A 1- and 4-year follow-up study of 55 men with alcoholism showed that abstinence and controlled drinking of up to 60 g/day (4 drinks) resulted in comparable improvement in left ventricular (LV) ejection fraction. Ten patients who continued to alcoholic cardiomyopathy symptoms drink higher amounts of alcohol all died during the follow-up period. Acetaldehyde is a potent oxidant and, as such, increases oxidative stress, leading to the formation of oxygen radicals, with subsequent endothelial and tissue dysfunction.
Health & Wellness
- Experts do not know what quantity of alcohol a person needs to consume to develop ACM.
- Pharmacological restoration of autophagic reflux by inhibition of soluble epoxide hydrolase has been described to ameliorate chronic ethanol-induced cardiac fibrosis in an in vivo swine model [151].
- Consulting with a healthcare professional can provide personalized advice and guidance.
- Since ACM is related to frequent perioperative events and high postoperative morbidity [139], detection and treatment of ACM is compulsory to avoid anesthetic and surgical complications [140].
- However, no differences were found in these parameters between the sub-group of individuals who had been drinking for 5 to 14 years and the sub-group of individuals who had a drinking history of over 15 years.
- They also have not established how long a person would need to consume alcohol before developing ACM.
Others have examined the potential effects of micronutrient deficiencies (such as zinc) on ethanol-induced changes in the heart. Wang et al. found evidence of ethanol-induced changes in mitochondrial structure that were more pronounced in a metallothionein knock-out mouse model compared to wild-type mouse (80). Metallothionein binds zinc within the cell and is important for overall zinc homeostasis. In that study, zinc supplementation suppressed some of the ethanol-induced changes in both the metallothionein knock-out mouse model and wild-type; however, ethanol-induced mitochondrial swelling and disorganization remained in both mouse groups. A summary of some of the potential cellular changes related to ethanol consumption are shown in Figure 1.
- Assessing differences between various forms of alcoholic beverages it should be noted that resveratrol leads in vitro to platelet inhibition in a dose-dependent manner [100] and has shown effects on all-cause mortality in a community-based study [101].
- It was suspected that malnutrition, frequently related to chronic alcohol misuse, was the origin of ACM [6,67].
6. Cardiac Hypertrophy and Remodeling in ACM
Other findings may include cool extremities with decreased pulses and generalized cachexia, muscle atrophy, and weakness due to chronic heart failure and/or the direct effect of chronic alcohol consumption. During the first half of the 20th century, the concept of beriberi heart disease (ie, thiamine deficiency) was present throughout the medical literature, and the idea that alcohol had any direct effect on the myocardium was doubted. Epidemics of heart failure in persons who had consumed beer contaminated with arsenic in the 1900s and cobalt in the 1960s also obscured the observation that alcohol could exhibit a direct toxic effect. In the 1950s, evidence began to emerge that supported the idea of a direct toxic myocardial effect of alcohol, and research during the last 35 years has been particularly productive in characterizing the disease entity of alcoholic cardiomyopathy (AC). Diastolic dysfunction is the earliest sign of ACM and is usually seen in approximately 30% of patients with a history of chronic alcohol abuse with no evidence of systolic dysfunction nor left ventricle hypertrophy.
- In fact, both molecules are directly cardiotoxic, decreasing structural protein synthesis and heart contractility and increasing oxidative and metabolic damage, leading to autophagy [20,75].
- Among the many ethanol and heart studies, mitochondrial dysfunction or evidence of impaired bioenergetics has been a common finding.
- 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).
- Moreover, alcohol may reduce the levels of transport proteins and diminish antioxidant activity by decreasing the plasma concentration of antioxidant enzymes.
Acknowledgments
In addition, ethanol is an immunosuppressive drug that is pro-inflammatory and pro-oncogenic [14,15,16,17]. Ethyl alcohol, also known as “ethanol” or usually just as “alcohol”, is the most consumed drug in human history [1]. At present, its consumption rates are still very high, with a widespread worldwide distribution, in a global uncontrolled scenario with easy access [2].
To assess the quality and validity of the included studies, we performed a critical appraisal using appropriate tools such as the Newcastle-Ottawa Scale for observational studies or the Cochrane Risk of Bias tool for clinical trials. This assessment allowed us to evaluate the methodological rigor of each study and determine its overall quality and potential impact on the literature review. Finally, we analyzed and presented the synthesized literature, along with relevant https://ecosoberhouse.com/ findings and conclusions from the included studies, in a coherent manner. We identified main themes and sub-themes to provide a comprehensive overview of the current state of knowledge regarding ACM. By following this methodology, we aim to contribute to the existing body of knowledge on ACM, providing a reliable and up-to-date understanding of its pathogenesis, clinical features, diagnostic approaches, treatment options, and potential preventive strategies.
Various pathophysiological mechanisms have been postulated in the development of cardiomyopathy however one key factor undergoing active research is the role of genetic mutation and susceptibility to develop cardiomyopathy. We reviewed the effects of ethanol on the cardiovascular system in 1996 [15], including aspects of inflammation [16], rhythm disturbances [17], and hypertension [18]. In 2001 we updated the data on the ambivalent relationship between alcohol and the heart [19] and in 2008 added new evidence on a larger cohort of patients with different forms of cardiomyopathy and increased alcohol intake from the German competence network on heart failure [20]. Also, low to moderate daily alcohol intake was proved to be a predictor of better prognosis for both ischemic cardiomyopathy and heart failure regardless of the presence of coronary disease[1,2].
Enlarged heart, in heart failure
In fact, there is an increasing consumption in particular groups, such as adolescents and young people [3,4]. In fact, Brandt et al.54 observed that in ALDH2-deficient mice, the most important increase in mitochondrial superoxide levels (which is the major species of ROS) is due to acetaldehyde, not ethanol. By inhibiting NOX2 (the most important superoxide-producing enzyme) with apocynin, they observed a decrease in ethanol- and acetaldehyde-induced superoxide levels. Furthermore, alcohol consumption has also been classified in the literature by ranges of consumption as mild, moderate, and heavy drinking.11 In this regard, these categories have the following consumption thresholds that also differ according to sex.
- Future studies with a strict classification of non-drinkers and drinkers will help clarify whether complete abstinence is mandatory for ACM patients.
- This can sometimes worsen the symptoms of heart failure and lead to abnormal heart rhythms (atrial fibrillation).
- Therefore, because of its multiple actions, acetaldehyde may influence ACM pathogenesis in addition to ethanol effect itself [20,76,77].
- Acute can be defined as large volume acute consumption of alcohol promotes myocardial inflammation leading to increased troponin concentration in serum, tachyarrhythmias including atrial fibrillation and rarely ventricular fibrillation.
Associated Data
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. Studies that have assessed the prevalence of ACM among IDCM patients have found high alcohol consumption in 3.8% to 47% of DCM patients. The lowest prevalence of ACM among DCM (3.8%) was obtained from a series of 673 patients admitted to hospital consecutively due to HF in the state of Maryland[27]. This study included not only DCM, but also all causes of left ventricular dysfunction, including hypertensive heart disease, ischemic cardiomyopathy and heart valve disease.