Abstract

Increased Plasma Nitrite Level in Cardiac Failure. Nitric oxide is implicated in the pathogenesis of cardiac failure. Plasma nitrite level (an end product of nitric oxide metabolism) is studied in 15 patients of chronic rheumatic valvular heart disease with myocardial contractile dysfunction and cardiac failure (Group I), 15 patients of chronic rheumatic valvular heart disease with similar valvular lesions, normal myocardial contractile function and without cardiac failure (Group II) and 15 healthy controls (Group III). Patients in Group I had higher nitrite level (242.2±31.7 nm) compared to Group II (142.6±24.4 nm) and Group III (102.7±15.9 nm). Among the patients with rheumatic heart disease, increasing nitrite level correlated significantly with worsening of contractile function [NitritevEnd systolic volume/Body surface area (Txy.z=0.23), NitritevEnd systolic dimension/Body surface area (Txy.z=0.32), Nitritevleft ventricular ejection fraction (Txy.z=−0.24), Nitritevtricuspid annular plane systolic excursion (Txy.z=−0.29)] and worsening New York Heart Association (NYHA) functional class (rs=0.5). We conclude that plasma nitrite, a stable end product of nitric oxide metabolism is increased in patients of rheumatic valvular heart disease with cardiac failure, suggesting increased nitric oxide production. Increased level of nitric oxide might be playing a significant role in myocardial contractile dysfunction and alteration of vascular response in cardiac failure.

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