We were also not able to further identify the ethnic minorities included under the “other” race category. Due to its significant toxicity, studies have avoided its direct instillation, as it produces indiscriminate cell damage alcoholic cardiomyopathy symptoms even at low doses. Alternatively, studies have analysed its effect by combining ethanol with cyanamide.
Epidemiological studies
- The diagnosis of alcohol-induced cardiomyopathy in our patient relied on the absence of known causes of dilated cardiomyopathy, the identification of excessive alcohol consumption and the improvement of cardiac function after the abstention from alcohol ingestion.
- Additionally, the accepted ACM definition does not take into account a patient’s sex or body mass index (BMI).
- Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports.
- Some have also suggested that lipid peroxidation may play a role in the pathogenesis of alcoholic cardiomyopathy (10).
- 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.
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. Regarding ICD and CRT implantation, the same criteria as in DCM are used in ACM, although it is known that excessive alcohol intake is specifically linked to ventricular arrhythmia and sudden cardiac death71. 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.
Signs and symptoms
Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users. It is estimated, approximately 21-36% of all non-ischemic cardiomyopathies are attributed to alcohol. The prevalance of alcoholic cardiomyopathy in addiction units is estimated around %. Overall data with regards to alcohol induced cardiomyopathy is insuffienct and does not illustrate significant available data. The outlook for people with alcoholic cardiomyopathy varies depending on how long alcohol was abused and how much alcohol was consumed during that time.
Acute reversible left ventricular dysfunction secondary to alcohol
- 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.
- In addition, people who receive early treatment for ACM, including medication and lifestyle modifications, have a better chance of improving their heart function and overall health.
- She received aggressive volume resuscitation, and 24 h after admission, she developed severe dyspnea.
- According to several articles, even moderate alcohol use has comparable effects to abstinence.
This is in comparison to other population based studies where they estimated the rates of liver cirrhosis to be as low as 0.27% and as high as 7% in ethnic minorities.20, 21 Rate of liver disease is expectedly higher in our population as we selected specifically patients with diagnosis of alcoholic cardiomyopathy. However, this data does not differentiate between alcoholic and nonalcoholic causes of liver disease and includes non‐cirrhotic liver involvement. Symptomatic management in people with secondary heart failure to address any related consequences is also vital in managing ACM.
Alcohol and the cardiovascular system
Moreover, there is a decrease in the left ventricular mass index and ejection fraction, falling below the normal range. Diastolic dysfunction, characterized by impaired left ventricular relaxation and reduced diastolic filling capacity, serves as an early indicator of ACM. Ventricular dilatation is the first echocardiographic change seen in alcohol use disorder patients, coming before diastolic dysfunction and hypertrophy. The symptoms of left ventricular diastolic function included waking up at night with shortness of breath, irregular heartbeat, extreme fatigue and weakness, dizziness and fainting, bouts of chest pain, and swelling in the feet, ankles, and abdomen 13. According to current knowledge, prolonged and excessive alcohol consumption plays a significant role in inducing oxidative stress within the myocardium.
Organ-Specific Toxicologic Pathology
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 years23; however, no differences in systolic function were observed. Finally, only Urbano-Márquez et al24 found a clear decrease in the ejection fraction, in a cohort of 52 alcoholics, which was directly proportional to the accumulated alcohol intake throughout the patients’ lives. Ethyl alcohol has detrimental effects on myocardial metabolism; nevertheless, the pathogenetic mechanisms of alcoholic cardiomyopathy remain uncertain. Reactive oxidative metabolites generated from the biotransformation of ethanol are thought to lead to lipid peroxidation of myocytes and oxidation of protein thiols. Acetaldehyde produced in the liver from metabolism via alcohol dehydrogenase may also reach the heart and produce adverse effects.
Acknowledgments
Eventually, the heart muscle and blood vessels may stop functioning properly due to the damage and strain. Cardiomyopathies (CMs) have many etiological factors that can result in severe structural and functional dysregulation. Fortunately, there are several potentially reversible CMs that are known to improve when the root etiological factor is addressed. In this article, we discuss several of these reversible CMs, including tachycardia-induced, peripartum, inflammatory, hyperthyroidism, Takotsubo, and chronic illness–induced CMs. Our discussion also includes a review on their respective pathophysiology, as well as possible management solutions.
Basic studies on molecular mechanisms of myocardial damage
Alcoholic cardiomyopathy refers to dilated cardiomyopathy due to toxic origin with left-ventricle systolic dysfunction, dilatation of cardiac chambers, and ultimately progression to heart failure. Prior studies have investigated the impact of ethanol on changes in the activity and levels of oxidative enzymes. Catalase activity is significantly increased in postmortem heart samples acquired from people who have been diagnosed with ACM. Other studies investigated the catalase levels and activity among rats with ACM with a control group.
Prediction of recovery after abstinence in alcoholic cardiomyopathy: role of hemodynamic and morphometric parameters
- We were unable to do any subgroup analysis especially to look into whether there is increased mortality among certain population subsets such as those with hypertension and coronary artery disease.
- Disrupted bioenergetics and oxidative phosphorylation indices and a change in the ultrastructure of the mitochondria may be the cause of such dysfunctions.
- Daily alcohol consumption of 80 g per day or more for more than 5 years significantly increases the risk, however not all chronic alcohol users will develop Alcohol-induced cardiomyopathy.
- Electron microscopic studies (7,8) of biopsies from patients with alcohol-induced cardiomyopathy have shown evidence of damage to the myofibres, including separation of filaments and loss of striation.
However, several pitfalls in the pathophysiology, natural history, diagnosis and risk stratification of this disease still exist. The authors are solely responsible for the study design, conduct and analyses, and drafting and editing of the manuscript and its final contents. We conducted our analysis on discharge data from the Healthcare Cost and Utilization Project‐Nationwide Inpatient Sample (HCUP‐NIS) from 2002 through 2014. We obtained data from patients aged ≥18 years with diagnosis of “Alcoholic Cardiomyopathy.” Death was defined within the NIS as in‐hospital mortality. By using International Classification of Disease‐9th edition‐Clinical Modification (ICD‐9CM) diagnoses and diagnosis‐related groups different comorbidities were identified.