Mathews and Kino found a small, but significant increase in left ventricular mass in individuals consuming at least 12 oz of whisky during 6 years and 60 g of ethanol per day, respectively[22,40]. More recently, Lazarevic found a modest increase in end-systolic and diastolic left ventricular volumes and a subsequent thickening of the posterior wall in a cohort of alcoholics consuming at least 80 g during 5 years[23]; however, no differences in systolic function were observed. Finally, only Urbano-Márquez et al[24] found a clear decrease in the ejection fraction, in a cohort of 52 alcoholics, which was directly proportional to the accumulated alcohol intake throughout the patients’ lives. The quantity of alcohol consumed daily and the duration of alcohol misuse are linked to the development of ACM, although the precise thresholds for causing cardiac dysfunction remain unknown.
- Data suggests patients with successful quitting of alcohol have improved overall outcomes with a reduced number of inpatient admissions and improvement in diameter size on echocardiogram.
- 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.
- One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al[64] in 2002.
- For comparison, the mean annual beer consumption in Bavaria is nowadays estimated to be 145 l and in the rest of Germany around 100 l beer per person and year [24].
- Clinical Review BoardAll Healthwise education is reviewed by a team that includes physicians, nurses, advanced practitioners, registered dieticians, and other healthcare professionals.
Who is At Risk of Alcoholic Cardiomyopathy?
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 al[22] 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. In another study on this topic, Lazarević et al[23] divided a cohort of alcoholic cardiomyopathy symptoms 89 asymptomatic individuals whose consumption exceeded 80 g/d (8 standard units) into 3 groups according to the duration of their alcohol abuse. Subjects with a shorter period of alcohol abuse, from 5 to 10 years, had a significant increase in left ventricular diameter and volume compared to the control group. However, a systolic impairment was not found as the years of alcoholic abuse continued. New strategies to improve the natural course of ACM have been proposed as promising agents in this field [112,147].
Derangements in Fatty Acid Metabolism and Transport
This mechanism is also important for cell and organism survival during stress and nutrient deprivation. Under the latter conditions, autophagy via degradation of macromolecular intracellular constituents becomes important in generating and recycling carbons https://ecosoberhouse.com/ and amino acids. However, there is evidence that there is enhanced autophagy in certain cardiac pathological conditions such as heart failure, cardiomyopathy, and cardiac hypertrophy, conditions in which there are increased levels of angiotensin II (69).
Pathological Aspects of ACM
In fact, the particular effects that ethanol produces in a specific organ depend on several factors [18,19]. One is the physical characteristics of ethanol itself, with a low molecular size, high distribution capacity, and high tissue reactivity. In addition, there is a relevant role on each organ, particularly on defense and adaptive mechanisms, with a clear induction of anti-oxidant, metabolic, and anti-inflammatory protective responses as a result of ethanol aggression [18,25,26]. This multi-factorial effect is attributed to genetic factors [27] and ethnic [28] variability. The final damage is an equilibrium between the intensity of damaging effects and the possibility of defense, plasticity, regeneration, and adaptation for every specific organ [29,30,31]. Thus, alcohol-dilated cardiomyopathy (ACM) is the result of dosage and individual predisposition [32].
Mitochondria play an essential role in cellular metabolism, and disruption of their function can have profound effects on the entire cell. The myocyte mitochondria in the hearts of persons exposed to alcohol are clearly abnormal in structure, and many believe that this may be an important factor in the development of AC. To identify the causative agent of AC, investigators administered ethanol to rats pretreated with inhibitors of ethanol metabolism. Use of ethanol alone or ethanol with an alcohol dehydrogenase inhibitor resulted in a 25% decrease in protein synthesis.
5. The effects of Moderate Consumption of Ethanol and Binge-drinking
- There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy.
- However, if alcoholic cardiomyopathy is caught early and the damage isn’t severe, the condition can be treated.
- In the setting of acute alcohol use or intoxication, this is called holiday heart syndrome, because the incidence is increased following weekends and during holiday seasons.
- Due to its significant toxicity, studies have avoided its direct instillation, as it produces indiscriminate cell damage even at low doses.
- Finally, we analyzed and presented the synthesized literature, along with relevant findings and conclusions from the included studies, in a coherent manner.
This refers to the finding in the last century that moderate alcohol consumption could be the reason for the relatively low cardiovascular disease incidence in wine-drinking regions [92]. Renaud and de Lorgeril [93] suggested that the inhibition of platelet reactivity by wine may be one explanation for protection from CAD in France. Unfortunately Lazarević et al[23], as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms. It is therefore possible that most of these studies may have also consistently omitted most alcohol abusers in whom alcohol had already caused significant ventricular dysfunction. Cardiac remodeling is a global process that myocardium establishes as a result of different aggressions [31,132]. Heart myocytes are relatively resistant to the toxic effect of ethanol, developing a functional and structural compensatory mechanism able to minimize or repair the ethanol-induced myocyte damage [20,31,39].
- During pregnancy, ethanol consumption should be clearly discouraged because of the possibility of fetal alcohol syndrome or the development of other congenital heart diseases [97].
- 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.
- It may be caused by a surge of hormones, particularly adrenaline, during a period of stress.
- The key to diagnosis is a personal history of chronic heavy alcohol use and the absence of other etiologies.
- Acetaldehyde is a potent oxidant and, as such, increases oxidative stress, leading to the formation of oxygen radicals, with subsequent endothelial and tissue dysfunction.
