Furthermore, for this review, certainty assessment was conducted by assessing the risk of bias, imprecision, inconsistency, and indirectness of the presented evidence. Through a thematic synthesis, we identified common trends, knowledge gaps, and emerging research areas related to ACM. To assess the quality and validity of the included studies, we performed a critical appraisal using appropriate tools such as the Newcastle-Ottawa Scale for observational studies or the Cochrane Risk of Bias tool for clinical trials. This assessment allowed us to evaluate the methodological rigor of each study and determine its overall quality and potential impact on the literature review. Finally, we analyzed and presented the synthesized literature, along with relevant findings and conclusions from the included studies, in a coherent manner. We identified main themes and sub-themes to provide a comprehensive overview of the current state of knowledge regarding ACM.
Diagnosis
Among patients who continued drinking heavily, transplant-free survival was significantly worse alcohol cardiomyopathy symptoms than in non-drinkers (27% vs 45%). The first paper to assess the natural history and long-term prognosis of ACM was published by McDonald et al69 in 1971. He recruited 48 patients admitted to hospital with cardiomegaly without a clear aetiology and severe alcoholism. The only factor to predict a poor outcome was the duration of symptoms before admission. The blood flow through the heart is slower than normal, especially when the heart is very enlarged (dilated).
Acknowledgments
In addition, the AHA advises against starting to drink alcohol solely for potential health benefits, as the risks can outweigh the advantages. It is crucial to exercise caution and be aware of individual tolerance and personal health circumstances when making decisions about alcohol consumption. Consulting with a healthcare professional can provide personalized advice and guidance. Furthermore, they specified the definition of “one drink” offer clarity when it comes to alcohol consumption.
- Excessive intake of alcohol may result in increased systemic blood pressure in a dose-response relationship, and this may contribute to chronic myocardial dysfunction.
- To treat the alcohol problem, a combined approach comprising pharmacologic and psychosocial therapy involving self-help groups or Alcoholics Anonymous is essential.
- A 2023 article notes that ACM carries a more positive outlook than ischemic cardiomyopathy, which refers to heart damage that typically occurs due to CAD.
- In addition, ethanol induces mitochondrial-dependent apoptosis pathways with Bax and caspase activation 101.
- In a nonhuman primate model (cynomolgus and rhesus monkeys) following 12 months of alcohol consumption (3.3 ± 0.2 g/kg alcohol/day), Cheng et al. found marked increases in plasma 8-isoprostane levels in animals consuming alcohol (124.8 ± 11 pg/ml) compared to controls (28 ± 5.1 pg/ml) (46).
- Illustrations of a typical heart, as shown on the left, and a heart with hypertrophic cardiomyopathy.
4. The dose-Related Effect of Ethanol and Beverage Types on the Heart
Structurally, hypertrophy of myocytes is seen in the early stages to avoid contractile depression 52,107,125. Myocytolysis progressively develops, disturbing the sarcomere contractile system. The heart output is progressively lower in a dose-dependent relationship with the lifetime accumulated total dose of alcohol consumed 38. Several growth factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage 119,133.
- Ethanol-induced changes may be related to oxidative or nonoxidative pathways of ethanol metabolism.
- It is important to note that, unlike other studies with more discrete alcohol consumption categories, alcohol use was nonspecifically defined in INTERHEART as the consumption of at least 1 alcoholic beverage within the previous 12 months (Leong et al. 2014).
- In pathophysiological terms, heart failure in liver cirrhosis belongs to the hyperdynamic cardiomyopathies.
- These changes, though subtle, were similar to those found by Ferrans and Hibbs in eight deceased individuals diagnosed with ACM42,43.
Data Availability
As noted in text the exact amount and duration of alcohol consumption that results in ACM in human beings is variable. The exact sequence for the development of ACM remains incompletely understood, data from animal models and human beings with a history of long-terms suggest oxidative stress maybe an early and initiating mechanism. Many cellular events, such as intrinsic myocyte dysfunction, which is characterized by changes in calcium homeostasis and regulation and decreased myofilament sensitivity, can come about due to oxidative stress.
