Division of Cardiology, Department of Medicine, University Hospital Split, 21000 Split, Croatia
The question of coronary calcification and its role in the process of atherogenesis, plaque stability, and occurrence of acute coronary events is a not completely resolved matter. Mark J. Pletcher et al. (1) recently reported that, among 3,037 participants aged 3345 years, those who on average consumed more alcohol were more likely to have coronary calcification. It has previously been proposed that calcium is a feature of stable coronary lesions (2
, 3
). At present, we know that coronary calcium correlates with the prognosis of coronary heart disease and predicts future coronary events (4
). Accordingly, it seems plausible that coronary calcium may indicate unstable and/or progressive coronary disease.
The beneficial association between alcohol and coronary heart disease is probably mediated through favorable effects on lipid profile, hemostatic factors, platelet aggregability, endothelial function, myocite protection, inflammation, and arrhythmogenesis (510
). However, a body of evidence suggests an increased cardiovascular risk in a group of the most frequent heavy drinkers (11
, 12
). The findings of Pletcher et al. support these data and a linkage between the level of alcohol consumption and unstable coronary disease. In their article, the authors also discussed the possibility that coronary calcium characterizes the process of plaque stabilization as a beneficial effect of alcohol, which could be associated with lower coronary risk among moderate drinkers. In that case, the more intense coronary calcification, like the one found in heavy drinkers, would be a sign of even more stable coronary lesions associated with a better prognosis, but this is in contrast with previous data (4
). It is more likely that the beneficial effects of alcohol in heavy drinkers are overrided by increased plaque vulnerability characterized by calcification. Such plaques would be more prone to rupture, particularly in the presence of hemodynamic and mechanic forces caused by external triggers (13
). Since alcohol consumption itself has been implicated as a trigger of sudden cardiac events (14
, 15
), frequent drinking increases the total amount of time at risk. A great advance in the understanding of the role of coronary calcium may be obtained by subsequent long-term follow-up of the middle-aged population of the present study. Nevertheless, coronary calcium may have different consequences or may reflect different proccesses at a younger or older age.
Pletcher et al. concluded that the association between usual alcohol consumption and coronary calcium is strongest among Black men. However, they failed to comment on an apparently even more impressive and also statistically significant association between the highest level of alcohol consumption (14 drinks/week) and coronary calcium among Black women. Although the overall interaction among different gender/ethnic groups was not statistically significant, it would be interesting if the authors continued with this subgroup analysis, for example, multivariable analysis. In the context of calcification and plaque vulnerability, such information may be useful for understanding the gender differences observed for the triggering of coronary incidents (13
, 16
). After all, the relation between alcohol consumption and coronary calcium may not be either linear or a J- or U-shaped curve. The amount of approximately 14 drinks/week may be a cutoff value where alcohol starts to exert its predominantly adverse effect.
Although coronary calcium is associated with a poorer cardiovascular prognosis, the meaning and impact of calcium on atherosclerotic plaque properties are not clear. It is still doubtful whether it may allow for identification of unstable plaques and estimation of coronary risk. If so, the measurement of coronary calcium will be a significant and useful method for cardiovascular prevention and decision-making.
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ACKNOWLEDGMENTS |
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