This requires close attention, considering the ill effect of high blood pressure on the cardiovascular system. The rate of liver disease including but not limited to cirrhosis in our cohort was between 15% and 19%. However, this data does not differentiate between alcoholic and nonalcoholic causes of liver disease and includes non‐cirrhotic liver involvement.
Left ventricular filling impairment in asymptomatic chronic alcoholics
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. Previous studies were conducted on rats that are fed alcohol for about eight months. They found that there is about 14% loss of myocardial cells in the left ventricle of those rats. It showed a significant increase in both acute and chronic alcohol intoxication. All previous mechanisms can induce myocyte apoptosis through the induction of mitochondrial damage and oxidative stress 12.
Treatment / Management
However, very few studies have investigated the relationship between clinical characteristics and prognosis in ACM. Complete alcohol withdrawal is usually recommended to all patients with ACM. For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence. 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).
Review
In patients exhibiting chronic alcohol use, other causes of dilated cardiomyopathy need workup. Investigative work up such as mean corpuscular volume (MCV), gamma-glutamyl-transpeptidase (GGT), elevated transaminases (AST, ALT) and elevated INR usually are seen in liver injury can be helpful as supportive evidence of alcohol use.1415. On physical examination, patients present with non-specific signs of congestive heart failure such as anorexia, generalized cachexia, muscular atrophy, weakness, peripheral edema, third spacing, hepatomegaly, and jugular venous distention. S3 gallop sound along with apical pansystolic murmur due to mitral regurgitation is often heard. However, if alcoholic cardiomyopathy is caught early and the damage isn’t severe, the condition can be treated. It’s very important to stick with the treatment plan and to stop drinking alcohol during recovery.
Treatment of alcohol-induced cardiomyopathy
This is where the heart has an increased need for oxygen that exceeds the body’s ability to supply it. Often, when a doctor suspects cardiomyopathy, they will order an echocardiogram. This test will assess the ejection fraction (EF), a measurement that expresses how much blood the LV pumps out with each contraction. Once doctors have found this, they will look for the cause of the weakened heart.
He compared the prevalence of different polymorphisms of the angiotensin-converting enzyme gene in 30 ACM patients and in 27 alcoholics with normal ventricular function. Furthermore, 89% of the alcoholics with a DD genotype developed ACM, whereas only 13% of those with an II or ID genotype developed this condition. However, this individual susceptibility mediated by polymorphisms of the angiotensin-converting enzyme gene does not appear to be specific to ACM insofar as several diseases, including some that are not of a cardiologic origin, have been related to this genetic finding65. Although some studies have detailed structural and functional damage in proportion to the amount of alcohol consumed during a patient’s lifetime24, a large majority of authors have discarded this theory21-23,25. Both the absence of a direct correlation and the theory of the existence of a threshold dose (above which some alcoholics develop ACM) require the presence of individual susceptibility to alcohol induced cardiac damage63.
- Your recovery time depends on your overall health, including whether you have cardiovascular disease or other health conditions.
- Consulting with a healthcare professional can provide personalized advice and guidance.
- In fact, Brandt et al.54 observed that in ALDH2-deficient mice, the most important increase in mitochondrial superoxide levels (which is the major species of ROS) is due to acetaldehyde, not ethanol.
Also, there were significant size variations in the myofibrils and they showed a relative decrease in the number of striations, in addition to swelling, vacuolisation and hyalinisation. Cell nuclei were larger than normal, morphologically difficult to define and they occasionally showed hyperpigmentation. The authors highlighted the presence of an extensive intracellular accumulation of neutral lipids, principally in the form of small cytoplasmic droplets. In a subsequent study using electron microscopy, the authors found histological features that could be superimposed onto those found in hearts that had suffered hypoxia, anoxia or ischemia43. Analogous to the sarcoplasmic reticulum, the mitochondria were swollen or oedema was present, with crest alterations and intra-mitochondrial inclusions suggesting degenerative processes (Figure 2). Moreover, myofibrils showed a progressively distorted structure, resulting in a homogeneous mass.
At the end of the first year, no differences were found among the non-drinkers, who improved by 13.1%, and among those who reduced consumption to g/d (with an average improvement of 12.2%). Conversely, those whose consumption remained in excess of 80 g/d showed an average decline of 3.8% in their ejection fraction. Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure.
- The diagnosis of alcohol-induced cardiomyopathy in our patient relied on the absence of known causes of dilated cardiomyopathy, the identification of excessive alcohol consumption and the improvement of cardiac function after the abstention from alcohol ingestion.
- 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.
- By using International Classification of Disease‐9th edition‐Clinical Modification (ICD‐9CM) diagnoses and diagnosis‐related groups different comorbidities were identified.
Diastolic function impairment in alcoholics
In a national inpatient sample study, some authors have reported ACM to be most common in white males aged between 45 and 59 2. The diagnosis of alcohol-induced cardiomyopathy in our patient relied on the absence of known causes of dilated cardiomyopathy, the identification of excessive alcohol consumption and the improvement of cardiac function after the abstention from alcohol ingestion. Specifically, there was no evidence of a preceding viral infection or presence of another toxin.
However, these limitations are counterbalanced by the considerable sample size and absence of selection bias. The findings of our study are limited to index stay and cannot be extrapolated to postdischarge events. It is also likely that the actual rate of AC may be underestimated because of undercoding given that a number of patients would present as heart failure exacerbations, thereby altering code used. In alcoholic cardiomyopathy symptoms addition to this, there is difficulty in actually making the diagnosis of AC itself clinically due to absence of specific diagnostic criteria and the need to rule out other causes of cardiomyopathy as well. However, looking into a big population database might be a good way to study such a difficult to diagnose disease process.
