25 de febrero de 2021 Por [email protected] Inactivo

The alcohol-induced cardiomyopathy: A cardiovascular magnetic resonance characterization

alcoholic cardiomyopathy decreased ast

However, results from tissue assays have been shown to be potentially helpful in distinguishing AC from other forms of DC. Physical examination findings in alcoholic cardiomyopathy (AC) are not unique compared with findings in dilated cardiomyopathy from other causes. Elevated systemic blood pressure may reflect excessive intake of alcohol, but not AC per se. Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption.

alcoholic cardiomyopathy decreased ast

5. Sarcomere Damage and Dysfunction in ACM

List of the 15 articles reviewed in this study, indicating the study authors, objectives, design, sample size, patient characteristics, experimental procedures, outcome measures, and main findings. Data suggests patients with successful quitting of alcohol have improved overall outcomes with a reduced number of inpatient admissions and improvement in diameter size on echocardiogram. Certain microscopic features may suggest damage secondary to alcohol causing cardiomyopathy. Commonly seen cellular structural alterations include changes in the mitochondrial reticulum, cluster formation of mitochondria and disappearance of inter-mitochondrial junctions.

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In the first of these studies, Fauchier et al11 studied 50 patients with ACM and 84 patients with DCM between 1986 and 1997. Although up to 81% of ACM patients received an ACEI, none received beta-blockers and the use of spironolactone was not specified, although it was probably quite low. Also, current common cardiac therapies such as ICD and CRT devices were not used because of the period when the study was conducted. After a follow-up period of 47 mo, a significantly higher survival rate was observed among patients with DCM compared to patients with ACM. In spite of the high prevalence of excessive alcohol consumption and of its consideration as one of the main causes of DCM, only a small number of studies have analysed the long-term natural history of ACM. Unfortunately, all the available reports were completed at a time when a majority of the current heart failure therapies were not available (Table 1).

6. The Effect of Low-dose Ethanol on ACM

alcoholic cardiomyopathy decreased ast

Comorbidities such as depression are often overlooked and many of these comorbidities could be potentially modifiable risk factors to help curb subsequent cardiovascular sequelae as a result of AC. Further studies are needed to address this subset of the heart failure population and validate the results. The uptrend for admissions among Caucasian patients, increased from approximately 40% to near 60% between 2002 and 2014. Both African American and Hispanic patients also saw slight uptrend in the proportion of patients admitted, but the absolute percent alcoholic cardiomyopathy symptoms increase by 2014 was much smaller in comparison.

  • We conducted our analysis on discharge data from the Healthcare Cost and Utilization Project‐Nationwide Inpatient Sample (HCUP‐NIS) from 2002 through 2014.
  • As it is not uncommon in ACM for patients to experience a significant recovery of systolic function, it is particularly challenging in this disease to decide the most appropriate time to implant an ICD and whether it is necessary to replace a previously implanted device.
  • The postulated mechanism includes mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis.
  • This was interpreted by the authors as suggesting that acetaldehyde plays a key role in the cardiac dysfunction seen after alcohol intake.
  • Various studies have shown that alcohol exerts a negative inotropic effect on the myocardium.

An echocardiogram performed within 24 h of admission and reviewed by two independent echocardiographers demonstrated severe global left ventricular systolic dysfunction, with an ejection fraction of 20% by modified Simpson’s biplane method. The end-systolic dimension was 4.1 cm and the end-diastolic dimension was 5.0 cm (Figure 1). It is estimated, approximately 21-36% of all non-ischemic cardiomyopathies are attributed to alcohol. Overall data with regards to alcohol induced cardiomyopathy is insuffienct and does not illustrate significant available data. Alcoholic cardiomyopathy is most common in men between the ages of 35 and 50, but the condition can affect women as well.

alcoholic cardiomyopathy decreased ast