fraction, which is a decreased volume of blood emptied from the left ventricle at the end of a heart contraction. Recent studies have suggested that certain psychosocial factors, such as depression, the interaction between social isolation and life stress, and type A-B behavior, may influence the development of heart disorders. The relation between biobehavioral or psychosocial factors and clinical cardiac events was evaluated, based on results obtained from the Cardiac Arrhythmia Pilot Study (CAPS). The study included 502 patients with 10 or more ventricular complexes per hour, or five or more episodes of nonsustained ventricular tachycardia (an abnormally rapid ventricular rate) which were recorded 6 to 60 days after a heart attack. In 66 percent of the patients psychosocial questionnaires were used to assess anxiety, depression, social desirability and support, and type A-B behavior patterns. Blood pressure and pulse rate were recorded when patients played a video game. Death or cardiac arrest were used as indicators of outcome. The results indicate that a type B behavior patterns, higher levels of depression and lower pulse rates while playing the video game were associated with an increased risk of death and cardiac arrest. (Consumer Summary produced by Reliance Medical Information, Inc.)