It is always advisable to be mindful of individual tolerance and consume alcohol responsibly 4-6. One common risk factor for CV disease is the composition of the lipids found in the blood, and the effects of alcohol consumption on lipid profiles have been extensively studied. 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 (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.
- They found that there is about 14% loss of myocardial cells in the left ventricle of those rats.
- The onset of symptoms is usually insidious, but acute decompensations are also observed, especially in patients with asymptomatic left ventricular dysfunction who develop atrial fibrillation or other tachyarrhythmia and, because of this, are unable to increase their cardiac output.
- In the ESC consensus document on the classification of cardiomyopathies, ACM is classified among the acquired forms of DCM19.
- This activity highlights the role of the interprofessional team in caring for patients with this condition.
Signs and symptoms
The alcohol causes the enlarged tissue to stop contracting, which expands in the area through which blood can flow out of your heart. Investigating the mechanisms, consequences, and potential treatment options for ACM remains a very important area of research. You will receive the first heart failure and transplantation email in your inbox shortly. When seeking answers, people often look to experts for clear and accurate information. By subscribing to heart failure content from Mayo Clinic, you have taken an important first step in gaining knowledge and using it for your overall health and well-being.
Risk factors
Subjects who drank wine more often, however, were less likely to have symptoms of depression and more likely to have a better perception of health status. They also had lower levels of circulating inflammatory markers, such as C-terminal proendothelin-1 and pentraxin-3 (Cosmi et al. 2015). Several studies and meta-analyses have been conducted to determine the relationship between alcohol consumption and the risk of developing heart failure in healthy subjects, as well as in those with a history of MI or CHD. Studies also have examined the “safety” of alcoholic beverage consumption in subjects with heart failure. Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption. Individuals with certain mitochondrial deoxyribonucleic acid (DNA) mutations and angiotensin-converting enzyme (ACE) genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol.
Acute and Long-term Effects of Alcohol on the Myocardium
- In some cases, ACM can cause arrhythmias or irregular heartbeats, which can be life-threatening.
- The researchers found that the alcohol-drinking subjects (particularly those who were insulin sensitive) had higher insulin levels and a slower rise in glucose levels after a low-carb meal.
- They try to control myocardial remodeling to avoid the progression of myocyte hypertrophy 39,148 or fibrosis 149 and ventricle dysfunction and dilatation, as well as to increase the degree of myocyte regeneration 150.
- Data from human and animal studies have revealed that within the myocardium, a number of adverse histological, cellular, and structural changes occur in response to and over the course of long-term heavy alcohol consumption.
At a pathological level, sarcomere Z-line distortion and disruption of the sarcomere pattern leads to myocytolysis 107,129. Myocytolysis is evident through focal myofiber dissolution, cell vacuolization, and fiber disarray 19 (Figure 2). The sarcomere complex is early affected by ethanol, decreasing the titin content, a protein that is responsible for sarcomere relaxation and LV distensibility 130. This damage first induces diastolic dysfunction, which is initially subclinical and later clinically apparent 57. In addition, contractile sarcomere proteins such as Myosin, Actin, and Troponin are also affected by ethanol, causing the functional progressive depression of myocyte contractility, inducing progression to heart failure 56,104,131.
Data from transgenic animal models and pharmacologic approaches strongly support a role for ethanol-induced oxidative stress in CV disease. In addition, there was no evidence of nitrative damage in mice bred to disrupt (i.e., knock out) the gene for angiotensin I receptor (AT1-KO) that had been given ethanol for a similar length of time (Tan et al. 2012). Both experimental approaches also prevented accumulation of ethanol-induced scarring (collagen and fibronectin); apoptotic cell death; and changes in the size, shape, and function of the heart after injury to heart muscle (ventricular remodeling). 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.
Acetaldehyde is produced at a lower quantity in the heart as compared to the liver, and systemic acetaldehyde does not achieve cardiomyopathy alcohol toxic heart concentrations 77. In addition, acetaldehyde is able to interact with proteins and produce protein-adduct compounds that are highly reactive and may induce additional inflammatory and immunologic heart damage 78. Therefore, because of its multiple actions, acetaldehyde may influence ACM pathogenesis in addition to ethanol effect itself 20,76,77. This ethanol misuse at high consumption rates causes a variety of health problems, ethanol being the sixth most relevant factor of global burden of disease and responsible for 5.3% of all deaths 5.
