Mortality from Alcoholic Cardiomyopathy: Exploring the Gap between Estimated and Civil Registry Data PMC

Prompt treatment can help prevent the disease from getting worse and developing into a more serious condition, such as congestive heart failure (CHF). Others have also found a significant decrease in intramitochondrial isocitrate dehydrogenase activity (20,24). Others have found an increased level of fatty acid ethyl esters in the alcoholic heart, which can attach to the mitochondria and disrupt mitochondria respiratory function (32). As pointed out before, the current accepted definition of ACM probably underestimates the number of women affected by the disease.

The denominator for calculating HF garbage code and ACM proportions was ‘all CVD’ and was calculated from the sum of all registered deaths from CVD and CVD garbage codes (for definition, see Appendix Table A1). Prior to building regression models, the data structure of the dependent variable (% of ACM deaths) was examined using scatter plots and bivariate correlations with % of HF garbage code deaths and alcohol exposure (for results see Appendix Table A2). 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.

What are the symptoms of alcoholic cardiomyopathy?

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. Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure. Symptoms include gradual onset worsening shortness of breath, orthopnea/paroxysmal nocturnal dyspnea.

All-cause mortality was assessed using Kaplan–Meier survival curves, and the risk factors were assessed using Cox regression. A receiver operating characteristic (ROC) curve analysis was performed to optimize the cutoff point for discriminating between the 2 risk groups. During this period, 10 women and 26 men fulfilled criteria for alcoholic cardiomyopathy. Considering the complete group of alcoholics who attended in this period, the prevalence of alcoholic cardiomyopathy was slightly higher in women (0.43%) than in men (0.25%). However, in patients admitted to the hospital, the prevalence of alcoholic cardiomyopathy was 0.08% in women and 0.19% in men. This latter result may be explained by the significantly lower NYHA functional class in alcoholic women than men.

Alcoholic Cardiomyopathy: Signs, Symptoms, And Treatment

The underlying mechanisms might include the impaired β‑receptor and calcium signaling, altered cardiomyocyte membrane physiology, elevated sympathetic nervous tone and increased activity of vasodilatory pathways [44]. In pathophysiological terms, heart failure in liver cirrhosis belongs to the hyperdynamic cardiomyopathies. The subject with excessive alcohol consumption, after more than 10 years of high ethanol consumption, usually develops subclinical heart functional changes before symptom appearance or signs of alcoholic cardiomyopathy heart failure [55,56]. These may be detected with echosonography in around one-third of high-dose chronic consumers with preliminary evidence of subclinical left-ventricle (LV) diastolic dysfunction before progression to subclinical LV systolic dysfunction [57]. Therefore, complete abstinence from ethanol is the most useful measure to control the natural course of ACM [51,56,135]. In fact, patients with ACM who abstain from alcohol have a better long-term prognosis than subjects with idiopathic dilated CMP [54].

The natural course of ACM is mainly related to the degree of persistence in alcohol consumption and the individual biological adaptive response [2,20,41,56,81]. Ethanol abstinence allows for recovery in the majority of cases, including in those with previous severe depression of LV EF [81,88,135]. Khanna et al. demonstrated that inducible nitric oxide synthase (iNOS) is increased in cardiomyocytes isolated from rats exposed to 1 month of ethanol (13 g/day, Lieber-DeCarli diet) (42). Increased cardiac tissue iNOS levels can lead to the formation of superoxide and peroxynitrite (16). Ethanol-fed animals had reduced systolic contractility and responses to adrenergic stimuli (isoproterenol) compared to control animals (42).

Treatment / Management

The risk of atrial and ventricular dysrhythmias and sudden cardiac death are also increased in this population already prone to these adverse events [36, 37]. Consequently, alcohol consumption should be avoided in all patients with substantial heart failure and in those whose cardiomyopathy is suspected to be primarily from alcohol regardless of severity. In ACM, it is relevant to consider the treatment of the other alcohol-induced systemic damage, such as liver cirrhosis, malnutrition, and vitamin and electrolyte disturbances [2,11,52]. 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.

Model results of random effects Poisson regressions are presented in Appendix Table A4. Data fit of regression models was measured in the correlation between observed and fitted data, which was satisfactory (greater than 0.7) in the young- and middle-age strata and poorer in the oldest age group (correlation below 0.5). Further, the variation in the dependent variable (% of ACM deaths) was lowest in the oldest age group, most pronounced among females.

Risk Factor Management and Lifestyle Modification in Heart Failure

For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence. 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. In this respect, a higher prevalence of excessive alcohol consumption has been reported among individuals diagnosed with DCM than in the general population[8].

• On physical examination, patients present with non-specific signs of congestive heart failure such as anorexia, generalized cachexia, muscular atrophy, weakness, peripheral edema, third spacing, hepatomegaly, and jugular venous distention.
• This is not surprising because mitochondria are a major target for free-radical injury; however, dysfunctional mitochondria are not only less bioenenergetically efficient, they can also generate increased amounts of ROS and are more likely to initiated apoptosis (55).
• As noted in text the exact amount and duration of alcohol consumption that results in ACM in human beings is variable.
• 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.
• As alcohol-attributable fractions are stratified by age groups, the decline in exposure in the elderly population can be reflected in lower alcohol-attributable fractions in these age groups.

Those who drink heavily may experience substantial increases in their blood pressure. Alcohol consumption may also lead to deficiencies in magnesium, potassium, phosphorus, and thiamine, which may further exacerbate existing dysfunction. Alcohol can also worsen hyperlipidemia, primarily by elevating the triglyceride levels, although it can also increase both the total cholesterol and low-density lipoprotein concentration [35]. In smaller quantities (less than 1–2 ounces a day), the high-density lipoprotein levels typically increase, thus alcohol may exert a slightly favorable effect. Overall, the risks of continued alcohol consumption outweigh this small benefit of this lipid improvement.

More research is required using more contemporary measures of mitochondrial function as well as determining changes in mitochondrial DNA. A second set of studies that are quoted when addressing this topic are those conducted in individuals who started an alcohol withdrawal program[21-24]. In these studies, the authors estimated the amount and chronicity of alcohol intake and subsequently related the figures to a number of echocardiographic measurements and parameters. Although all of the studies reported an increase in left ventricular mass and volume, it cannot generally be stated that they provided the alcohol consumption dosage required to cause ACM. Despite the key clinical importance of alcohol as a cause of DCM, relatively few studies have investigated the effects of alcohol on the heart and the clinical characteristics of DCM caused by excessive alcohol consumption (known as alcoholic cardiomyopathy).

• Unfortunately, cause-specific results of the redistribution models are not available, thus, it remains unknown how many of the estimated ACM deaths have been redistributed from which garbage code.
• Alcoholic cardiomyopathy (ACM) is a cardiac disease caused by chronic alcohol consumption.
• In particular, mitochondrial DNA is highly susceptible to oxidative stress because of the close proximity to ROS generation and lack of protective histones and DNA repair mechanisms compared to nuclear DNA (55).
• A descriptive summary of the mortality data compiled for this study can be found in Table 1.
• Once free from alcohol, substance abuse treatment and medical treatments for alcoholic cardiomyopathy can begin.