Alcoholic Cardiomyopathy: Symptoms, Causes, and Treatment

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. It was characterized by congestive heart failure, pericardial effusion, and alcoholic cardiomyopathy an elevated hemoglobin concentration. Cobalt was used as a foam stabilizer by certain breweries in Canada and in the USA. As the syndrome could be attributed to the toxicity of this trace element, the additive was prohibited thereafter.

Fatty acid ethyl esters: Potentially toxic products of myocardial ethanol metabolism

Nitrocellulose membranes (Amersham) were blocked with 5% non-fat milk dissolved in a solution of PBS-0.1% Tween20 (PBS-T). We obtained antibodies for Abl1 (clone 8E9, sc-56887) and GAPDH (clone 6C5, sc-32233) from Santa Cruz Biotechnology, and PARP from https://ecosoberhouse.com/ Cell Signaling Technology (Euroclone, Milan, Italy; #9542). To confirm p53 activation in response to doxorubicin treatment, we assayed p53 (clone DO-1, sc-126) and the p53 targets p21 (clone C-19, sc-397) and MDM2 (SMP14, sc-965) by Western blotting.

Alcohol and the heart

• This reinforces the notion of an, as yet, undefined physiological role of p73 in the cellular differentiation of lymphocytes of control animals.
• Ventricular dilatation is the first echocardiographic change seen in alcohol use disorder patients, coming before diastolic dysfunction and hypertrophy.
• Your outlook may also improve depending on other treatments you receive, such as medication or surgery.
• The resulting effect in those multiple sites may be additive and synergistic, increasing the final damage [20,52] (Figure 1).

Doxorubicin treatment caused marked ultrastructural changes of cardiomyocytes (panels E and F) with sub-sarcolemmal bleb formation (E1) and protrusions of sarcolemma surrounding individual mitochondria (E1, F1). Panel E2 and E3 depict a swollen vascular endothelial cell and myofibrillar disarray (E3), which is characterized by the loss of regular cross striations. The distinct organisation of sarcomeres into bands, zones and lines is vanished, and harmed mitochondria display loss of the cristae structure. Shown in panel F2 is a myofibroblast as part of the wound healing process and the scaring of the tissue. The ultrastructure of control animals reveals a regular arrangement of the myofibrils; the mitochondria vary in size and shape and form smaller aggregates (D1–3). The contractile apparatus is intact, and the Z bands of the cardiac sarcomere are clearly visible (D3).

Validation of doxorubicin-regulated genes in cell lines and iPS-derived human cardiomyocytes

However, it has been evidenced that ACM may develop in the absence of protein or caloric malnutrition [38]. However, nutritional factors may worsen the natural course of ACM and should be avoided [18,19]. Ethyl alcohol, also known as “ethanol” or usually just as “alcohol”, is the most consumed drug in human history [1].

Comparison of long-term outcome of alcoholic and idiopathic dilated cardiomyopathy

Together, the four treatments (T1-T4) resulted in 102, 52, 20 and 79 unique and therefore distinct gene regulations with no overlap between them (Fig. 4A1, Venn diagram and supplementary Table S5). Nonetheless, we identified up to 3 commonly regulated genes in the comparison of three different treatments (Fig. 4B), whereas the results of a comparison between two treatments are given in supplementary Figure S2. For instance, T2 caused repressed and T4 induced expression of dedicator of cytokinesis protein 9 (Dock 9), i.e. a protein highly expressed in heart tissue that functions in the signaling networks of small G proteins. Collectively, we observed strict treatment dependent genomic responses with little overlap between the different regimens, and the results imply considerable heterogeneity in cardiomyocyte responses to doxorubicin treatment.

Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies

• Wang et al. found evidence of ethanol-induced changes in mitochondrial structure that were more pronounced in a metallothionein knock-out mouse model compared to wild-type mouse (80).
• 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.
• Additionally, in T1 and T4, the centromere protein F (Cenpf) is repressed and although its functions are only partly understood, its cardiac-specific deletion resulted in dilated cardiomyopathy, disruption of the microtubule network and aberrant cellular morphology [114].
• 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.

How is alcoholic cardiomyopathy treated?