Many researchers have found that alcohol intake increases HDL cholesterol (HDL-c) levels, HDL (“good cholesterol”) particle concentration, apolipoprotein A-I, and HDL-c subfractions (Gardner et al. 2000; Muth et al. 2010; Vu et al. 2016). Findings have been equivocal for other lipids, such as low-density lipoprotein cholesterol (LDL-c) (the estimated amount of cholesterol within LDL particles, or “bad cholesterol”) and triglyceride levels https://ecosoberhouse.com/ (Rimm et al. 1999; Volcik et al. 2008; Waskiewicz and Sygnowska 2013). High triglyceride levels in the blood stream have been linked to atherosclerosis and, by extension, increased risk of CHD and stroke. However, in a recently conducted Mendelian randomization study, Vu and colleagues (2016) reported that low-to-moderate alcohol consumption reduced triglyceride and LDL-c and increased HDL-c, in particular the HDL2-c subfraction.
Acknowledgments
In light of the available data, new studies will help to clarify the current prognosis of ACM compared to DCM and to determine prognostic factors in ACM that might differ from known prognostic factors in DCM. The latest two papers to be published, unlike previous papers, reported worse outcomes for ACM patients compared to DCM patients. In the first of these studies, Fauchier et al[11] studied 50 patients with ACM and 84 patients with DCM between 1986 and 1997. Although up to 81% of ACM patients received an ACEI, none received beta-blockers and the use of spironolactone was not specified, although it was probably quite low.
What tests will be done to diagnose this condition?
- In skeletal muscle, ubiquitin E3 ligases, such as atrogin-1 and muscle RING Finger 1 (MuRF1), accelerate protein breakdown and lead to muscle atrophy (67,68).
- Of the 56 patients included in the study, 28 were former drinkers and 28 continued consuming alcohol during the study.
- Excessive alcohol consumption represents one of the main causes of non-ischemic dilated cardiomyopathy.
Experimental studies analysing the depressive properties of alcohol on the cardiac muscle invariably use similar approaches[31-39]. Accordingly, a given amount of alcohol is administered to volunteers or alcoholics, followed by the measurement of a number of haemodynamic alcoholic cardiomyopathy is especially dangerous because parameters and, in some cases, echocardiographic parameters. Generally, following alcohol intake, healthy, non-drinking individuals showed an increase in cardiac output due to a decline in peripheral arterial resistance and an increase in cardiac frequency[31].
Histologic Findings
- However, when alcoholic patients with ACM received thiamine therapy or other nutritional supplements, myocardial structural and functional changes were often not reversed.
- That scar tissue can also cause potentially life-threatening arrhythmias (irregular heart rhythms).
- Most likely, the decrease in contractility was offset by corresponding decreases in afterload (end-systolic wall stress), systemic vascular resistance, and aortic peak pressure, which maintained cardiac output.
In this review, we discuss these mechanisms, as well as the potential importance of drinking patterns, genetic susceptibility, nutritional factors, ethnicity, and sex in the development of ACM. Prognosis in individuals with low or moderate consumption up to one or two drinks per day in men and one drink in women is not different from people who do not drink at all. In CAD, diabetes, and stroke prevention the J‑type mortality curves even indicate some benefit apart from the social ”well-being“. In patients with chronic alcohol use disorders and severe heart failure prognosis is poor, since continued alcohol abuse results in refractory congestive heart failure.
- At present ACM is considered a specific disease both by the European Society of Cardiology (ESC) and by the American Heart Association (AHA)[18,19].
- All-cause mortality was assessed using Kaplan–Meier survival curves, and the risk factors were assessed using Cox regression.
- 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.
He recruited 48 patients admitted to hospital with cardiomegaly without a clear aetiology and severe alcoholism. The only factor to predict a poor outcome was the duration of symptoms before admission. In spite of numerous studies, the sequence of events that occur in alcohol-induced myocardial damage is still highly controversial. Although some authors contend that the initial event is the appearance of hypertrophy, the majority accept that the core event is the loss of cardiomyocytes. They commonly include fatigue, shortness of breath, and swelling of the legs and feet. The best way to reduce your risk of developing alcohol-induced cardiomyopathy is to only drink in moderation.
Is this condition only a chronic (long-term) problem?
Alcohol in moderation may lower stress-related risk of heart disease, study finds – The Guardian
Alcohol in moderation may lower stress-related risk of heart disease, study finds.
Posted: Mon, 12 Jun 2023 07:00:00 GMT [source]
The first study, which specifically focused on the amount of alcohol necessary to cause ACM, was conducted by Koide et al[20] in 1975. The authors examined the prevalence of cardiomegaly by means of chest x-rays and related it to alcohol consumption among a consecutive series of Japanese males of working age. They found that 2 of the 6 individuals (33%) whose alcohol consumption exceeded 125 mL/d had cardiomegaly. In contrast, an enlarged heart was found in only 1 of 25 subjects with moderate consumption (4%), in 6 of 105 very mild consumers (5.7%), and in 4.5% of non-drinking individuals. Alcohol-induced cardiomyopathy, especially when more severe, leads to deadly problems like heart attack, stroke or heart failure.
Coronary angiography, coronary artery computed tomography (CT), or nuclear medicine testing was performed to rule out coronary heart diseases. The effect measure for each outcome was conducted using the mean differences effect measure, where the outcomes were assessed in identical units across the various literature reviews used in the study. Furthermore, for this review, certainty assessment was conducted by assessing the risk of bias, imprecision, inconsistency, and indirectness of the presented evidence. Through a thematic synthesis, we identified common trends, knowledge gaps, and emerging research areas related to ACM. 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.
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. Furthermore, the inclusion criteria for ACM were very strict and required a minimum consumption of 8 oz of alcohol (200 g or 20 standard units) each day for over 6 mo. In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients[9-12] (Figure (Figure11). Changes in mitochondrial function have been reported from a number of animal studies in different species, under various alcohol consumption paradigms (ethanol in water or liquid diet), and after variable durations of chronic ethanol consumption (6 weeks to 6 months). Through the process of oxidative phosphorylation, the mitochondria generate ~90 percent of cellular ATP.
