Ib. Puddey et al., Influence of pattern of drinking on cardiovascular disease and cardiovascular risk factors - a review, ADDICTION, 94(5), 1999, pp. 649-663
Citations number
127
Categorie Soggetti
Public Health & Health Care Science","Clinical Psycology & Psychiatry
There is an established inverse relationship between the regular light cons
umption of alcohol (5-10g/day) and the incidence of coronary artery disease
(CAD). This association has several biologically plausible mechanisms with
dose-dependent effects of alcohol to increase HDL cholesterol, lower plasm
a fibrinogen and inhibit platelet aggregation. However, such a protective e
ffect against atheroma cannot be considered in isolation from known adverse
effects on blood pressure and triglycerides or possible detrimental effect
s of episodic or binge drinking on several other cardiovascular end-points
and risk factors. In subjects with pre-existing CAD, an alcoholic binge can
increase both silent myocardial ischaemia and angina. During withdrawal fo
llowing binge drinking, marked fluctuations in blood pressure together with
heightened platelet activation and adverse changes in the balance of fibri
nolytic factors, may offer an explanation for the reported association betw
een episodic heavy drinking and ischaemic stroke. This has been seen partic
ularly in young males and extends further to an increase in both subarachno
id haemorrhage and intracerebral haemorrhage after binge drinking. Interven
tion studies in man have shown acute increases in blood pressure in men who
drink predominantly at weekends, compared to longer-term presser effects i
n regular daily drinkers. We have been unable, however, to reproduce the fi
nding of unfavourable effects of binge drinking on the lipid profile that h
ave been reported in animal studies and man. Binge drinking may also induce
cerebrovascular spasm or cause both ventricular and supraventricular arrhy
thmias, especially atrial fibrillation. Alcohol-induced arrhythmia has been
postulated as the basis for alcohol-related sudden coronary death in those
subjects with pre-existing CAD. Hence, further exploration of any protecti
ve association of alcohol against CAD needs to carefully consider the impli
cations of pattern of drinking for the relationship. The modulating influen
ces of co-timing of drinking with meals, cigarette smoking or illicit drug
use also need to be evaluated. Without such vital information, public healt
h advice on alcohol and CAD will be limited in its scope and potentially fl
awed in its impact.