Abstract

The habitual mild intake of alcohol (510 g/day) and the incidence of coronary artery disease are known to be inversely related (CAD). This link includes many physiologically plausible mechanisms, including alcohol's amount of the drug effects on HDL cholesterol, plasma fibrinogen, and platelet aggregation. However, such a preventive impact against atheroma must be weighed against known negative regulation of blood pressure and triglycerides, as well as the potential negative consequences of episodic or binge drinking on a variety of other cardio -vascular final and risk factors. An alcoholic binge may worsen both silent myocardial ischaemia and angina in those who already have CAD. When people go through withdrawal after binge drinking, they experience a lot of symptoms. Blood operating pressure, together with increased platelet activation and changes in the balance of fibrinolytic factors, may explain the observed link between episodic excessive drinking and ischemic stroke. This has been observed in young men in particular, and it extends to an increase in both subarachnoid and intracerebral haemorrhage following binge drinking. Acute elevations in hypertension have been seen in males who drink mostly on weekends, compared to longer-term pressure effects in habitual daily drinkers, according to intervention studies in men. However, we have not been able to replicate the findings of unfavorable effects of binge drinking on the lipid profile that were reported in both animal and human research. Binge drinking may produce cerebrovascular spasms as well as ventricular and supraventricular arrhythmias, including atrial fibrillation. Alcohol-induced arrhythmia is thought to be the cause of alcohol-related sudden coronary mortality in those who already have CAD. As a result, future research into potential protective effects of alcohol against CAD must carefully examine the implications of drinking patterns for the connection. Co-timing of drinking with meals, cigarette smoking, and illegal drug use all have modifying effects that must be examined. Without this crucial knowledge, public health recommendations on alcohol and coronary artery disease would be restricted in breadth and possibly in effective.

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