Until the second part of the 20th century, there was no scientific evidence on the direct and dose-dependent effect of ethanol on the heart as cause of ACM [6,38]. This is a longstanding accumulated effect that usually appears when a subject has, in their lifetime, consumed more than 7 Kg of ethanol per Kg of body weight in men (equivalent to 60 drinks per month), and 5 Kg of ethanol per Kg of body weight in women (equivalent to 43 drinks per month) [19,46]. However, there is a clear personal susceptibility of this effect that creates a wide variability range and supposes significant inter-individual differences [50,66]. In fact, ACM is considered to be the result of dosage and individual predisposition [32]. In Fabry disease, deficiency in α-galactosidase A promotes lysosomal accumulation of globotriaosylceramide.
Management and Treatment
After several months, the same dilated ventricle can result from diffuse scar with little or no inflammation. The transition from acute myocarditis to chronic fibrotic DCM probably occurs over months, with substantial individual variability, which creates a window for personalized therapies. Breastfeeding in women with PPCM is controversial, and conflicting data exist. A retrospective study has suggested better outcomes among women who breastfeed178; however, other investigators have suggested that prolactin subfragments will have negative effects on myocardial recovery and are specifically involved in the pathogenesis of PPCM.
Cardiac Catheterization
As mentioned, those are all steps in the right direction to make a heart attack less likely. Losing even a few pounds can significantly improve your heart health and reduce your heart attack risk. “Belly fat” around your alcoholic cardiomyopathy midsection can lead to increased buildup of plaque in the walls of your arteries, making a heart attack more likely. A BMI of 30+ is the traditional benchmark for obesity; 25 to 29.9 is categorized as overweight.
- Pharmacological restoration of autophagic reflux by inhibition of soluble epoxide hydrolase has been described to ameliorate chronic ethanol-induced cardiac fibrosis in an in vivo swine model [151].
- Therefore, physicians should be aware of the risk of new cardiomyopathy in patients with these overlapping diagnoses [144].
- It also appears that the changes emerging in ACM patients only differ from idiopathic DCM in quantitative terms, with histological changes being more striking in idiopathic DCM than in ACM[44].
- Finally, it should be noted that McKenna and co-workers, in one of the most frequently cited papers in the ACM field, reported an incidence of 40% in 100 individuals suffering from idiopathic DCM, but in this case the consumption threshold used was only g/d[8].
AMOUNT OF ALCOHOL REQUIRED TO PRODUCE ACM
A colleague working in the publishing industry asked if I’d see his 30-year-old son for a medical evaluation. A business executive in Philadelphia, the son was in good health with no prior illness. But, some tachycardia was puzzling the primary care physician, who requested a consultation. This table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all reviewers are required to complete and submit.
- In patients exhibiting chronic alcohol use, other causes of dilated cardiomyopathy need workup.
- Muscular weakness may also be present because of the effect of alcohol on muscles (alcoholic myopathy).
- For more than 3000 years, alcoholic beverages have been consumed in multiple societies through the centuries and cultures.
- It is always advisable to be mindful of individual tolerance and consume alcohol responsibly [4-6].
Therefore, physicians should be aware of the risk of new cardiomyopathy in patients with these overlapping diagnoses [144]. Control of these alcohol-related systemic diseases, as well as the strict control of the presence of other heart risk factors (tobacco, cocaine, arterial hypertension, diabetes mellitus, or anemia) contributes to ACM improvement [10,20,23,37,52]. Atrial fibrillation should be controlled with chronotropic drugs such as digoxin or diltiazem and anticoagulant treatment to avoid arterial embolisms [60,145]. 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.
Get regular health screenings
In fact, ACM is related to systemic damage induced by ethanol misuse and its global biological response [10,11,31]. Recent advances in the understanding of T-cell plasticity have influenced this model and are now under investigation in human disease. Measurement of multiple viral titers in the blood is expensive and has not proven to be very useful over the years. The role of EMB in the evaluation of PPCM remains limited, and in general, EMB does not assist in therapy or the determination of recovery potential.
- The best approach to treat alcohol-induced cardiomyopathy is addressing the source of the disease.
- Early cardiotoxicity of doxorubicin consists mainly of sinus tachycardia or electrocardiographic abnormalities such as nonspecific ST-T–wave changes, reduction of the QRS voltage, or QRS prolongation, but the ECG is not a sensitive or specific method for monitoring anthracycline-related cardiotoxicity.
- Hyperthyroidism and hypothyroidism can both lead to cardiovascular injury, including HF.
Alcohol causes cardiomyopathy by directly damaging heart muscle cells, impairing their function. Prolonged alcohol abuse weakens the heart muscle, leading to enlargement of the heart chambers, reduced pumping ability and ultimately heart failure. Acute cases of alcohol-induced cardiomyopathy may be reversible under total abstinence from alcohol, with first signs of improvement within the first month. Left ventricular function can improve within six months, with complete recovery within 18 months.
