ABSTRACT
The heart failure syndrome (HF) has diverse etiologies. In a 22-year study of predictors of HF in 126,235 persons, we attempted to identify etiologic factors independent of associated coronary heart disease (CAD) in 2594 persons hospitalized for the condition. For this purpose, subjects were stratified according to whether CAD was present. Of the subjects, 60% had evidence for CAD (CAD-HF). Because we also wished to study HF predictors in subjects without associated CAD according to specific HF etiology, the paper records of the other 40% of subjects (non-CAD-HF) underwent a detailed review so that we could determine the apparent primary etiology and contributory factors. A random sample of all subjects with CAD-HF underwent a similar paper record review so that we could ascertain contributory factors. The primary etiology among the subjects with non-CAD-HF was categorized as systemic hypertension (HTN) in 354, valve disease in 110, cardiomyopathies (including alcoholic and idiopathic) in 93, other specific miscellaneous in 55, and primary etiology not evident (unclear) in 423. The unclear-group subjects generally had multiple probable contributing factors. In addition to the preponderant etiology in subjects with non-CAD-HF, the mean number of contributory factors was 1.5; among subjects with CAD-HF, the mean number of contributory factors was 1.9. Frequent additional factors, in both CAD-HF and non-CAD-HF, were HTN, diabetes mellitus, atrial fibrillation, and heavy alcohol consumption. These data show that primary HF etiology is often uncertain and that HF etiology is usually multifactorial, whether or not CAD is present.
ABSTRACT
Myocardial damage from heavy alcohol intake can cause the heart failure (HF) syndrome, but the relation of lighter alcohol intake to HF has rarely been studied. We examined the risk of HF hospitalization among 126,236 subjects who supplied data about alcohol during health examinations from 1978 to 1985. Among 2,594 subjects who were subsequently hospitalized for HF, record review established an association between coronary artery disease (CAD) and HF (CAD-HF) in 1,559 patients. Among the remaining 1,035 subjects who had HF (non-CAD-HF), we attempted determination of preponderant etiologic and contributory factors. Analyses used Cox models that were controlled for 7 covariates, with usual alcohol intake studied categorically compared with that in subjects who did not drink alcohol. Heavier drinkers (> or =3 drinks/day) but not light to moderate drinkers had increased risk of non-CAD-HF; e.g., relative risk for subjects who reported > or =6 drinks/day was 1.7 (95% confidence interval 1.1 to 2.6). This association of non-CAD-HF with heavy drinking was limited to subsets with cardiomyopathy or of unclear preponderant etiology. Alcohol drinking was inversely related to risk of CAD-HF (e.g., at 1 to 2 drinks/day, relative risk 0.6, 95% confidence interval 0.5 to 0.7), with consistency across subgroups of age, gender, ethnicity, education, smoking status, interval to diagnosis, and presence or absence of baseline heart disease or systemic hypertension. Moderate drinking was inversely related to non-CAD-HF only in subjects who had diabetes mellitus (n = 252). In conclusion, heavy, but not light, alcohol drinking is associated with increased risk of non-CAD-HF and that apparent protection by alcohol drinking against CAD-HF risk provides confirmation of a protective effect of alcohol against CAD.
