Editor—As Martyn notes in an editorial, the Monday peak in cardiovascular mortality and morbidity has been documented in various settings.1 We would like to develop further the notion that alcohol consumption is at least partly responsible. In countries with known weekend binge drinking the Monday peak is pronounced and is accompanied by slight increases in mortality on Saturdays and Sundays. This has been shown in countries of the former Soviet Union2 and in Scotland.3
The epidemiological evidence on high alcohol consumption and cardiovascular mortality supports this hypothesis. Studies that look at the pattern of drinking, either directly or indirectly, have consistently found an increased risk of cardiovascular death (particularly sudden death) with binge drinking.4
Physiological studies have also shown that the effects of regular moderate drinking versus binge drinking differ greatly.5 In binge drinkers, cardioprotective changes in high density lipoproteins are not seen and adverse changes in low density lipoproteins are acquired. Binge drinking seems capable of predisposing the heart to arrhythmia, both by reducing the threshold for ventricular fibrillation and by causing scarring of the myocardium.
The myocardium may be especially sensitive during withdrawal, as will occur after weekend binges. In addition, irregular drinking is associated with an increased risk of thrombosis, which is most likely to occur after heavy drinking stops. These physiological mechanisms may explain the observed increase in cardiovascular events during the weekend and on Mondays.
We hypothesise that alcohol, particularly when drunk in binges, acts as a catalyst on acute ischaemic heart diseases, possibly by being synergetic to other triggering factors.
References
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