Nitric oxide is implicated in the pathogenesis of cardiac failure. Plasma n
itrite level (an end product of nitric oxide metabolism) is studied in 15 p
atients of chronic rheumatic valvular heart disease with myocardial contrac
tile dysfunction and cardiac failure (Group I), 15 patients of chronic rheu
matic valvular heart disease with similar valvular lesions, normal myocardi
al contractile function and without cardiac failure (Group IT) and 15 healt
hy 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 funct
ion [Nitrite v End systolic volume/Body surface area (T-xy.z = 0.23), Nitri
te v End systolic dimension/Body surface area (T-xy.z = 0.32). Nitrite v le
ft ventricular ejection fraction (T-xy.z = -0.24), Nitrite v tricuspid annu
lar plane systolic excursion (T-xy.z = -0.29)] and worsening New York Heart
Association (NYHA) functional class (r(s) = 0.5). We conclude that plasma
nitrite, a stable end product of nitric oxide metabolism is increased in pa
tients of rheumatic valvular heart disease with cardiac failure, suggesting
increased nitric oxide production. Increased level of nitric oxide might b
e playing a significant role in myocardial contractile dysfunction and alte
ration of vascular response in cardiac failure, (C) 1999 Academic Press.