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Barnett and Dobson performed meta-analysis of data about weekly distribution of cardiovascular events and found a slight excess in events on Mondays, more pronounced in men or associated with greater alcohol consumption.1 However, a debate about the underlying mechanisms is wide open.
The meta-analysis provided little evidence to support the possibility that registration data collection or recording procedures play a significant part in the phenomenon. Another part of the hypothesis lies in regard to increased stress on Mondays, particularly in employed people. A lack of data on work schedules in the original studies prevents a firm conclusion regarding this issue. Today, a growing number of people do not have a classic workweek with completely free weekends, work in shifts is common, and the line between work and free periods seems to be blurred. Furthermore, anger, quarrelling, sleep disturbances and other emotional stresses are well recognised triggers of cardiovascular events2 and, besides some habitual differences between extreme population subgroups, a random distribution of such triggers over the week probably exists in the general population. Last but not least, emotional stress seems to be more important for triggering cardiovascular events in women,2 whereas a Monday peak is present only in men.1
Increased alcohol consumption during weekend remains an appealing explanation. However, both alcohol consumption and deaths related to alcohol intoxication are at their lowest on Mondays, and peak on weekend days.3 So, what may cause this hypothetical, approximately one day delay in cardiovascular risk on Monday?
During alcohol hangover, an increase in concentrations of interleukin 12 (IL12) and interferon γ (INF γ) has been seen.4 Inflammation and its reactants are now regarded as markers of increased risk of acute coronary incident, but also as possible contributors to the initiation of that very incident. Increased serum IL12 and both serum and intracellular IFNγ, and associated increase in T-helper 1 activity are found in patients with unstable coronary disease.5,6 Perhaps, it takes some time before impaired cytokine and T-helper 1 function induce plaque vulnerability, and coupled with other consequences of alcohol consumption, for example, increased coagulability and likelihood of ventricular arrhythmias, increase cardiovascular risk, which usually falls on Monday.
Alcohol induced cytokine dysregulation and subsequent plaque destabilisation may be the core mechanisms of delayed cardiovascular risk on Mondays, but extensive research is necessary to confirm and to further develop this notion. Although Monday excess accounts only for less than 1 event in 100, in terms of epidemy of coronary disease it is highly significant rather than slight.