Data derived from systematic reviews and meta-analyses suggest that alcohol-dose and CV-health relationships differ for various CV conditions. For example, certain levels of alcohol consumption that lower risk for CHD may increase it for other CV conditions, such as stroke. In addition, data from studies using new research methods, including Mendelian randomization, suggest that the relationship between low-to-moderate alcohol consumption and cardioprotection merits more critical appraisal (Holmes et al. 2014). In various biologic systems, oxidative stress can be measured or inferred by several biologic indexes. Also, low to moderate daily alcohol intake was proved to be a predictor of better prognosis for both ischemic cardiomyopathy and heart failure regardless of the presence of coronary disease[1,2].

sharing your story in recovery

If you have the condition, your health care provider might recommend that your family members be checked. Alcohol use is an important cause for non-ischemic cardiomyopathy and accounts for 10% of all cases of dilated cardiomyopathies. Electrolyte abnormalities, including hypokalemia, hypomagnesemia, and hypophosphatemia, should be corrected promptly because of the risk of arrhythmia and sudden death. Chest radiographs usually show evidence of cardiac enlargement, pulmonary congestion, and pleural effusions.

Nutritional causes of “alcoholic” cardiomyopathy

For example, a slight increase in the pre-ejection period/left ventricular ejection time ratio (PEP/LVET) was found by some authors, suggesting a sub-clinical impairment of systolic function[21,33]. 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]. More recently, Lazarevic found a modest increase in end-systolic and diastolic left ventricular volumes and a subsequent thickening of the posterior wall in a cohort of alcoholics consuming at least 80 g during 5 years[23]; however, no differences in systolic function were observed. Finally, only Urbano-Márquez et al[24] found a clear decrease in the ejection fraction, in a cohort of 52 alcoholics, which was directly proportional to the accumulated alcohol intake throughout the patients’ lives. Askanas et al[21] found a significant increase in the myocardial mass and of the pre-ejection periods in drinkers of over 12 oz of whisky (approximately 120 g of alcohol) compared to a control group of non-drinkers.

Markers for chronic alcohol consumption rely on liver enzymes such as gamma-glutamyltransferase (GGT) [119], glutamic oxalacetic transaminase (GOT), and glutamic pyruvic transaminase (GPT). 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]. An excellent marker is carbohydrate deficient transferrin (CDT), which best detects chronic alcohol consumption alone [122, 123] or in combination with the other markers such as GGT [8, 124]. Markers such as ethyl sulphate, phosphatidyl ethanol, and fatty acid ethyl esters are not routinely done. In 1887, Maguire reported on 2 patients with severe alcohol consumption who benefitted from abstinence.

What are the symptoms?

In all three ethanol groups, compared to control groups there was a significant increase in heart weight-to-body weight ratios. In terms of cardiac function and structure, significant decreases in fractional shortening and ejection fraction were found in all ethanol groups, but no other changes were found in other echocardiography-derived parameters between the alcohol and control groups. Intra-myocardial lipid accumulation, which was direct contact with the mitochondria, was found in all ethanol-fed groups and was significantly correlated with increased myocardial triglyceride content. LCFA uptake was evaluated in isolated cardiomyocytes obtained from ethanol-fed rats and was increased in a dose-dependent manner (i.e., greatest in 18% ethanol group) (33). Among the LCFA transport genes examined in all ethanol groups, increases were found in Cd36 and Scd-1 expression. The Cd36 gene encodes for proteins involved with transport of long-chain fatty acids.

However, certain symptoms may start to improve even sooner, depending on treatments and the severity of your case. In more severe or complicated cases, especially ones involving surgery, some symptoms may not improve for even longer. Overall, your healthcare provider is the best source of information and answers when it comes to your recovery.

Cardiac cirrhosis or cirrhotic cardiomyopathy

Zhang et al. found significant increases in myocardial protein carbonyl and superoxide levels in mice fed an ethanol (4% v/v) diet for 6 weeks (22). These oxidative stress biomarkers corresponded to myocardial fibrosis development and decreases in fractional shortening and cardiac output. Interestingly, these changes were prevented by the co-administration of the cytochrome P450 2E1 (CYP2E1) inhibitor, diallyl sulfate (100 mg/kg/d). Data from Jing et al., also support a role for CYP2E1 activation and changes in oxidative stress markers, such as superoxide dismutase, glutathione peroxidase and malondialdehyde protein levels (30). These investigators found that cardiac microsomal CYP2E1 activity was increased and corresponded to decreased superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde levels in dogs that received alcohol (22%) in their water once per day for 6 months (30).

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