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Zagrosek A, Messroghli D, Schulz O, Dietz R, Schulz-Menger J. Effect of Binge Drinking on the Heart as Assessed by Cardiac Magnetic Resonance Imaging. JAMA. 2010;304(12):1328–1330. doi:https://doi.org/10.1001/jama.2010.1343
To the Editor: Excessive consumption of alcohol over a short period of time (binge drinking) induces a systemic inflammatory reaction,1,2 which might lead to alcohol-induced myocardial inflammation. We investigated whether excessive consumption of alcohol induces myocardial changes detectable by cardiac magnetic resonance (CMR) techniques commonly used for the diagnosis of myocardial inflammation.3
From March 2007 to July 2008, we studied 31 healthy volunteers. In 23, binge drinking was simulated by excessive consumption of vodka over 3 to 4 hours (blood alcohol level [BAL] >0.6 g/L following a standardized protocol).4 Participants were examined in 1.5-T MR systems (Sonata and Avanto; Siemens Medical Solutions, Erlangen, Germany) 10 to 12 hours before, 1 day after, and 1 week after alcohol intake. Blood alcohol level was assessed 1 hour after alcohol intake. Blood cell count, C-reactive protein, creatine kinase, troponin T, myoglobin, lactate dehydrogenase, and serum creatinine were assessed before each CMR examination. High-sensitivity cardiac troponin I (cTnI) was evaluated in 12 participants.
The CMR protocol included cine imaging for assessing left ventricular function, T2-weighted techniques for detecting myocardial edema, contrast-enhanced T1-weighted techniques for global relative enhancement (gRE, quantification of myocardial hyperemia), and late gadolinium enhancement for detecting myocardial necrosis.3 Eight control participants underwent CMR twice within 24 hours to test for effects of repeated contrast exposure. Assessors were blinded to exposure status.
Data underwent the Shapiro-Wilkinson test for normality, and Friedman and Wilcoxon tests were used for nonparametric data. Analyses were performed with Analyze-it version 2.11 (Analyze-it Software, Leeds, United Kingdom), and significance was set at 2-sided P < .05. Written informed consent was obtained from all participants and the local ethics committee approved the study.
The study was completed by 28 of 31 participants; 2 from the intervention group and 1 from the control group were excluded because of claustrophobia or pathological CMR findings at baseline. The median peak BAL was 1.3 g/L (interquartile range [IQR], 1.1-1.5). All individuals experienced hangover symptoms after alcohol exposure.
Left ventricular volumes and systolic function remained unchanged throughout the study. There was a significant increase in median myocardial T2-signal intensity (1.9 [IQR, 1.8-2.0] vs 1.7 [IQR, 1.6-1.8]; P = .001) and gRE (6.0 [IQR, 5.2-7.4] vs 4.1 [IQR, 3.4-5.0]; P = .008) 1 day after drinking (Table). No areas of focal late gadolinium enhancement were detectable. Three participants with abnormal T2 images developed mild pericardial effusion after alcohol exposure. In 6 of 12 participants tested, cTnI levels increased, suggesting subtle cardiac injury.5 There were significant differences between the intervention and control groups 1 day after drinking for median T2-signal intensity (1.9 [IQR, 1.8-2.0] vs 1.6 [IQR, 1.6-1.7]; P = .003) and gRE (6.0 [IQR, 5.2-7.4] vs 3.6 [IQR, 2.8-4.4]; P = .002). Other laboratory results remained unchanged except for myoglobin level, which was increased 1 day after drinking (median, 38.5 [IQR, 31.5-40.3] vs 35.0 [IQR, 28.0-38.5] μg/L; P = .02) (to convert myoglobin to nmol/L, multiply by 0.0571). Cardiac magnetic resonance parameters returned to baseline within 1 week (Table).
Despite possible reduction in the sensitivity of gRE and T2-weighted imaging due to co-involvement of the CMR reference (skeletal muscle), this study demonstrated transient myocardial changes accompanied by an increase in serological markers of myocardial injury after binge drinking. This reversible myocardial injury is most likely caused by an inflammatory reaction.
Because left ventricular systolic function remained normal and there were no CMR signs of irreversible tissue injury, the study does not provide evidence of an acute risk of cardiac events involved with binge drinking, and the clinical significance of the findings requires further investigation. However, in patients with acute viral myocarditis, additional myocardial stress (eg, unrestricted physical exercise) can promote inflammatory processes and cause severe reduction of cardiac function.6 Accordingly, repeated exposure to excessive amounts of alcohol might prevent the myocardium from full recovery and lead to alcoholic cardiomyopathy by triggering chronic inflammation. Serial animal studies with histopathological confirmation are needed to test this hypothesis.
Author Contributions: Dr Zagrosek had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Zagrosek, Dietz, Schulz-Menger.
Acquisition of data: Zagrosek, Messroghli, Schulz, Schulz-Menger.
Analysis and interpretation of data: Zagrosek, Messroghli, Schulz-Menger.
Drafting of the manuscript: Zagrosek, Schulz.
Critical revision of the manuscript for important intellectual content: Zagrosek, Messroghli, Dietz, Schulz-Menger.
Statistical analysis: Zagrosek, Messroghli.
Administrative, technical, or material support: Zagrosek, Schulz.
Study supervision: Dietz, Schulz-Menger.
Financial Disclosures: None reported.
Additional Contributions: Kerstin Kretschel, Evelyn Polzin, and Denise Kleindienst provided magnetic resonance technical assistance; Sascha Aiche, MD, provided help conducting the study; and Florian von Knobelsdorff-Brenkenhoff, MD, and Ralf Waßmuth, MD, provided careful reading of the manuscript. All are affiliated with the Clinic for Cardiology at Charité-Campus Buch. None of these persons received financial compensation for their roles in this study.
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