Impact of Genetic Variation in Aldehyde Dehydrogenase 2 and Alcohol Consumption on Coronary Artery Lesions in Chinese Patients with Stable Coronary Artery Disease

Abstract

The aim of this study is to investigate the impact of aldehyde dehydrogenase 2 (ALDH2) genotype and alcohol consumption on coronary artery lesions in Chinese patients with stable coronary artery disease (CAD). A total of 753 Chinese patients (73.6% male) diagnosed with stable CAD by coronary angiography were included in the sample. The frequency of the mutated type ALDH2^*2 (including ALDH2^*1/^*2 and ALDH2^*2/^*2) was 44.1% in CAD patients. The mutated ALDH2 carriers were more susceptible to multivessel lesions. Low to moderate alcohol consumption is related to higher plasma HDL-C level and fewer coronary artery lesions in CAD patients with ALDH2 wild genotype, while these effects were not observed in CAD patients with ALDH2 mutated genotype. Furthermore, we divided the mutated group into heterozygous and homozygous subgroups, and no obvious relationships were observed among drinking and HDL-C and coronary lesions. To explore the metabolic effects of ALDH2 modified by alcohol, we examined the impact of ALDH2 genotype and alcohol intake on HDL-C levels in ALDH2 wild type and knockout mice. The results showed HDL-C levels were significantly higher post low to moderate alcohol consumption in wild type rather than in knockout mice. CAD patients with mutated ALDH2 genotype are inclined to suffer with coronary artery lesions than wild type subjects. Low to moderate ethanol intake contributes to fewer multivessel lesions in CAD patients with ALDH2 wild type, which might be related to higher HDL-C level.