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An epidemiologic study was carried out to examine the possible role of beta-agonists and other respiratory medications in the development of idiopathic dilated cardiomyopathy. Associations with respiratory medications, bronchial asthma, emphysema, and chronic bronchitis were examined by comparing newly diagnosed cases (n = 129) ascertained from five Washington, DC, area hospitals for the period 1990-1992 with neighborhood controls (n = 258) identified by using a random digit dialing technique. The cases and controls were matched on sex and 5-year age intervals and were compared in the analysis using conditional logistic regression methods. A statistically significant association was observed between idiopathic dilated cardiomyopathy and history of emphysema or chronic bronchitis (adjusted odds ratio (OR) = 4.4, 95% confidence interval (CI) 1.6-12.4). The association with bronchial asthma was of borderline significance (adjusted OR = 1.9, 95% CI 0.9-4.2). Associations were also observed with use of oral beta-agonists (adjusted OR = 3.4, 95% CI 1.1-11.0) and beta-agonist inhalers or nebulization (adjusted OR = 3.2, 95% CI 1.4-7.1), as well as with use of oral corticosteroids, inhaled corticosteroids or cromolyn, and theophylline medications. A total of 20.0% (23 of 115) of the cases had a reported history of beta-agonist inhaler use compared with 6.7% (17 of 254) of the controls. The strength of these associations was diminished when the temporal relation between exposure to beta-agonist inhalers or oral preparations and clinical diagnosis of idiopathic dilated cardiomyopathy was taken into account, however, and the associations with duration of beta-agonist medication use were not statistically significant (p > 0.05). The results of this study suggest, but do not prove, that use of beta-agonists has an etiologic role in idiopathic dilated cardiomyopathy.

A regression method that utilizes an additive model is proposed for the estimation of attributable risk in case-control studies carried out in defined populations. In contrast to previous multivariate procedures for the estimation of attributable risk, which have utilized logistic regression techniques to adjust for confounding factors, the model assumes an additive relation between the covariates included in the regression equation. As an empirical example, additive and logistic models were fitted to matched case-control data from a population-based study of childhood astrocytoma brain tumors. Although both models fitted the data well, the additive model provided a more satisfactory estimate of the risk attributable to multiple exposures, in the absence of significant additive interaction. In contrast to the results from the logistic model, the adjusted estimates of the risk attributable to each factor included in the additive model summed to the overall estimate for all of the factors considered jointly. Thus, the additive approach provides a useful alternative to existing procedures for the multivariate estimation of attributable risk when the additive model is determined to be appropriate on the basis of goodness-of-fit.

Possible predictors of mortality from idiopathic dilated cardiomyopathy were studied in 356,222 men who were screened as part of the Multiple Risk Factor Intervention Trial. The vital status of each member of this cohort was ascertained through 1986. Death certificates were obtained from state health departments and coded by a trained nosologist. Individuals with a history of myocardial infarction were excluded. A total of 206 deaths due to idiopathic dilated cardiomyopathy occurred in the cohort of 356,222 men after an average of 12 years of follow-up. The age-specific rates of mortality from idiopathic dilated cardiomyopathy increased from 0.10 per 10,000 person-years among men aged 35-39 years to 1.16 per 10,000 person-years among men aged 55-57 years. The proportional hazards model was used to obtain adjusted estimates of relative risks. Statistically significant, independent associations were observed with cigarettes smoked per day (p < 0.001), diastolic blood pressure (p < 0.001), and diabetes mellitus (relative risk (RR) = 2.97, p < 0.001). Black race was also associated with an increased risk of death from idiopathic dilated cardiomyopathy (RR = 1.59 and p = 0.045 without adjustment for income; RR = 1.58 and p = 0.058 with adjustment for income). No association was found with serum cholesterol or income. The information about possible risk factors obtained in this study may contribute to future preventive programs for idiopathic dilated cardiomyopathy.

An epidemiologic study of idiopathic dilated cardiomyopathy was carried out in order to identify possible risk factors for this often fatal cause of heart failure in young adults. Possible associations with black race and other genetic and environmental factors were examined by comparing newly diagnosed cases ascertained from four Baltimore hospitals (n = 95) with neighborhood controls (n = 95), matched on sex and 5-year age intervals. Matched and unmatched relative odds and conditional logistic regression coefficients were obtained to describe the associations. Statistically significant, independent associations were observed between idiopathic dilated cardiomyopathy and black race, low annual income, and history of asthma (p less than 0.05). The black predominance (relative odds = 2.7, 95% confidence interval 2.0-3.4) was not explained by income, alcohol consumption, cigarette usage, body mass index, hypertension, or asthma. A possible interactive effect was observed between black race and history of asthma and other atopic diseases. Thus, blacks, especially those with a history of hypersensitivity, may represent a high-risk subgroup in need of preventive care or early intervention.

There is increasing interest in identifying children at risk for later development of cardiovascular disease. The authors studied 1,457 children who were first examined as part of the Bogalusa Heart Study in 1973 and again 15 years later as young adults. Age-, race-, and sex-specific quartiles were defined for each of three risk factor variables-ponderal index (weight/height3), systolic blood pressure, and cholesterol--for both the child and adult measures. Adults were classified as clustered if they were in the top quartile for each of the variables. Clustered adults had higher levels of several risk factor variables, in addition to the criteria variables, than did nonclustered individuals. Of children who placed in the top quartile on three factors, 21.8% were clustered as adults. Only 1.1% of those with no risk factor levels in the top quartile were clustered as adults (p < 0.0001). Logistic regression was used to predict adult cluster status from childhood variables levels. All three factors were significant predictors, with blood pressure being the most powerful. This well-fitting model is easily interpretable in terms of standard deviations and can be a useful model for identifying at-risk children.

The authors used noninvasive techniques, including flow velocity by Doppler ultrasound, to accurately assess and distinguish between large and small vessel peripheral arterial disease in a population study in southern California, 1978-1981. In 565 men and women aged 38-82 years, there were 69 cases of large vessel peripheral arterial disease, 19 of which were severe, and 90 cases of isolated small vessel peripheral arterial disease. In cross-sectional multivariate analysis in men, large vessel peripheral arterial disease was significantly associated with age, pack-years of cigarettes smoked, systolic blood pressure, fasting plasma glucose, and marginally with obesity. Similar analysis in women revealed significant associations only for age and systolic blood pressure, although the associations for pack-years of cigarettes, obesity, and low density lipoprotein cholesterol were suggestive. By contrast, isolated small vessel peripheral arterial disease was not significantly associated with any of the major cardiovascular disease risk factors, including two measures of carbohydrate metabolism, fasting plasma glucose and glycosylated hemoglobin. These findings, coupled with our earlier report that large vessel peripheral arterial disease but not isolated small vessel peripheral arterial disease was independently predictive of subsequent mortality, suggest that large vessel peripheral arterial disease and isolated small vessel peripheral arterial disease are epidemiologically, as well as pathophysiologically, distinct entities.