Intake of fermented beverages protect against acute myocardial injury: target organ cardiac effects and vasculoprotective effects
Mild-to-moderate alcohol consumption has been associated with reduced risk of morbi/mortality from coronary artery disease. However, whether beer intake affords cardioprotection remains unclear. We investigated whether beer intake (alcohol-containing and alcohol-free brew) provides cardioprotection in a pig model of myocardial infarction (MI). Pigs were randomly assigned to: (1) be fed for 10 days a high-cholesterol diet (HC); (2) HC + low-dose beer (LB; 12.5 g alcohol/day); (3) HC + moderate-dose beer (MB; 25 g alcohol/day); or IV) HC + alcohol-free-MB (0.0 g alcohol/day) before MI induction and kept 21 days with the same regime. Scar size, echocardiography, biochemical and oxidative parameters were assessed. Myocardial tissue was obtained for molecular analysis and histology. All beer-fed animals were less prone to arrhythmogenesis during ischemia. At sacrifice, beer intake was associated with lower oxidative stress and higher HDL-antioxidant capacity. Within the ischemic myocardium beer-fed animals showed higher Akt/eNOS and AMPK activation and reduced sirtuin1-related apoptosis. Compared to controls beer intake was associated with lower lipid infiltration, higher TGFβ-related collagen fibril formation and diminished MMP9 activity in the fibrous tissue limiting scar size (HC + LB and HC + MB P < 0.05 and HC + alcohol-free-MB P = 0.068 vs. HC). Systolic-related parameters were similarly worsen post-MI in all groups and further deteriorated in control animals (P ≤ 0.05 vs. post-MI). At sacrifice, all animals showed a worsening in diastolic-related parameters but overall cardiac performance was improved in beer-fed animals regardless of the dose or alcohol content (P ≤ 0.05). In conclusion, beer intake reduces oxidative stress and apoptosis, activates RISK components and favors reparative fibrosis improving global cardiac performance.