National trends in hospitalizations and outcomes in patients with alcoholic cardiomyopathy

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symptoms of alcoholic cardiomyopathy

Alcoholic cardiomyopathy is most common in men between the ages of 35 and 50, but the condition can affect women as well. People with alcoholic cardiomyopathy often have a history of heavy, long-term drinking, usually between five and 15 years. Heavy drinking is alcohol consumption that exceeds the recommended daily limits. While the overall admissions among patients with AC decreased over time, the proportion of patients with high‐risk characteristics such as smoking, depression, and drug abuse increased.

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Conversely, those whose consumption remained in excess of 80 g/d showed an alcoholic cardiomyopathy symptoms average decline of 3.8% in their ejection fraction. Ethanol-induced changes may be related to oxidative or non-oxidative pathways of ethanol metabolism. More than one mechanism may be activated that lead to the multitude of ethanol-induced changes in cellular proteins and cell function. As reviewed in text, data from pharmacologic and transgeneic approaches, have revealed an important role for oxidative stress and the hormone, angiotensin II.

  • 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).
  • They demonstrated a much higher catalase activity among rats suffering from ACM.
  • Within the month before presentation, she had increased her alcohol intake by drinking a large glass of 70% ethanol per day.
  • It is characterized by ventricular dilation and impairment in cardiac function.
  • Notably, in patients with a history of chronic alcohol consumption complicated by significant myocardial dysfunction and chronic malnutrition, re-feeding syndrome may increase the cardiac dysfunction.

4. Ethanol Disruption of Transients and SR Activation

symptoms of alcoholic cardiomyopathy

The latest two papers to be published, unlike previous papers, reported worse outcomes for ACM patients compared to DCM patients. 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.

Heartache in a Bottle: Understanding Alcoholic Cardiomyopathy

However, during the time that these haemodynamic changes appeared, some researchers identified a possible decrease in the ejection fraction and other parameters related to systolic function32-39. This was questioned by other authors, who pointed out that these conclusions could not be drawn, as alcohol itself also induces changes in the pre-load and after-load conditions, which influence cardiac contractility35. However, in this context, experimental in vitro studies using cardiomyocytes have shown that alcohol depresses the contractile capacity of the myocardium, regardless of the sympathetic tone and the haemodynamic conditions36.

symptoms of alcoholic cardiomyopathy

Demakis et al70 in 1974 divided a cohort of 57 ACM patients according to the evolution of their symptoms during follow-up. The sub-group of patients in whom symptoms improved was made up of a larger proportion of non-drinkers (73%), compared to 25% in the group who did not improve, or 17% in the group whose condition worsened. However, a possible confusion factor was identified because the group with clinical improvement also exhibited a shorter evolution of the symptoms and the disease. The suspicion that there may be an individual susceptibility to this disease is underscored by the finding that only a small group of alcoholics develop ACM, and that a proportional relationship between myocardial damage and alcohol intake has not been proven. Epidemiological studies analysing the relationship between excessive alcohol consumption and the development of DCM have found the existence of a reciprocal link between both disorders. The existence of a direct causal link between excessive alcohol consumption and the development of DCM is a controversial issue.

  • Thus, Nicolás et al73 studied the evolution of the ejection fraction in 55 patients with ACM according to their degree of withdrawal.
  • They typically require fewer hospitalizations and show improved heart function on ECG readings.
  • In the interim it seems appropriate to continue discouraging any alcohol consumption in these patients, as it would be difficult for them to maintain a limited alcohol intake considering their history of alcohol dependence and abuse.
  • Both African American and Hispanic patients also saw slight uptrend in the proportion of patients admitted, but the absolute percent increase by 2014 was much smaller in comparison.
  • In contrast, an enlarged heart was found in only 1 of 25 subjects with moderate consumption (4%), in 6 of 105 very mild consumers (5.7%), and in 4.5% of non-drinking individuals.

Ways to stay healthy

Since cardiac myocytes are excitable cells, and ethanol may easily damage this excitation–contraction mechanism, disruption of this coupling mechanism is involved in the ACM pathogenic process 19,58. Ethanol may produce the modification of sarcolemmal membrane L-type Ca2+ channels, leading to a decrease in transmembrane electrically induced Ca2+ transients 85,103,127. One of the most relevant targets of ethanol in the membrane is the disruption of membrane receptor composition and activities 86. The ryanodine L-type Ca2+ receptor at the sarcoplasmic reticulum (SR) is also significantly affected by ethanol in a dose-dependent manner 86,102. This causes a decrease in sarcolemmal contraction and also disturbance in other intercellular organelles dependent of i.c.

  • Others have also found a significant decrease in intramitochondrial isocitrate dehydrogenase activity (20,24).
  • It is always advisable to be mindful of individual tolerance and consume alcohol responsibly 4-6.
  • Congestive symptoms, such as the expression of right ventricular failure, with peripheral edema or anasarca, are characteristic of advanced cases of ACM 42,56.
  • She received aggressive volume resuscitation, and 24 h after admission, she developed severe dyspnea.

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. The guidelines typically define one drink as specific quantities for different types of alcoholic beverages.

The final damage is an equilibrium between the intensity of damaging effects and the possibility of defense, plasticity, regeneration, and adaptation for every specific organ 29,30,31. Thus, alcohol-dilated cardiomyopathy (ACM) is the result of dosage and individual predisposition 32. The preponderance of data suggests that drinking one to two drinks in men and one drink in women will benefit the cardiovascular system over time. Moderate drinking below that threshold might even reduce the incidence of coronary artery disease, diabetes, and heart failure. The pathologic and histologic findings of alcoholic cardiomyopathy (AC) are essentially indistinguishable from those of other forms of dilated cardiomyopathy (DC). Findings from gross examination include an enlarged heart with 4-chamber dilatation and overall increased cardiac mass.

AMOUNT OF ALCOHOL REQUIRED TO PRODUCE ACM

symptoms of alcoholic cardiomyopathy

This fact has been assessed with echocardiographic monitoring in women consuming high doses of ethanol both in the subclinical period of disease 46 as well as in the clinical period when congestive heart failure appears 95. At the experimental level, some gender differences also are evident in functional proteomic analysis, with sex-dependent differences in structural and energy-producing myocardial proteins in a rat model of alcoholic cardiomyopathy 96. The biological reason for this gender difference is based on different ethanol absorption rates, distribution pattern, and metabolism in women compared to men 52.

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