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See also Sandset PM. Hormone replacement therapy and risk of venous thromboembolism -still unresolved questions. This issue, pp 68-9.Grandone E, Margaglione M. New epidemiological risk factors for venous thromboembolism (VTE) after menopause. This issue, pp 70.Summary. Background: Lifetime estrogen exposure has been related to breast cancer risk, osteoporosis, and cardiovascular disease but data on venous thromboembolism (VTE) risk are limited. Methods: Data from a hospital-based casecontrol study among 608 postmenopausal women (191 with a first episode of idiopathic VTE and 417 age-matched controls) were used to determine whether estrogen exposure, as assessed by age at menopause [classified as early(£ 45 years), normal (46-54 years) and late menopause ( ‡ 55 years)] and parity, was associated with the risk of VTE. Results: After adjustment for potential confounding variables, the risk of VTE was increased with each year's delay in the menopause [odds ratio (OR) ¼ 1.06, 95% confidence interval (CI) ¼ 1.02-1.10, P < 0.0075]. When compared with women with normal menopause used as a reference, the adjusted OR for VTE was 0.59 (95% CI ¼ 0.36-0.97) and 2.53 (95% CI ¼ 1.28-4.99) for women with early menopause and late menopause, respectively (P ¼ 0.001). Adjusted OR for VTE was also higher for women with more than two children when compared with those with less than or equal to two children (1.56, 95% CI ¼ 1.03-2.34, P ¼ 0.03). The lowest risk of VTE was observed in women with early menopause and lower parity (adjusted OR ¼ 0.60, 95% CI ¼ 0.30-1.24), the highest risk was among women with late menopause who have had more than two children (adjusted OR ¼ 3.41, 95% CI ¼ 1.46-9.25). Conclusion: These results show that the longer exposure to endogenous estrogen is associated with an increased VTE risk.

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It is now well established that oxidative stress resulting from reactive oxygen species (ROS) that are generated in cardiac myocytes subjected to ischemia/reperfusion plays a causative role in the development of heart failure and may contribute to promote cell death. During the last decade, several groups have reported that, in animal models of myocardial ischemia/reperfusion, certain nutrients, including ethanol and nonethanolic components of wine, may have a specific protective effect on the myocardium, independent of the classical risk factors implicated in vascular atherosclerosis and thrombosis. Mechanisms through which the consumption of alcoholic beverages protects against ischemia-induced cardiac injury are still unknown. One major open question is whether ethanol and nonethanolic components of wine are cardioprotective, at least in part, by interfering with the myocardial prooxidant/antioxidant balance. Important concepts, such as cardiac preconditioning, are now entering the field of nutrition, and recent experimental evidence suggests that ethanol and/or nonethanolic components of wine might exert preconditioning effects in animal models of myocardial ischemia/reperfusion. There is no doubt that such an observation, if confirmed in human subjects, might open new perspectives in the prevention and treatment of ischemic coronary heart disease.

Moderate ethanol drinking (ED) and n-3 fatty acids have both been associated with low cardiac mortality. However, there are few data evaluating the interactions of ED with n-3. We recently reported that moderate ED results in increased n-3 in cardiac patients. The main aim of the present study was, through a well-controlled experimental model, to confirm that chronic ED actually results in increased n-3. Secondary aims were to examine the effects of chronic ED on cardiac mitochondria, cardiac function and experimental myocardial infarction. We studied the fatty acid profiles of plasma, cell membranes and cardiac mitochondria phospholipids in a rat model of chronic ED. In plasma and cell membranes, ED actually resulted in higher n-3 (P¼0·005). In mitochondria phospholipids of ED rats, n-3 were also increased (P, 0·05) but quite modestly. Cardiac mitochondrial function and left ventricular function were not significantly different in ED and control rats, while infarct size after 30 min ischaemia and reperfusion was smaller (P, 0·0001) in ED rats. This is the first animal study confirming interaction of alcohol drinking with n-3. We found no harmful effect of chronic ED on the heart in that model but a significant cardioprotection. Further studies are warranted to investigate the mechanisms by which moderate ED alters the metabolism of n-3 and whether n-3 are the mediators of the ED-induced cardioprotection.