Key result
Chronic ingestion of 36% alcohol for 12 weeks in mice significantly reduced cardiac conduction velocity and increased the incidence of ventricular tachyarrhythmia (62% vs 31%).
Why the study?
Does chronic 36% alcohol ingestion induce cardiac structural and electrophysiological remodeling in mice?
Does chronic 36% alcohol ingestion induce cardiac structural and electrophysiological remodeling in mice?
Absolute Event Rate: 62% vs 31%
p-value: p=<0.05
Chronic excessive alcohol intake in mice induces extensive cardiac remodeling, including reduced cardiomyocyte size, altered gap junction distribution, and decreased myocardial conduction velocity, increasing vulnerability to ventricular tachyarrhythmias.
Chronic alcohol alters mouse cardiac gap junctions and electrophysiology; leaves open human arrhythmia mechanisms and translation.
BACKGROUND: Long-term heavy alcohol drinkers are prone to the development of cardiac arrhythmia. To understand the mechanisms, we evaluated the cardiac structural and electrophysiological changes in mice chronically drinking excessive alcohol. RESULTS: Male C57BL/6J mice were given 36% alcohol in the drinking water. Those given blank water were used as control. Twelve weeks later, the phenotypic characteristics of the heart, including gap junctions and electrical properties were examined. In the alcohol group the ventricles contained a smaller size of cardiomyocytes and a higher density of capillary networks, compared to the control. Western blots showed that, after drinking alcohol, the content of connexin43 (Cx43) protein in the left ventricle was increased by 18% (p < 0.05). Consistently, immunoconfocal microscopy demonstrated that Cx43 gap junctions were up-regulated in the alcohol group with a disorganized distribution, compared to the control. Optical mapping showed that the alcohol group had a reduced conduction velocity (40 ± 18 vs 60 ± 7 cm/sec, p < 0.05) and a higher incidence of ventricular tachyarrhythmia (62% vs 30%, p < 0.05). CONCLUSION: Long-term excessive alcohol intake resulted in extensive cardiac remodeling, including changes in expression and distribution of gap junctions, growth of capillary network, reduction of cardiomyocyte size, and decrease of myocardial conduction.
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Lai et al. (2011) studied Alcoholic cardiomyopathy and cardiac arrhythmia (n=94). 36% alcohol vs. Water was evaluated on Incidence of ventricular tachyarrhythmia (p=<0.05). Chronic ingestion of 36% alcohol for 12 weeks in mice significantly reduced cardiac conduction velocity and increased the incidence of ventricular tachyarrhythmia (62% vs 31%).
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