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. Polyphenols of red barrique wines and flavonoids have been shown to inhibit endothelin-1 synthase 102 and PDGF-induced vasoproliferation thus also contributing to cardiovascular protection 103. As early as in 1915, Lian 45 reported in middle-aged French servicemen during the first world war that heavy drinking could lead to hypertension. It took almost 60 years before further attention was paid to the complex interaction between the heart and the peripheral vasculature in various cross-sectional and prospective epidemiologic studies, which have empirically confirmed this early report.
- No changes in heart weight-to-body weight ratios were found, however the myocardium from ethanol-treated animals showed fibrosis, and an irregular, disorganized myocyte pattern.
- According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases68.
- There is also an established link between the development of ACM and apoptosis because of myocardial cell death, which contributes to heart pathology and dysfunction.
- The use of carvedilol, trimetazidine with other conventional heart failure drugs have been proven to be beneficial in some studies.
- Of the 56 patients included in the study, 28 were former drinkers and 28 continued consuming alcohol during the study.
- 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.
When should I see my healthcare provider about alcohol septal ablation?
This suggests a direct or indirect role for ethanol-mediated oxidative stress in the heart (Jiang et al. 2012; Tan et al. 2012). In humans, endothelial function is assessed by measuring the widening (i.e., dilation) of the brachial artery under different conditions. Some research noted that endothelial function is impaired in abstinent individuals with a long-term history of alcohol abuse or alcoholism(Di Gennaro et al. 2007, 2012; Maiorano et al. 1999). Other studies have examined the effect of a single binge-drinking episode and found impairment in brachial artery endothelial-dependent and -independent vasodilation (Bau et al. 2005; Hashimoto et al. 2001; Hijmering et al. 2007). Therefore, as in animal studies, the effects of ethanol on endothelial function in humans likely depend on the dose and duration of ethanol consumption. Hypertension due to alcohol may be a confounding comorbidity in that it may contribute to LV dysfunction; therefore, LV dysfunction due to hypertension must be differentiated from pure AC.
General Health
- Studies that have assessed the prevalence of ACM among IDCM patients have found high alcohol consumption in 3.8% to 47% of DCM patients.
- Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption.
- As with all patients with congestive heart failure, ACE inhibitors and beta-blockers should be prescribed as initial therapy.
In spite of the high prevalence of excessive alcohol consumption and of its consideration as one of the main causes of DCM, only a small number of studies have analysed the long-term natural history of ACM. Unfortunately, all the available reports were completed at a time when a majority of the current heart failure therapies were not available (Table 1). Indeed, the first account of the possible harmful effects of alcohol specifically on heart muscle was reported in the latter half of the 19th century. Expressions referring to “the heart of a wine drinker in Tubingen” and particularly a “Munich beer heart” were used and known in Germany during this time13. A summary of some of the potential cellular changes related to ethanol consumption are shown in Figure 1. There may be more than one cellular event happening and similar to other chronic health conditions, mechanisms maybe synergistic and inter-related.
Coronary artery disease and atherosclerosis
When it comes to wine, one drink is defined as a 5-ounce (148 ml) serving, which typically contains about 12% ABV. Distilled spirits, such as vodka, whiskey, rum, or tequila, are measured as 1.5 ounces (44 ml) per drink, with a typical ABV of around 40%. It is important to note cardiomyopathy alcohol that the size and strength of different alcoholic beverages can vary, so these definitions serve as general guidelines.
- The sub-group of patients in whom symptoms improved was made up of a larger proportion of non-drinkers (73%), compared to 25% in the group who did not improve, or 17% in the group whose condition worsened.
- However, since it includes moderate alcohol consumption of red wine, this aspect should be clearly avoided in subjects affected by ACM.
- In these patients, only early and absolute abstinence of alcohol can reverse myocardial dysfunction 56, 57, 126 which in a historic study by McDonald and Burch was achieved with prolonged bedrest for several months without further access to alcoholic beverages.
- However, genetic polymorphisms, the use of other concomitant drugs (tobacco, cocaine), and the presence of other cardiac risk factors (hypertension, diabetes) may influence and worsen the natural course of ACM in each specific individual 27,72,98.
The signs and symptoms of alcoholic cardiomyopathy (ACM) can vary depending on the severity of the condition.6 In the early stages, people with ACM may not experience any symptoms. 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. Askanas et al21 found a significant increase in the myocardial mass and of the pre-ejection periods in drinkers of over 12 oz of whisky (approximately 120 g of alcohol) compared to a control group of non-drinkers. 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. Kino et al22 found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption.
Heart remodeling is an adaptive mechanism, susceptible to being modified in ACM by the use of cardiomyokines (FGF21, Metrnl) and growth factors (IGF-1, Myostatin) 112,119. Recently, apoptosis and necrosis have been also attributed to autophagy in ACM 18. In order to maintain cardiac homeostasis, the removal of defective organelles and cell debris by autophagy is essential both in physiological and pathological conditions 115. Dysregulated excessive autophagy, together with other factors such as oxidative stress, neurohormonal activation, and altered fatty acid metabolism, contributes to cardiac structural and functional damage following alcoholism.
Myocytolysis progressively develops, disturbing the sarcomere contractile system. The heart output is progressively lower in a dose-dependent relationship with the lifetime accumulated total dose of alcohol consumed 38. Several growth factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage 119,133. Antioxidant, anti-inflammatory, anti-apoptotic, and antifibrogenic mechanisms try to avoid myocyte necrosis and heart fibrosis 14,30,58.
Quebec‘s beer drinker disease
Excessive intake of alcohol may result in increased systemic blood pressure in a dose-response relationship, and this may contribute to chronic myocardial dysfunction. Patients who consume more than two drinks per day have a 1.5- to 2-fold increase in hypertension compared with persons who do not drink alcohol, and this effect is most prominent when the daily intake of alcohol exceeds five drinks. Because hypertension may directly contribute to left ventricular (LV) dysfunction, this may be a confounding comorbidity in persons who abuse alcohol, and it should be differentiated from pure forms of alcoholic 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.