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Original research: Clinical profile and prognostic factors of alcoholic cardiomyopathy in tribal and non-tribal population PMC

Alterations caused by heavy alcohol intake have also been studied from the perspective of histopathology. Emmanuel Rubin analysed muscle biopsies from individuals who were previously non-drinkers and were submitted to a balanced diet with heavy alcohol intake during one month[41]. These changes, though subtle, were similar to those found by Ferrans and Hibbs in eight deceased individuals diagnosed with ACM[42,43]. On histological examination, various degrees of fibrosis, patchy areas of endocardial fibroelastosis, intramural blood clots and focal collections of swollen cells in both the epicardium and endocardium were found. 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 findings were analysed taking into account the amount and chronicity of intake and they were compared with the same parameters measured in a control group of non-drinkers. From the studies reviewed in this group, 6 clinically significant abnormal ST segment findings were reported as 3 depressed ST segment, 1 prolonged ST segment, and 2 nonspecific ST segments. From the studies reviewed in this group, 20 clinically significant abnormal ST segment findings were reported as 1 prolonged ST segment, 1 horizontal ST segment, 1 elevated ST segment, 6 depressed ST segments, and 11 nonspecific ST segments. Research studies of varying designs, methodologies and length were included to investigate ECG abnormalities reported in exposure to excessive oral alcohol consumption in humans. The selection of papers for this systematic review followed the Preferred Reporting Items for Systematic Reviews, and Meta-Analysis (PRISMA) (Schulz, Altman, & Moher, 2010) (Figure 1). Three electronic databases (PubMed, Embase, and CINAHL) for studies published from database inception to April 19, 2019 were included for this systematic review.

Sex Differences in the Clinical Presentation and Natural History of Dilated Cardiomyopathy.

However, during the time that these haemodynamic changes appeared, some researchers identified a possible decrease in the ejection fraction and other parameters related to systolic function[32-39]. This was questioned by other authors, who pointed out that these conclusions could not be drawn, as alcohol itself also induces changes in the pre-load and after-load conditions, which influence cardiac contractility[35]. However, in this context, experimental in vitro studies using cardiomyocytes have shown that alcohol depresses the contractile capacity of the myocardium, regardless of the sympathetic tone and the haemodynamic conditions[36].

Absorption levels of Indium-111 were high in 75% of patients who continued drinking and in only 32% of those who had withdrawn from consuming alcohol. Guillo et al[17] in 1997 described the evolution of 9 ACM patients who had been admitted. He divided this cohort into two groups according to the evolution of the ejection fraction during 36 mo in which no deaths were recorded. The 6 subjects who experienced a clear improvement in their ejection fraction had fully refrained from drinking. Conversely, the 3 subjects recording a less satisfactory evolution had persisted in their consumption of alcohol.

Treatment of alcohol use disorders in patients with alcoholic liver disease

Future directions include investigating whether a real-time assessment, such as the ECG, in conjunction with other key behavioral and cardiac measures can help clinicians and patients realize the progressive and insidious cardiac damage due to excessive alcohol consumption. This theory guided nurse science review supports the development of personalized symptom monitoring to deliver tailored feedback that illuminate risk factors as a potentially transformative approach in the management of AUD. Alcoholic cardiomyopathy (ACM) is a cardiac disease caused by chronic alcohol consumption. The major risk factor for developing ACM is chronic alcohol use; however, there is no cutoff value for the amount of alcohol consumption that would lead to the development of ACM.

  • Considering all the works conducted to date, it is clear that new studies on the natural history of ACM are needed, including patients treated with contemporary heart failure therapies.
  • (A) Kaplan-Meier plots displaying the estimated survival probability in groups categorised according to QRS duration.
  • Clinically significant T-wave abnormalities were reported in all sample groups reviewed.
  • The authors examined the prevalence of cardiomegaly by means of chest x-rays and related it to alcohol consumption among a consecutive series of Japanese males of working age.
  • Expressions referring to “the heart of a wine drinker in Tubingen” and particularly a “Munich beer heart” were used and known in Germany during this time[13].
  • This activity highlights the role of the interprofessional team in caring for patients with this condition.

This includes a combination of beta-blockers, an angiotensin-converting enzyme inhibitor, diuretics, aldosterone receptor antagonist and angiotensin blocker-neprilysin inhibitor (if LVEF is less than or equal to 40%). The use of carvedilol, trimetazidine with other conventional heart failure drugs have been proven to be beneficial in some studies. Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports. In these studies, haemodynamic and echocardiographic parameters were measured in individuals starting an alcohol withdrawal program.

2. Estimation of prognosis and risk factors in ACM

In spite of numerous studies, the sequence of events that occur in alcohol-induced myocardial damage is still highly controversial. Although some authors contend that the initial event is the appearance of hypertrophy, the majority accept that the core event is the loss of cardiomyocytes. Finally, it should be noted that a large alcoholic cardiomyopathy majority of studies on the long-term prognosis of ACM used the cut-off point of 80 g/d for a minimum of 5 years to consider alcohol as the cause of DCM. Since those initial descriptions, reports on several isolated cases or in small series of patients with HF due to DCM and high alcohol intake have been published[15-17].

natural history and prognostic factors in alcoholic cardiomyopathy

This aggregative synthesis assimilates key patterns related to the physiological response in the healing process of AUD and provides fertile ground for theoretical development ergo actionable knowledge in a participatory nurse practice. We encourage nurse scientists to use this data-inspired synthesis to develop creative new ways to approach AUD that have yet to be configured. Clinically significant T-wave abnormalities were reported in all sample groups reviewed. Clinically significant P-wave abnormalities were reported in all sample groups reviewed except for the Acute on Chronic Use group. Many changes can be observed including premature atrial or ventricular contractions, supraventricular tachycardias, atrioventricular blocks,  bundle branch blocks, QT prolongation, non-specific ST and T wave changes and abnormal Q waves.


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