Alcoholic Cardiomyopathy: Causes, Symptoms, and Treatment Options

It was characterized by congestive heart failure, pericardial effusion, and an elevated hemoglobin concentration. As the syndrome could be attributed to the toxicity of this trace element, the additive was prohibited thereafter. For more than 3000 years, alcoholic beverages have been consumed in multiple societies through the centuries and cultures. In the 16th century Paracelsus Theophrastus Bombastus from Hohenheim used this term for distilled liquor and called it alcohol 15.

• Consistently high blood pressure and thickened heart muscle suggest hypertensive heart disease, while alcoholic cardiomyopathy typically shows a weakened heart muscle.
• Your lifestyle choices can also worsen your condition, especially when you use substances that affect your heart, lungs, and circulatory system.
• As the heart’s function deteriorates, the kidneys may become less efficient at removing excess fluid from the body, leading to weight gain.
• Genetics may play a role in determining susceptibility to alcohol-induced heart damage.
• If you see any signs of alcoholic cardiomyopathy, contact emergency medical services immediately.
• Finally, it should be noted that a large majority of studies on the long-term prognosis of ACM used the cut-off point of 80 g/d for a minimum of 5 years to consider alcohol as the cause of DCM.

Mental Health Treatment at Five Palms

Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence. The signs and symptoms of alcoholic cardiomyopathy (ACM) can vary depending on the severity of the condition.6 In the early stages, people with ACM may not experience any symptoms. However, as the condition progresses, they may experience symptoms such as fatigue, shortness of breath, palpitations, and swelling of the legs and ankles.6 They may also experience chest pain, dizziness, and fainting. In some cases, ACM can cause arrhythmias or irregular heartbeats, which can be life-threatening.

3. Ethanol-induced Heart Fibrosis

Conversely, those whose consumption remained in excess of https://ecosoberhouse.com/ 80 g/d showed an average decline of 3.8% in their ejection fraction. 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). Unfortunately Lazarević et al23, as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms.

Pathological Aspects of ACM

It took almost 60 years before further attention was paid to the complex interaction between the heart and the peripheral vasculature in various cross-sectional and prospective epidemiologic studies, which have empirically confirmed this early report. One is aware today that alcohol may cause an acute but transient vasodilation, which may lead to an initial fall in blood pressure probably mediated by the atrial natriuretic peptide (ANP) 46. But also short- and long-term pressor effects mediated by the renin–aldosterone system and plasma vasopressin have been described 47, 48.

Some cardiomyokines, such as FGF21, may regulate this process of alcohol-induced cardiac fibrosis 119. Apoptosis may be induced by ethanol through mitochondrial membrane permeabilization and the release of pro-apoptotic factors (cytochrome c) from the mitochondrial inter-membrane space to the cytosol. Chronic ethanol exposure, in combination with other stress signals, provides a trigger for cardiac apoptosis through activation of the drug addiction treatment mitochondrial permeability transition pore by physiological calcium oscillations 111. Mortality in ACM is related to the progression of heart failure and malignant arrhythmias 58,65.

Seek Treatment At Vertava Health

However, there is a clear personal susceptibility of this effect that creates a wide variability range and supposes significant inter-individual differences 50,66. In fact, ACM is considered to be the result of dosage and individual predisposition 32. Another curious hypothesis from Germany suspected that some ethanol additives, such as anti-foam beer products with arsenic or cobalt content, produced cardiac toxicity and development of ACM 71. Therefore, it is evident that ACM may develop with normal serum thiamine and electrolyte levels 38,66.

• To diagnose alcoholic cardiomyopathy, your doctor will conduct a physical exam and ask about your medical history.
• Although the severity of histological alterations on endomyocardial biopsy correlates with the degree of heart failure in one of our studies, biopsy is not in common use for prognostic purposes 117.
• However, it has been evidenced that ACM may develop in the absence of protein or caloric malnutrition 38.
• Growth factors and cardiomyokines are relevant molecules that may modify this process.

How to Know if You Might Have Hypertensive Heart Disease vs Alcoholic Cardiomyopathy

Alcoholic cardiomyopathy treatment may include medications, surgery, or a combination. In the course of ethanol-induced cardiac damage, one of the more relevant findings is that ethanol exerts its deleterious effects on cardiac myocytes at multiples sites (membrane, receptors, mitochondria, ribosomes, sarcolemma, DNA, or cytoskeleton) 18,19,98 (Table 1). Before recognizing that ethanol itself is the etiological factor of ACM, different theories and hypotheses emerged 1,66.

A history of high blood pressure is common in hypertensive heart disease but not in alcoholic cardiomyopathy. However, ischemic heart disease often causes chest pain during physical activity or stress (angina), which is less common in alcoholic cardiomyopathy. Ischemic heart disease is also linked to risk factors like high cholesterol, high blood pressure, smoking, and diabetes, rather than alcohol use. Experimental studies analysing the depressive properties of alcohol on the cardiac muscle invariably use similar approaches31-39. Accordingly, a given amount of alcohol is administered to volunteers or alcoholics, followed by the measurement of a number of haemodynamic parameters and, in some cases, echocardiographic parameters. Generally, following alcohol intake, healthy, non-drinking individuals showed alcoholic cardiomyopathy is especially dangerous because an increase in cardiac output due to a decline in peripheral arterial resistance and an increase in cardiac frequency31.

• Many changes can be observed including premature atrial or ventricular contractions, supraventricular tachycardias, atrioventricular blocks,  bundle branch blocks, QT prolongation, non-specific ST and T wave changes and abnormal Q waves.
• By being more susceptible to the damaging effects of alcohol, you’re more likely to develop alcoholic cardiomyopathy.
• Dependence is characterized by uncontrollable drinking patterns and a strong urge to drink alcohol.

Echocardiographic and haemodynamic studies in alcoholics

At present, ACM is defined as a dilated cardiomyopathy of toxic origin with low left-ventricle ejection fraction, chamber dilatation, and progression to congestive heart failure 18,52,53. Excessive EtOH consumption is one of the main causes of non-ischemic dilated cardiomyopathy (CMP), representing around one-third of cases 30. Alcoholic cardiomyopathy (ACM) is a disease in which the long-term consumption of alcohol leads to heart failure.1 ACM is a type of dilated cardiomyopathy.

Pharmacological treatment for heart failure

A second set of studies that are quoted when addressing this topic are those conducted in individuals who started an alcohol withdrawal program21-24. 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. 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.