Search

Survival rates and antiarrhythmic drug use were determined in 941 consecutive patients resuscitated from prehospital cardiac arrest due to ventricular fibrillation between March 7, 1970, and March 6, 1985. Of these patients, 18.7 0/0 were treated for at least a portion of the period with quinidine, 17.5 0/0 with procainamide, and 39.4 0/0 received no antiarrhythmic agent. Beta blockers were prescribed for 28.3 0/0 of the patients. Unadjusted comparisons of survival estimates showed dramatically lower survival rates for patients who received antiarrhythmic drugs independent of [beta]-blocker therapy and significantly improved survival for patients receiving [beta]-blocker therapy independent of antiarrhythnic use. Patients for whom antiarrhythmic therapy was prescribed also had more adverse baseline risk factors, whereas patients taking [beta] blockers had fewer such risk factors. After adjustment for these baseline risk factors, the use of antiarrhythmics was weakly (p, Heart arrhythmias, abnormalities in the rhythm of the heartbeat, are a major cause of death after heart attacks. Arrhythmias such as ventricular fibrillation (extremely rapid beating of the ventricles, the major pumping chambers), if prolonged, may cause heart arrest, and in the past, antiarrhythmic drugs were used routinely to treat the condition. This type of management was succeeded by administration of these medications only after evaluation of the ventricular arrhythmia. The effectiveness of this approach has not been proven, however. To better understand the effect of these drugs, the outcome from use of antiarrhythmic drugs in 941 patients who had out-of-hospital heart attacks caused by ventricular fibrillation was evaluated. Patients also received another type of medication, beta-blockers. Subsequent heart arrest was related to older age, having been resuscitated during the early 1970s, and a history of heart attack or congestive heart failure. After adjusting for these factors, the relative risk for recurrent heart arrest was significantly increased with antiarrhythmic therapy, by a factor of 1.17 times. Procainamide was associated with a greater risk than quinidine. Beta-blocker therapy was associated with a significant decrease, by 38 percent. The study suggests that antiarrhythmic agents may be hazardous, rather than helpful, in patients who have had ventricular fibrillation. (Consumer Summary produced by Reliance Medical Information, Inc.)

In a retrospective survey of 1,195 survivors of out-of-hospital ventricular fibrillation, 43 patient were identified in whom left ventricular ejection fraction was [greater than or equal to] 0.50 and in whom no coronary artery stenosis of [greater than or equal to] 50% luminal diameter were present. Thirteen (30%) of these patients had hypokinesia on left ventriculography, and 20 patients (47%) had a persistently abnormal electrocardiogram. Seven patients (16%) had recurrent out-of-hospital cardiac arrest during an average follow-up of 86 [plus or minus] 54 months. The presence of either wall motion or electrocardiographic abnormalities defined patients with a several-fold higher risk of recurrent cardiac arrest than those without such abnormalities. The risk for recurrent cardiac arrest within 5 years was 30% in those with abnormal electrocardiograms versus 5% in the others (p [less than] 0.03). Age was an independent predictor of recurrent cardiac arrest in this group (p [less than] 0.01); surprisingly, recurrent cardiac arrest was occurring more often among younger patients. Although cardiac arrest is unusual in patients with major structural heart disease, its recurrence in such survivors is common. Patients at relatively high risk for recurrent ventricular fibrillation can be identified by their youth and by abnormalities detected on the surface 12-lead electrocardiogram or by contrast left ventriculography. (Am J Cardiol 1991;67:704-708), Most individuals who suffer from out-of-hospital cardiac arrest, even young and ostensibly healthy patients, usually have significant structural heart disease. The likelihood of recurrent cardiac arrest in these individuals is related to the severity of coronary artery disease (narrowing of the arteries supplying the heart with blood) and the severity of left ventricular dysfunction. Among the population of cardiac arrest victims in whom there is no or little cardiac disease, the predictors of recurrence are less well known. To identify which patient variables might predict recurrence of cardiac arrest, 1,195 survivors of out-of-hospital ventricular fibrillation (an often fatal type of cardiac arrest) were evaluated. From this group, 43 patients (ranging in age from 20 to 73 years) were selected with relatively normal left ventricular function (ejection fraction greater than or equal to 50 percent) and no (or very mild) narrowing of the coronary arteries. Thirty percent of these patients had abnormalities of cardiac wall motion, and 47 percent had frequently abnormal electrocardiograms. Over a five-year follow-up period, patients with either wall motion abnormalities or abnormal electrocardiograms had a several-fold higher risk of suffering recurrent cardiac arrest; 30 percent of the patients with abnormal electrocardiograms suffered recurrent cardiac arrest compared with five percent of the other patients. Age was inversely related to the frequency of recurrence; younger patients were significantly more likely to have a second episode of cardiac arrest than older patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Since 1988, 641 black and 11,892 white patients with chest pain of presumed cardiac origin have been admitted to coronary care units in 19 hospitals in metropolitan Seattle. Mack men and women were younger (58 vs 66, p Questions about the premature onset of coronary artery disease, excess systemic hypertension, and the differential use of interventions in black persons have been raised by other investigators. Despite differences in age, referral patterns and the use of coronary angioplasty and bypass surgery, black and white patients with AMI in metropolitan Seattle had similar outcomes. (Am J Cardiol 1991;67:18-23), Coronary artery disease (CAD) is a condition in which stenosis (narrowing) develops in the blood vessels supplying the heart muscle (coronary arteries). This results in a reduction of blood flow to that organ and can cause chronic insufficient blood flow to the heart (myocardial ischemia) or, if the occlusion becomes worse, acute myocardial infarction (AMI), a heart attack. The prevalence and history of CAD and AMI in black populations is coming under increasing study. To ascertain whether blacks are less likely than whites to seek medical care for symptoms of CAD, whether the time from symptom onset to initiation of hospital care differs for the two races, whether similar or different treatment strategies are used, and the relative rates of mortality for blacks and whites suffering from CAD, the records of 641 black and 11,892 white patients with symptoms of CAD were analyzed. All patients were admitted to hospitals in the metropolitan Seattle area between January 1988 and January 1990. Blacks were significantly younger than whites (56 vs. 66 years), were more likely to be admitted to central city (rather than suburban) hospitals, and developed evidence of AMI less often than whites. Blacks also had less incidence of prior coronary artery bypass graft surgery, but a higher incidence of hypertension (high blood pressure). During hospitalization, whites were more likely to undergo coronary angioplasty or bypass surgery as treatment; the administration of thrombolytic (clot-dissolving) drugs was utilized equally for blacks and whites. Mortality rates were higher for white patients (13.1 percent) than blacks (7.4 percent), but when statistical correction for confounding variables (such as medical history and risk factors) was made, there was no difference in mortality from heart disease between the races. (Consumer Summary produced by Reliance Medical Information, Inc.)

The basis for the excess mortality with age after acute myocardial infarction (AMI) is not clear, nor is it known whether the mode of death is altered with age. Age-related factors predictive of mortality and age-related mechanisms of the 333 deaths were examined in 2,466 patients who were enrolled in a placebo-controlled trial to determine the effect of diltiazem on mortality and reinfarction after AMI. There were 3 age groups with increasing mortality rates: ages 25 to 49 (n = 499), 50 to 64 (n = 1,228) and 6S to 75 years (n = 739). There was a significant age-related increase in the proportion of patients with baseline risk factors. These baseline characteristics did not differ by treatment (placebo vs diltiazem). However, multivariate survivorship analysis still identified age as an independent risk factor for cardiac death. The proportion of arrhythmic and myocardial failure deaths did not differ by treatment or age group. (Am J Cardiol 1990;65:559-566), The likelihood of death after a heart attack (myocardial infarction, MI) is associated with advanced age, but the basis for this increased mortality risk is not known. Some identifiable factors such as impaired function of the left ventricle (the major pump of the heart muscle) are more prevalent in the elderly than in younger patients after MI, but this does not adequately explain the increased risk. Factors predictive of mortality were examined during a study which was evaluating the effects of diltiazem on 2,466 survivors of acute MI during a one- to five-year period. Prognosis, risk predictors, mechanism of death, and presence of ischemia (deficient blood supply) before death were studied. There was a similar incidence of arrhythmias (abnormal heart rhythms) and ischemia preceding death in younger and older age groups. The older group of patients had more risk factors, including previous MI, advanced New York Heart Association Classification, and decreased ventricular function or abnormal heart beat. Nevertheless, age still predicted mortality risk independently of these other factors. Possibly, older patients may have had more coronary vessel obstructions, but there was a similar incidence of MI recurrence in younger and older patients. Much of the current knowledge about MI relates to a younger population, but the US population is rapidly aging. Further studies are needed to broaden the understanding of heart physiology following MI in the elderly, so as to improve the survival rate in these patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Whether the dietary intake of long-chain n-3 polyunsaturated fatty acids (PUFAs) from seafood reduces the risk of ischemic heart disease remains a source of controversy, in part because studies have yielded inconsistent findings. Results from experimental studies in animals suggest that recent dietary intake of long-chain n-3 PUFAs, compared with saturated and monounsaturated fats, reduces vulnerability to ventricular fibrillation, a life-threatening cardiac arrhythmia that is a major cause of ischemic heart disease mortality. Until recently, whether a similar effect of long-chain n-3 PUFAs from seafood occurred in humans was unknown. We summarize the findings from a population-based case-control study that showed that the dietary intake of long-chain n-3 PUFAs from seafood, measured both directly with a questionnaire and indirectly with a biomarker, is associated with a reduced risk of primary cardiac arrest in humans. The findings also suggest that 1) compared with no seafood intake, modest dietary intake of long-chain n-3 PUFAs from seafood (equivalent to 1 fatty fish meal/wk) is associated with a reduction in the risk of primary cardiac arrest; 2) compared with modest intake, higher intakes of these fatty acids are not associated with a further reduction in such risk; and 3) the reduced risk of primary cardiac arrest may be mediated, at least in part, by the effect of dietary n-3 PUFA intake on cell membrane fatty acid composition. These findings also may help to explain the apparent inconsistencies in earlier studies of long-chain n-3 PUFA intake and ischemic heart disease. Am J Clin Nutr 2000;71(suppl):208S-12S. KEY WORDS n-3 Fatty acids, diet, risk factors, arrythmia, sudden death, cardiac arrest, ischemic heart disease