alcoholic cardiomyopathy

For more than 3000 years, alcoholic beverages have been consumed in multiple societies through the centuries and cultures. Pulverized antimony was used as eye shadow by Egyptian women and named al-Kol. In the 16th century Paracelsus Theophrastus Bombastus from Hohenheim used this term for distilled liquor and called it alcohol [15].

3. Ethanol-induced Heart Fibrosis

alcoholic cardiomyopathy

Although these reports were isolated, the routine use of propranolol and subsequently all β-blockers were considered relatively contraindicated in treating cocaine-induced cardiovascular emergencies. As a result, benzodiazepines have been the drug of choice in treating the cerebrovascular and subsequent systemic hyperadrenergic complications of cocaine, and nitroprusside or phentolamine being advocated for peripheral vasodilatory effects. It is now becoming apparent that treatment of cardiovascular effects of cocaine should involve a multifactorial approach to combat both central nervous system and peripheral vasospastic effects of cocaine. The risk of developing alcoholic cardiomyopathy appears to be related to both the amount and duration alcohol intake.

Clinical work-up for alcoholic cardiomyopathy

alcoholic cardiomyopathy

The guidelines typically define one drink as specific quantities for different types of alcoholic beverages. For instance, a single drink of beer is typically considered as a 12-ounce (355 ml) serving of regular beer, usually containing around 5% alcohol by volume (ABV). When it comes to wine, one drink is defined as a 5-ounce (148 ml) serving, which typically contains about 12% ABV. Distilled spirits, such as vodka, whiskey, rum, or tequila, are measured as 1.5 ounces (44 ml) per drink, with a typical ABV of around 40%. It is important to note that the size and strength of different alcoholic beverages can vary, so these definitions serve as general guidelines. It is always advisable to be mindful of individual tolerance and consume alcohol responsibly [4-6].

Is there an immediate risk of alcohol intake?

Until the second part of the 20th century, there was no scientific evidence on the direct and dose-dependent effect of ethanol on the heart as cause of ACM [6,38]. However, there is a clear personal susceptibility of this effect that creates a wide variability range and alcoholic cardiomyopathy supposes significant inter-individual differences [50,66]. In fact, ACM is considered to be the result of dosage and individual predisposition [32]. It has been said that ethanol is the “perfect drug” because of its pleasant effects but damaging long-term effect [1,6].

alcoholic cardiomyopathy

Occidental Berberi is the term used for the clinical scenario caused by thiamine deficit, a situation commonly present in chronic alcohol misuse, and was attributed as the cause of ACM [68,69]. Similarly, electrolyte (Na, K, Ca, Mg, P) deficiencies or disturbances may play a major role https://ecosoberhouse.com/ in cardiac function, and ethanol misuse may be related to them [52]. Selenium deficit (Keshan disease in China) could also induce ACM in specific areas [70]. Based on epidemiological evidence, ACM is recognized as a significant contributor to non-ischemic DCM in Western countries.

alcoholic cardiomyopathy

What can I expect if I have this condition?

ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition.

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