Impact of lifetime alcohol consumption on left ventricular myocardial reserve in athletes

Background Excessive alcohol consumption is a risk factor for impaired left ventricular (LV) function. Although current guidelines limit weekly alcohol intake to ≤ 14 units (U). The impact of cumulative lifetime exposure on cardiac contractile reserve is unknown. We investigated the relationship between alcohol consumption and the ability to augment peak LV ejection fraction (LVEF) during stress echocardiography (myocardial reserve) in athletic individuals with a dilated LV. Methods 62 control athletes with a normal LVEF [> 55%], 52 athletes with dilated cardiomyopathy (DCM) and mildly impaired LVEF (45-54%) and 68 asymptomatic athletes with borderline low LVEF(45-54%) (grey zone) were studied. All participants completed a comprehensive alcohol consumption questionnaire and underwent stress echocardiography. The questionnaire assessed multiple patterns of alcohol intake to calculate the average U per day and week and total lifetime consumption. Age-adjusted cumulative exposure was calculated by dividing the total lifetime units consumed by age. Participants exercised on a supine bicycle with a 25 W increment every 2 minutes until volitional exhaustion. Echocardiograms images were acquired at rest and peak exercise. Normal myocardial reserve was defined as a >10% increase in LVEF from baseline to peak Spearman’s Rho correlation, ROC curve analysis, and Youden’s Index were used to assess the correlation between alcohol consumption and the ability to augment LVEF to determine detrimental alcohol thresholds and identify optimal cut-off points. Results There were no differences in mean age (p=0.3), size (p=0.79) or number of weekly hours of exercise (p=0.22) between the three groups. Total lifetime consumption was highest in individuals with DCM, followed by grey zone athletes and athletes with normal LV function (mean = 29,949 U,17,612 U and 17,431 U and median =11,096 U, 16,790 U, 7,800 U, respectively). The quantity of alcohol consumed did not impact indexed LV cavity size (R2 = 0.001). Lifetime consumption >12,191 U was associated with impaired myocardial reserve (Sensitivity = 71%, Specificity = 64%); p= 0.001. Age-adjusted consumption was highest in DCM, followed by control athletes and grey zone athletes (mean=650, 425, 407 U/year and median = 429, 250 and 344 U/year, respectively)(Picture 1). Consuming >278 U/year increased the risk of impaired myocardial reserve (Sensitivity=71%, Specificity=52%); p = 0.001. An average daily alcohol intake >3.67 U and an average weekly intake >25 U were associated with impaired myocardial reserve with low sensitivity (32% and 33%, respectively) and high specificity (80% and 80%). Conclusion Alcohol consumption is potentially associated with impaired myocardial reserve in athletes. Cumulative lifetime exposure and age-adjusted consumption were the strongest predictors. Lifetime consumption >12,000 U or > 270 U/year age-adjusted is associated with impaired myocardial reserve in athletic individual.