Alcoholic cardiomyopathy: Treatments, outlook, and more

However, consistent heavy drinking strains those protective processes — especially in your liver — making them less effective. Ultimately, your body can’t keep up with the damage to multiple organ systems, including your heart. The Centers for Disease Control and Prevention (CDC) defines heavy alcohol use — also known as heavy drinking — as more than eight drinks per week for women and more than 15 drinks per week alcoholic cardiomyopathy is especially dangerous because for men. One drink is equal to 14 grams of pure alcohol, which can take many different forms because some forms have a higher concentration of alcohol than others. The mainstay of management is providing support, resources including but not limited to alcoholic anonymous and encouragement for alcohol abstinence and address underlying stressors if any which requires assistance from nursing staff and pharmacy.

2 Estimation of prognosis and risk factors in ACM

The aim of this narrative review is to describe clinical characteristics of alcoholic cardiomyopathy, highlighting the areas of uncertainty. Others have demonstrated that long-term ethanol administration decreases myocardial protein expression and synthesis and accelerates protein degradation, suggesting that these alterations may represent a key pathophysiologic mechanism underlying the adverse effects of ethanol (62). Histopathologic examination of hearts from individuals with https://ecosoberhouse.com/ the diagnosis of ACM have revealed contractile protein loss, fragmentation, and disarray, supporting the concept of altered protein physiology/composition (11, 29,31). Using a mass spectrometric-based proteomic analysis, Fogle et al. examined the effects of 16 weeks of ethanol consumption on rat cardiac muscle protein expression (45). These investigators also found decreases in peroxiredoxin 5, antioxidant protein 2, and glutathione transferase 5, important anti-oxidant enzymes.

Is this condition only a chronic (long-term) problem?

Data on the amount of alcohol consumption required to cause ACM are limited and controversial. In general, you should talk to your healthcare provider if you notice changes in your symptoms over time, especially if they are starting to affect your normal life and routine. However, you should talk to your healthcare provider about symptoms that mean you should call their office because each case is different. The only way to completely prevent alcohol-induced cardiomyopathy is not to drink alcohol at all. Alcohol-induced cardiomyopathy can affect anyone who consumes too much alcohol, even those who don’t have alcohol use disorder.

Oxidative Stress and Apoptosis: Linked Mechanisms

Alterations caused by heavy alcohol intake have also been studied from the perspective of histopathology. Emmanuel Rubin analysed muscle biopsies from individuals who were previously non-drinkers and were submitted to a balanced diet with heavy alcohol intake during one month[41]. These changes, though subtle, were similar to those found by Ferrans and Hibbs in eight deceased individuals diagnosed with ACM[42,43]. On histological examination, various degrees of fibrosis, patchy areas of endocardial fibroelastosis, intramural blood clots and focal collections of swollen cells in both the epicardium and endocardium were found.

How is this condition treated, and can it be cured?

• Other treatments aim to treat the symptoms of ACM and prevent any disease complications.
• When it comes to wine, one drink is defined as a 5-ounce (148 ml) serving, which typically contains about 12% ABV.
• In summary, there appears to be a number of ways in which mitochondrial perturbations could contribute to both the development and progression of ACM.
• NIAAA defines binge drinking as a pattern of drinking alcohol that brings the blood alcohol concentration to 0.08 percent or above.
• As noted in the text, the exact amount and duration of alcohol consumption that results in ACM in human beings varies.
• The Cd36 gene encodes for proteins involved with transport of long-chain fatty acids.

Data from isolated papillary and heart muscle cell (myocyte) experiments demonstrate that acute physiologic intoxicating doses of alcohol (80 mg% to 250 mg%) can have a negative inotropic effect (Danziger et al. 1991; Guarnieri and Lakatta 1990). These effects also may involve an irregular and often very fast heart rate (arrhythmia) during which the heart’s upper chambers (atria) contract chaotically out of coordination with its lower chambers (ventricles), known as atrial fibrillation, or (rarely) sudden cardiac death. Some adverse BP-related mechanisms that may be triggered by alcohol include changes in intracellular calcium levels, baroreflex control, and heart rate and activation of other neurohormonal systems besides the RAAS, such as the sympathetic nervous system (Marchi et al. 2014). Results from another meta-analysis of 12 cohort studies found a similar dose–response relationship between alcohol consumption and HTN for males. A J-shaped relationship for females showed protective effects at or below consumption levels of 15 g/day (Taylor et al. 2009). These data highlight how gender may be an important modifier of the alcohol threshold level and can shape the alcohol benefit–risk relationship.

Long-term Effects

• Alcohol also can increase levels of co-enzymes or reducing equivalents (e.g., reduced nicotinamide adenine dinucleotide phosphate [NADPH]), which lead to increases in ROS formation and decreases in eNOS activity (Ceron et al. 2014).
• Detailed study design and findings related to investigations reporting changes in oxidative phosphorylation are summarized in Table 2.
• Alcoholic cardiomyopathy (ACM) is a heart disease that occurs due to chronic alcohol consumption.
• Elevations of the transaminases (GOT, GPT), especially a ratio of GOT/GPT higher than 2 might be indicative of alcoholic liver disease instead of liver disease from other etiologies [120, 121].
• In a national inpatient sample study, some authors have reported ACM to be most common in white males aged between 45 and 59 [2].
• The prevalance of alcoholic cardiomyopathy in addiction units is estimated around %.
• It’s important to note that alcoholic cardiomyopathy may not cause any symptoms until the disease is more advanced.

• Despite the progress in standardizing measurement of alcohol, studies still vary in how they define the different levels of drinking, such as low-risk or moderate and heavy drinking.
• Consulting with a healthcare professional can provide personalized advice and guidance.
• Mathews and Kino found a small, but significant increase in left ventricular mass in individuals consuming at least 12 oz of whisky during 6 years and 60 g of ethanol per day, respectively[22,40].

Basic studies on molecular mechanisms of myocardial damage