A Study on N-terminal-pro Brain-type Natriuretic Peptide in Cirrhosis of Liver

is due to neurohormonal activation in response to ventricular volume and pressure overload.10 The BNP and atrial natriuretic peptide (ANP) may be deemed as counterregulatory hormones acting against the sympathetic and renin-angiotensin-aldosterone systems (RAAS). Secretion of BNP and ANP cause natriuresis, vasodilation activation with a concomitant inhibition of the RAAS and adrenergic activity, inhibition of cardiomyocyte hypertrophy, angiogenesis promotion, and delay in the activation of cardiac fibroblasts, all of which give rise to improved myocardial relaxation.11,12 However, in heart failure with cirrhosis, elevated levels of N-terminal proBNP (NT-proBNP),were more confirmatory than elevated plasma levels of BNP as the latter correlated best with diastolic dysfunction mainly.13-16 However, there was no significant relation of NT-proBNP levels to other measures of hyperdynamic circulation, such as cardiac output or systemic vascular resistance.15 A study that evaluated the severity of disease compared to plasma levels of BNP in nonalcoholic cirrhotic patients found no significant BNP INTRODUCTION