Increased plasma nitrite level in cardiac failure

Citation
G. Ramesh et al., Increased plasma nitrite level in cardiac failure, J MOL CEL C, 31(8), 1999, pp. 1495-1500
Citations number
24
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
ISSN journal
00222828 → ACNP
Volume
31
Issue
8
Year of publication
1999
Pages
1495 - 1500
Database
ISI
SICI code
0022-2828(199908)31:8<1495:IPNLIC>2.0.ZU;2-F
Abstract
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.