Potential Therapeutic Targets in Cirrhotic Cardiomyopathy

Abstract

Cirrhotic cardiomyopathy is a recently identified pathological condition defined as "a chronic cardiac dysfunction in patients with cirrhosis characterized by blunted contractile responsiveness to stress and/or altered diastolic relaxation with electrophysiological abnormalities, in the absence of known cardiac disease". Overall there seems to be a link between the progression of liver function impairment, the development of portal hypertension and the degree of hyperdynamic circulation, the hallmark of the deranged cardiovascular function in advanced liver diseases. Although mechanical factors contribute to much of the increased resistance within the liver in portal hypertension, there is clearly a vasculogenic component to the development, perpetuation and progression of this syndrome as well. The vascular component of portal hypertension includes an increase in splanchnic blood flow, as well as an increase in intrahepatic vascular resistance. Dysregulation of the nitric oxide system appears to play a key role in both these processes with a paradoxical reduction of intrahepatic availability despite increased disposal in the splanchnic and other vascular districts with adverse effects on cardiac function and structure. Nevertheless, other putative mediators of cardiac damage in cirrhosis have been proposed and their role in the pathogenesis of cirrhotic cardiomyopathy investigated. This review involves a discussion of data achieved on pathogenesis and clinical features of cirrhotic cardiomyopathy but mainly focuses on considerations on potential therapeutic targets, in the light of the evidence that this mainly subclinical condition merges to clinical relevance when challenged with those therapeutic interventions and procedures currently employed to treat the major complications of cirrhosis that might produce a negative impact on the cardiovascular system.

A study of cardiovascular abnormalities among cirrhosis of liver cases

“…There was significant difference in the values of LAD compared to the controls among which only 2 of them had an elevated value more than 40. These findings were in line with the studies conducted by Wong et al and Pozzi et al 8 The echo findings showed that in all patients in our study group, the value of LVIDd was more than 56, which was the value taken as the cut off. This shows that almost all cirrhotic patients will have some sort of cardiac enlargement during the course of the disease.…”

“…As the follow up of the patients were not done, it was not able to assess the rate of progression and its rapidity. The findings correlated with the studies conducted by Wong et al and Pozzi et al 8 The machine calculated LV mass was abnormal in 71 of the cirrhotic patients as compared to 6 of the controls. Among this 33 of them were alcoholics and 38 were non alcoholics.…”

“…The increase in LV mass was mostly among those in the age group 41-60 years, which could be explained by the increased number of subjects in that age group. The findings correlated with studies by pozzi et al 8 The major cardiac structural abnormality of the myocardium in such patients was myocardial hypertrophy. One possible explanation for this would be myocardial adaptation to a chronically elevated blood volume.…”

Cirrhotic Cardiomyopathy

“…Researches have shown that portal venous tension can be decreased using alpha-adrenergic antagonists (prazosin), beta-adrenergic antagonists (propranolol), angiotensin-II antagonists, cyclooxygenase isoenzyme blockers, and TX antagonists. Results of these researches support the pathogenesis [22,[29][30][31][32][33][34].…”

Heart Function and Myocardial Tissue Characterization in Patients with HCV Related Cirrhosis: Diastolic Dysfunction and Cardiac Hypertrophy

“…These findings also introduce new considerations on the potential role of drugs such as beta blockers, angiotensin II receptor antagonists and aldosterone antagonists: their therapeutic application in earlier stages of the cirrhotic disease might prove useful in the clinical management of cirrhotic cardiomyopathy before decompensation of disease develops [63][64][65].…”