Serum lipoprotein(a) concentrations and alcohol consumption in hypertension: possible relevance for cardiovascular damage

Objectives To evaluate the relationships between alcohol intake and serum lipoprotein(a) [Lp(a)], a powerful predictor of organ damage, in patients with essential hypertension with a wide range of alcohol intake, and to investigate whether the association between alcohol intake and serum Lp(a) concentrations occurs over the entire spectrum of apo(a) phenotypes. Design Cross-sectional study of a case series. Setting University medical centre. Patients Four hundred and two patients with untreated essential hypertension recruited at a hypertension clinic. Main outcome measures Serum Lp(a) concentrations, apo(a) isoforms, alcohol consumption, smoking habits and cardiovascular status. Results No difference in Lp(a) concentrations was observed between teetotalers and occasional drinkers. Light drinkers (1 -20 g/day ethanol), moderate drinkers (21-50 g/day), and heavy drinkers (>50 g/day) had, respectively, 21, 26 and 57% lower median Lp(a) concentrations than teetotalers and occasional drinkers. Similar findings were obtained when male and female patients were analysed separately. Log Lp(a) concentrations were inversely and independently correlated with alcohol consumption in both men and women with hypertension. The frequency distributions of apo(a) isoforms and liver function parameters were comparable across the different alcohol intake groups. Patients with evidence of cardiovascular damage had greater concentrations of serum Lp(a) and higher frequency of low-molecular weight apo(a) isoforms as compared with patients without such evidence. Conclusions Serum Lp(a) is inversely and dose-dependently related with alcohol intake in patients with hypertension, and this relationship is independent of the size distribution of apo(a) isoforms. Reduction of Lp(a) concentrations by regular consumption of alcohol might favourably affect the atherosclerotic risk profile of patients with hypertension and thereby decrease cardiovascular morbidity. J Hypertens 21:281-288 (C) 2003 Lippincott Williams Wilkins.