Without an adequate supply of blood and oxygen, the body’s organs and tissues can no longer function properly. Electrocardiographic findings are frequently abnormal, and these findings may be the only indication of heart disease in asymptomatic patients. Results from resting and stress nuclear imaging techniques (eg, stress testing with thallium and sestamibi imaging, multiple gated acquisition [MUGA] scanning, positron emission tomography [PET scanning]) may be useful for evaluating cardiac size and function and for screening for coronary alcoholic cardiomyopathy is especially dangerous because disease. A 12-month observational study of 20 patients with AC noted smaller cavity diameters, better clinical evaluation findings, and fewer hospitalizations in the 10 patients who abstained from alcohol use. 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. Myocardial depression secondary to alcohol is initially reversible however prolonged sustained alcohol use leads to irreversible dysfunction.
- Medications typically include beta-blockers (for heart rhythm and blood pressure issues) and diuretics (to help your body get rid of excess fluid and swelling).
- The regulatory mechanisms of mitochondrial dysfunction mainly include mitochondrial dynamics, oxidative stress, calcium handling, uncoupling, biogenesis, mitophagy, and insulin signaling.
- Liang et al. treated SD diabetic rats induced by STZ with triptolide (100, 200, or 400 μg/kg/d) for 6 weeks and evaluated cardiac energy metabolism using P-31 nuclear magnetic resonance spectroscopy.
- Therefore, we did not include medication use and alcohol abstinence as evaluation indices in this study, although these factors may influence all-cause mortality.
2. Estimation of prognosis and risk factors in ACM
- Based on the essential role of mitochondrial dynamics in regulating DCM, some targeted drugs that normalize mitochondrial dynamics are used to treat hyperglycemia induced myocardial injury.
- Alcohol-induced cardiomyopathy is a condition that can have major impacts on your life over time.
- Cardiotoxicity refers to heart damage that occurs in response to certain drugs, such as alcohol.
- These strategies targeting the treatment of mitochondrial dysfunction may help prevent and treat DCM.
- In some cases, a pacemaker or other implantable device might be necessary to treat more severe heart rhythm problems.
Continued heavy alcohol use, on the other hand, will continue to make alcoholic cardiomyopathy worse. Others have examined the potential effects of micronutrient deficiencies (such as zinc) on ethanol-induced changes in the heart. 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). Metallothionein binds zinc within the cell and is important for overall zinc homeostasis.
6 Mitochondrial calcium handling
These findings suggest that astragaloside IV may exert a protective effect on DCM by promoting mitochondrial biogenesis and inducing mitophagy. Secondary metabolites derived from plants have the properties of being safe, effective, and low in toxicity. Research on the prevention and treatment of diabetes and its complications using these metabolites has attracted increasing attention (Sukhikh et al., 2023). Previous studies have reported that the research on plant secondary metabolites for diabetes mainly focuses on regulating lipid and protein metabolism pathways, insulin signaling pathways, anti-inflammatory responses, and anti-oxidant stress (Shehadeh et al., 2021).
- 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.
- Mitochondria are double-membrane organelles that maintain a highly dynamic and multifunctional network (Iannetti et al., 2015).
Regulatory mechanism of mitochondrial dysfunction in diabetic cardiomyopathy
The content of n-hexane extract was 97.65%, petroleum ether extract was 98.05%, dichloromethane extract was 98.93%, and the content of steam-distilled extract was 99.68%. In vitro pharmacology studies have shown that the n-hexane extract of carthami flos has the best in vitro anti-diabetic activity against protein tyrosine phosphatase 1B (PTP1B), demonstrating potential for the treatment of diabetes and obesity (Li et al., 2012). Ethyl alcohol has detrimental effects on myocardial metabolism; nevertheless, the pathogenetic mechanisms of alcoholic cardiomyopathy remain uncertain. Reactive oxidative metabolites generated from the biotransformation of ethanol are thought to lead to lipid peroxidation of myocytes and oxidation of protein thiols. Acetaldehyde produced in the liver from metabolism via alcohol dehydrogenase may also reach the heart and produce adverse effects.
Among them, polysaccharides, flavonoids, and saponins have biological activities such as hypoglycemic, antioxidation, and immune regulation, and are important components of the pharmacological effects of astragali radix. In previous reports, it has been indicated that astragaloside IV can significantly delay the excessive generation of mitochondrial ROS. It can also exert a protective effect on diabetic cardiomyopathy by upregulating the activities of antioxidant enzymes SOD2, catalase, GSH-Px, and downregulating the expression of c-Jun N-terminal kinase and p38 MAPK (Chen et al., 2018). Astragalus polysaccharides can prevent the occurrence of diabetic cardiomyopathy through the mitochondrial-mediated cell apoptosis pathway (Sun et al., 2017).
Abnormal heart sounds, murmurs, ECG abnormalities, and enlarged heart on chest x-ray may lead to the diagnosis. More specifically, atrial fibrillation with rapid ventricular response is a cause of arrhythmia-induced cardiomyopathy,61 which can potentially worsen LVEF in https://ecosoberhouse.com/article/writing-a-goodbye-letter-to-alcohol/ AC patients, on top of the direct toxic effect of ethanol, acetaldehyde damage, or the aforementioned genetic factors. Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction.
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It also suppressed the expression of UCP2 protein, thereby improving cardiac function in diabetic rats (Diao et al., 2019). In conclusion, resveratrol may have a positive impact on the prevention and treatment of diabetic cardiomyopathy by regulating mitochondrial uncoupling. Recent research has highlighted the close relationship between ferroptosis and mitochondrial oxidative damage. Research shows that abnormal mitochondrial ferroptosis occurs in the heart of diabetes mice, which is mainly manifested by the decrease of Δψm, the downregulation of the expression of SOD and glutathione peroxidase 1 (GPX 1) in mitochondria, and the significant increase in mitochondrial ROS levels (Fang et al., 2020).