The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy.

Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.

Extracorporeal membrane oxygenation for cardiogenic shock due to alcoholic cardiomyopathy: a long-term follow-up of 4 cases.

Even though alcoholism is a major health concern, alcoholic cardiomyopathy is a little-known pathology. The exact prevalence remains elusive (20-40% of dilated cardiomyopathy). However, it can lead to dilated cardiomyopathy, heart failure and refractory cardiogenic shock. The literature on cardiogenic shock in alcoholic cardiomyopathy is limited. We report 4 cases of patients with refractory cardiogenic shock due to heavy alcohol consumption, who were treated with venoarterial extracorporeal membrane oxygenation. The evolution was favourable with recovery in 3 patients and the need for heart transplantation in 1 patient. After 3-5 years, all patients are alive, 2 of 4 are sober, all of them are on cardiac follow-up and none of them have presented with a cardiac relapse.

Late ventricular structure after partial left ventriculectomy.

Nine months after partial ventriculectomy, a 53-year-old man died of progressive heart failure. His heart was examined to determine the alignment of the muscle fibers around the ventricular scar, which was 11 cm long, 1.3 cm thick and 4 cm wide. The scar reached 2 to 12 mm beyond the surgical suture line. The fibers in the middle and subendocardial layers were malaligned, resulting in convergence, compression and regional necrosis.

[Alcoholic cardiomyopathy and heart transplantation]. / Cardiomyopathie éthylique et transplantation cardiaque.

The recognition of alcoholic cardiomyopathy in patients with dilated cardiomyopathy is essential as they may regress, at least partially in a relatively short period, with abstention. The clinical history is the key to diagnosis because no other specific feature can identify the cause. Between January 1984 and July 1995, 26 candidates for cardiac transplantation with dilated cardiomyopathy and chronic alcoholism improved after withdrawal of alcohol. None of these patients was placed on the surgical waiting list. Patients with ischaemic cardiomyopathy, valvular disease or previous surgery for valvular hypertensive or congenital heart disease, documented viral myocarditis or connective tissue diseases, were excluded. The diagnostic criterion of chronic alcoholism was a total alcohol consumption of 292 kg and a duration of alcohol abuse of over 10 years. In addition to the clinical features, biological, electrocardiographic, echocardiographic and haemodynamic parameters were analysed. The mean age of the patients was 48 +/- 8 years. There were 25 men and 1 woman. The total mean alcohol consumption was 1,492 kg. The average follow-up period was 63 +/- 41 months. The interval between the onset of symptoms and abstention was 25 months. Haemodynamic improvement was observed in 25 cases. The average interval between alcoholic abstention and recovery was 11.7 months. One patient died suddenly. Improvement of symptoms, decrease of the cardiothoracic ratio and improvement of echocardiographic parameters were statistically significant. The increase in angiographic or isotopic ejection fraction and cardiac index and the decrease in mean pulmonary artery pressures were also statistically significant. These results confirmed the diagnosis of alcoholic cardiomyopathy. Therefore, patients with chronic alcohol abuse and dilated cardiomyopathy must be identified and treated for this problem and not placed on the waiting list for cardiac transplantation unless no improvement is observed after about 3 months of abstention.

The effect of chronic alcohol use on the heart before and after transplantation in an experimental model in the rat.

BACKGROUND: Alcohol has potential deleterious effects on donor heart function. This study was conducted in rats to determine whether long-term alcohol ingestion produces impaired hemodynamic performance while maintaining a normal left ventricular ejection fraction in donor hearts before transplantation and whether donor cardiac function is affected after heart transplantation. METHODS: Rats fed 30% alcohol in their drinking water for 12 weeks were compared with rats fed a normal diet. Left ventricular ejection fraction was measured by echocardiography with Simpson and single plane Dodge formulas in living sedated rats after 10 and 12 weeks of alcohol feeding. Explanted heart function was assessed before and 3 days after heterotopic heart transplantation (no immunosuppression) with a Langendorff preparation. RESULTS: Blood ethanol levels at 4 and 8 weeks were 0.08 +/- 0.04 and 0.08 +/- 0.09 gm/dl. Left ventricular ejection fraction was similar in the group fed an alcohol diet for 12 weeks when compared with the control group (65.4% +/- 1.6% vs. 66.5% +/- 2.9%, p = 0.33). Explanted alcohol-fed hearts before transplantation had significantly lower maximum and developed pressures and had a blunted response to 0.1 ml 10(-9) mol/L isoproterenol. After transplantation alcohol-fed hearts had significantly lower maximum and developed pressures and decreased maximum rates of pressure rise and pressure decline. Allografts (ACI to Lewis) exhibited decreased function in comparison with isografts (ACI to ACI). CONCLUSIONS: Alcohol feeding for 12 weeks in rats does not affect pretransplantation left ventricular ejection fraction, but it impairs explanted heart function, both before and after transplantation, resulting in a subclinical cardiomyopathy that is worsened by the presence of allograft rejection. Long-term alcohol exposure and rejection have independent, additive detrimental effects on left ventricular performance of the transplanted heart. Alcohol-exposed hearts may not be suitable donors.