More indirect effects also may play a role. For example, alcohol may increase the risk of hypertension by enhancing the activity of the sympathetic nervous system, which results in greater constriction of the blood vessels and makes the heart contract more strongly. In addition, alcohol possibly decreases the sensitivity of the body��s internal blood pressure sensors (i.e., baroreceptors), thereby CP127374 diminishing its ability to regulate blood pressure. Alcohol��s protective effects against the risk of ischemic heart disease as well as against hypertension in women is hypothesized to result from its ability to increase HDL levels and/or reduce platelet aggregation on arterial walls. Differences in the effects of alcohol in men and women may stem from differing drinking patterns, with men more likely to engage in binge drinking, even at low average levels of consumption.

These heavy-drinking occasions may lead to an increased risk of hypertension for men compared with women at similar alcohol consumption levels (Rehm et al. 2003b). Alcohol��s effect on hypertension also contributes to the risk of hemorrhagic stroke (Taylor et al. 2009), with a hypothesized dose-response effect. The mortality and morbidity from alcohol-attributable hemorrhagic stroke differ by sex (see figure 4). As with hypertension, differences in drinking pattern between men and women most likely are responsible for the differing RR functions for hemorrhagic stroke by sex. Three possible explanations have been put forth to explain the effects of drinking pattern on RR: Heavy drinkers also may have other comorbidities that may increase the probability of a fatal hemorrhagic stroke.

Alcohol consumption may worsen the disease course through biological mechanisms and by decreasing compliance with medication regimens. Alcohol��s effects on morbidity may be underestimated because of a stigmatization of heavy alcohol consumption in women, thereby potentially decreasing the probability that female heavy drinkers will be treated for stroke. Large cohort studies and meta-analyses have shown that alcohol consumption leads to an increase in the risk for conduction disorders and dysrhythmias (Samokhvalov et al. 2010b). These effects are caused by changes in the electrical activity of the heart, including direct toxic effects of alcohol on the heart (i.e., cardiotoxicity), excessive activity of the sympathetic nervous system (i.

e., Carfilzomib hyperadrenergic activity) during drinking and withdrawal, impairment of the parasympathetic nervous system (i.e., of vagal tone), and increase of intra-atrial conduction time (Balb?o et al. 2009). Alcohol interacts with the ischemic system to decrease the risk of ischemic stroke and ischemic heart disease at low levels of consumption; however, this protective effect is not observed at higher levels of consumption.