Alcoholic cardiomyopathy: Treatments, outlook, and more

In addition, ethanol induces mitochondrial-dependent apoptosis pathways with Bax and caspase activation [101]. Until the second part of the 20th century, there was no scientific evidence on the direct and dose-dependent https://ecosoberhouse.com/ effect of ethanol on the heart as cause of ACM [6,38]. However, there is a clear personal susceptibility of this effect that creates a wide variability range and supposes significant inter-individual differences [50,66].

Acknowledgments

In patients exhibiting chronic alcohol use, other causes of dilated cardiomyopathy need workup. Investigative work up such as mean corpuscular volume (MCV), gamma-glutamyl-transpeptidase (GGT), elevated transaminases (AST, ALT) and elevated INR usually are seen in liver injury can be helpful as supportive evidence of alcohol use.[14][15]. Although the most common cause of heart failure is coronary artery disease, ischemic cardiomyopathy is unlikely in the absence of a clear history of prior ischemic events or angina and in the absence of Q waves on the ECG strip. In most patients, exercise or pharmacologic stress testing with echocardiographic or nuclear imaging is an appropriate screening test for heart failure due to coronary artery disease. In patients with dilated cardiomyopathy, if additional questions remain after a history is obtained and noninvasive testing is performed, cardiac catheterization may be used to help exclude other etiologies of heart failure. A summary of some of the potential cellular changes related to ethanol consumption are shown in Figure 1.

• The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review.
• 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].
• 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].
• In the mid-1960s, another unexpected heart failure epidemic among chronic, heavy beer drinkers occurred in two cities in the USA, in Quebec, Canada, and in Belgium.
• 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.

Impact of Drinking Patterns and Types of Alcoholic Beverages on Risk

This suggests that alcoholic beverage type may be an important mediator, because in countries such as Russia, spirits are the alcoholic beverage of choice. However, the negative associations between alcohol consumption and CV outcomes in these countries also may relate to pervasive patterns of binge drinking (Leon et al. 2009). Some investigators have suggested that drinking wine may offer alcoholic cardiomyopathy is especially dangerous because more protection against CV disease because it contains polyphenols, such as resveratrol and flavonoids, which are micronutrients with antioxidant activity (Tangney and Rasmussen 2013). However, among studies designed to examine the influence of beverage type, no differences have been found in CV disease outcomes or biologic markers, such as HDL-c (Mukamal et al. 2003a; Volcik et al. 2008).

Hemostatic Factors

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. In summary, there appears to be a number of ways in which mitochondrial perturbations could contribute to both the development and progression of ACM. However, it remains to be determined whether changes in mitochondrial function are cause or consequence.

Ischemic Preconditioning

In some cases, ACM can cause arrhythmias or irregular heartbeats, which can be life-threatening. Despite the progress in standardizing measurement of alcohol, studies still vary in how they define the different levels of drinking, such as low-risk or moderate and heavy drinking. Most often, low-risk or moderate drinking has been defined as 1 to 2 standard drinks per day and heavy alcohol consumption as 4 or more standard drinks per day. However, ascertaining the exact alcohol consumption threshold for determining both the benefit and risk has been challenging, and threshold levels continue to differ across studies.

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]. The postulated mechanism includes mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis. Studies have shown an increase in reactive oxygen species (ROS) level in myocytes following alcohol consumption and thus causes oxidation of lipids, proteins, and DNA leading to cardiac dysfunction. These changes are related to both direct alcohol toxicity on cardiac cells and the indirect toxicity of major alcohol metabolites such as acetaldehyde. As noted in the text, the exact amount and duration of alcohol consumption that results in ACM in human beings varies.

Basic studies on molecular mechanisms of myocardial damage

Clinical Review BoardAll Healthwise education is reviewed by a team that includes physicians, nurses, advanced practitioners, registered dieticians, and other healthcare professionals. They typically require fewer hospitalizations and show improved heart function on ECG readings. Around 40–80% of people with ACM who continue drinking alcohol die within 10 years of their diagnosis. Despite these features, the structural changes do not seem to be specific, furthermore, they are not qualitatively different from those found in idiopathic DCM and they do not allow us to differentiate between the two conditions[44].

Mechanisms Related to Alcohol’s Positive and Adverse Effects on CV Conditions