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Abstract: The association of alcohol intake with ischemic heart disease (IHD) and all-cause mortality may depend on ABO phenotype. We tested this hypothesis in a 16-year follow-up of 3,022 Caucasian men aged 53–74 years without overt cardiovascular disease. Potential risk factors and confounders included were ABO phenotypes, alcohol intake (wine, beer, and spirits), tobacco smoking history, leisure-time physical activity, social class, and age. During 16 years, 1985–1986 to end of 2001, 197 subjects (6.5%) died due to IHD, and 1,204 (39.8%) from all causes. Among non-O phenotypes (A, B, and AB) significantly fewer men who died due to IHD were wine consumers, 43.9% versus 55.7%, P <.01; with respect to all-cause mortality corresponding figures were 47.0% versus 60.1%, P <.001. No difference was found among men with phenotype O. Among men with phenotype A, compared to alcohol abstainers, in Cox analysis, the hazard ratio (HR) (95% confidence limit) for men drinking up to 8 beverages/wk was 0.5 (0.3–1.02), and among men consuming >8 beverages/wk (the highest quintile) the HR was 0.3 (0.2–0.8), P <.01. Among men with phenotype O, the association of wine intake with IHD mortality was slightly and not significantly U-shaped. The difference in the predictive role of wine intake between phenotype O and phenotype A men was supported in a statistical test for interaction. A similar association was found for all-cause mortality. The results suggest that the effect of wine intake on IHD and all-cause mortality among middle-aged and elderly men may depend on ABO phenotypes. [Copyright &y& Elsevier]

Increased ventricular ectopic activity and even more complex arrhythmias are not uncommon in subjects without apparent heart disease. However, their prognostic significance has been controversial and not updated in recent years. The prevalence and prognostic significance of different ventricular arrhythmias were studied in a cohort of middle-aged and elderly subjects without apparent heart disease. Six hundred seventy-eight men and women aged 55 to 75 years without a history of heart disease or stroke were included. Baseline examinations included physical examinations, fasting laboratory testing, and 48-hour ambulatory electrocardiographic monitoring. All patients were followed for up to 5 years. Combined events were defined as all-cause mortality or acute myocardial infarction. A cardiovascular event was defined as cardiovascular death or acute myocardial infarction. In total, 84% had 0 to 10 ventricular premature complexes (VPCs)/hour, 8% had 11 to 30 VPCs/hour, and 8% had >30 VPCs/hour; 10.8% had ≥1 run of ≥3 VPCs. Frequent VPCs (≥30/hour) was a significant predictor of combined (hazard ratio 2.47, 95% confidence interval 1.29 to 4.68, p = 0.006) and cardiovascular (hazard ratio 2.85, 95% confidence interval 1.16 to 7.0, p = 0.023) event rates, after adjustment for conventional risk factors. Runs of ≥4 VPCs/day or ≥2 doublets/day were also associated with a poor prognosis, but only in the presence of frequent VPCs. The detection of a single VPC on standard electrocardiography was a significant predictor of frequent VPCs and an independent predictor of events (hazard ratio 2.6, 95% confidence interval 1.02 to 6.66, p = 0.045). In conclusion, apparently healthy, middle-aged and elderly subjects with frequent VPCs (≥30/hour) have a poor prognosis. According to current guidelines, strict risk-factor modification and primary prevention are justified in these high-risk subjects. [Copyright &y& Elsevier]