Abstract 294: Heavy Alcohol Use Worsens Peripheral Artery Disease-Associated Myopathy

Abstract

Heavy alcohol use can induce skeletal muscle dysfunction referred to as alcoholic myopathy. Likewise, peripheral artery disease (PAD) is characterized by an acquired skeletal muscle metabolic myopathy in ischemic muscles of the lower extremity. Although epidemiological studies have shown that heavy alcohol consumption is associated with a greater risk of PAD, data are lacking on the contribution of alcohol-related myopathy on PAD-associated skeletal muscle pathology. We compared myofiber morphometrics, mitochondrial respiration, and oxidative stress measures in gastrocnemius biopsies from PAD patients with heavy alcohol use (>7 or >14 drinks per week, for females and males, respectively) (n=13) to PAD patients (n=13) and non-PAD controls (n=17) consuming moderate to low/no alcohol. Myofiber area and diameter were lower in heavy-drinking PAD patients compared to low/moderate drinkers (p=0.03 and p=0.04, respectively) and non-PAD controls (p=0.02 and p<0.001, respectively). Myofiber roundness was significantly higher in heavy-drinking PAD patients compared to low/moderate drinkers (p=0.04) and non-PAD controls (p<0.001). Although there were no significant differences between PAD groups in mitochondrial respiration, PAD patients with heavy alcohol consumption tended to have lower respiration for Complex I (p=0.14), Complex II (p=0.10), and Complex IV (p=0.16) compared to PAD patients without heavy alcohol use. Both PAD groups had significantly reduced respiration of all Complexes compared to non-PAD controls (p<0.05). These data suggest that alcohol abuse may accentuate skeletal muscle pathology in PAD patients.