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The prevalence of Rose Questionnaire angina and its association with coronary heart disease risk factors and manifestations were investigated in representative samples of the US population. The study populations included 1,135 black and 8,323 white subjects aged 25-74 years examined in the Second National Health and Nutrition Examination Survey, 1976-1980, and 2,775 Mexican-American subjects aged 25-74 years examined in the Hispanic Health and Nutrition Examination Survey, Mexican-American portion, 1982-1983. Age-adjusted prevalence rates of Rose angina were similar among black, white, and Mexican-American women (6.8%, 6.3%, and 5.4%, respectively). An excess in the prevalence of Rose angina was observed in women compared with men for white and Mexican-American persons under age 55 years, but not for those over age 55. Electrocardiographic evidence of myocardial infarction and self-reported heart attack were strongly associated with prevalent Rose angina among white men and women aged 55 years and over, but not among those below age 55. Serum cholesterol, body mass index (weight (kg)/height (m)2), current cigarette smoking, and dyspnea were independently associated with an increased risk of prevalent angina in multivariate logistic models for white women, excluding those with a prior heart attack. Because many younger women with chest pain who may consult physicians are likely to have elevations in cardiovascular risk factors, their self-reported chest pain can be used as an opportunity to intervene and reduce their future risk of cardiovascular disease.

The relationship of alcohol consumption, measured in 1965-1968 by the 24-hour recall method, to incident coronary heart disease morbidity at eight years and mortality at 12 years of follow-up was investigated in a cohort of 9150 Puerto Rican males 35-79 years of age. After adjustment for age, cigarettes, exercise, urban/rural status, and income, there was clear evidence of a "U-shaped" relationship between alcohol and total mortality, and also the suggestion of a "J-shaped" relationship for angina pectoris, nonfatal myocardial infarction, and nonsudden coronary heart disease death. There was no association of alcohol with sudden cardiac death. The adjusted odds ratio for drinkers versus nondrinkers was 0.6 for angina pectoris (p less than 0.05), 0.7 for nonfatal myocardial infarction (p less than 0.1), and 0.7 for nonsudden coronary heart disease death (p less than 0.05). The inverse association of alcohol consumption to nonsudden coronary heart disease death was found to be dependent on age and income: the adjusted odds ratio for subjects under age 60 (0.4) or over the median income (0.3) strongly favored drinkers, while there was no evidence for a "protective effect" of alcohol consumption in the older and poorer segments of the population. It is concluded that available evidence does not justify the assertion that the inverse association between moderate alcohol intake and coronary heart disease risk is a causal one.

Results from twin studies in older children and adults indicate that there is significant genetic variance for blood pressure (BP). Utilizing date which were collected in 12 US university-affiliated hospitals in 1966-1973 in the Collaborative Perinatal Project (NCPP), the authors sought to determine if the effects of heredity on BP variability are apparent in younger twins. BP was determined in 197 pairs of like-sexed twins at seven years of age. Significant genetic variability for diastolic blood pressure (DBP) was found in the twins, with a heritability estimate of 0.53. Systolic blood pressure (SBP) results tended in the same direction but were not statistically significant. The trends were comparable for both sexes and races. These findings suggest that even at a young age substantial genetic influences on DBP variability are detectable.

In the Puerto Rico Heart Health Program, a prospective epidemiologic study, 9824 men living in defined urban and rural areas of Puerto Rico have been followed for approximately eight years. Periodic examinations have been used to assess potential cardiovascular risk factors and to monitor coronary heart disease events. Although the emphasis of the study has been oriented to cardiovascular disease, all causes of death have been closely monitored. During the observation period, 179 deaths from cancer have occurred in the age group 45--64 years. The distribution of cancer deaths varies from that of the mainland, with a greater percentage being oral, pharyngeal and stomach, and a lesser frequency being lung. Serum cholesterol measured at the first examination in 1965 was found to vary inversely with subsequent mortality from cancer. This trend was significant overall for the rural area and in the age group 45--54 years in the urban area. Multivariate analysis with other covariables did not eliminate the cholesterol relationship in the rural men, although relative weight, ventricular rate, hematocrit and cigarette smoking made independent contributions in certain age groups in both locations. The association between serum cholesterol and cancer mortality in the rural area and in the young urban area suggests that further investigation is needed to determine whether the relationship is causal, a secondary association to some other unidentified set of primary factors, or merely a physiological reaction to early and undiagnosed stages of the cancer process.

HDL, VLDL, and LDL cholesterol as well as total cholesterol were measured in young adult offspring of Framingham Heart Study participants. Parental total cholesterol levels measured in the early 1950s were found to be significant predictors of present total cholesterol in the offspring. While both maternal and paternal cholesterol levels made an independent contribution to the prediction of the offspring's cholesterol, the mother's contribution was significantly greater than the father's for male offspring with a similar but less striking relationship for female offspring. The correlation for LDL cholesterol levels for siblings was higher than for HDL cholesterol or log VLDL choles terol. When adjustments were made for age, body weight, alcohol intake and cigarette smoking, slight reductions in the correlations were noted, but all adjusted correlations remained significantly different from zero. The spouse correlations for lipoproteins, however, did not differ from zero after adujustment. Since the significant association for lipoproteins in spouse pairs disappears on adjustment for correlates but the association for siblings does not, it is likely that the sibling lipoprotein associations result from either genetic or environmental factors shared early in life.