- Poster presentation
- Open Access
Nitric oxide in ischemic heart disease. Defective production or impaired function?
© BioMed Central Ltd. 2004
- Published: 15 March 2004
- Nitric Oxide
- Ischemic Heart Disease
- Smooth Muscle Cell Proliferation
- Coronary Arteriography
- Defective Production
Among the mediators released by coronary arterial endothelium, namely prostacyclin, endothelin, thrombomodulin, and so on, nitric oxide (NO) (i.e. endothelial-derived relaxing factor) has been the subject of our intense research. A biologic link between endothelial damage and atherosclerotic coronary arterial disease has been presumably related to decreased arterial bioavailability of NO through predisposing to leucocyte and platelet adhesion, vasoconstriction and smooth muscle cell proliferation.
The present study is intended to re-evaluate the potential role of NO in the pathophysiology of coronary heart disease through assessing the serum NO metabolites (nitrites and nitrates) in 150 patients (patients) with ischemic heart disease (118 male, 32 female; mean age 53.4 ± 8.3 years, range 33–80 years). Of the latter, 77 patients (51.3%) had unstable angina (AP), and 73 (48.7%) had recent myocardial infarction (MI). Twenty subjects with normal coronary arteriography (15 male, 5 female; mean age 55.4 ± 4.5 years) served as a control group. Of the studied patients, 89 (59%) were smokers, 68 (45%) were diabetics, 60 (40%) were hypertensives and 63 (43%) were dyslipidemic.
Following clinical evaluation including 12-lead ECG, all patients were subjected to routine laboratory testing (including liver and kidney functions, lipid profile, CBC, and random blood sugar). Specific laboratory tests included serum fibrinogen and plasma NO expressed as its metabolites, nitrites and nitrates (NOx), as measured by the Griess reaction.
All patients and controls were subjected to diagnostic coronary arteriography with assessment of the extent of coronary disease (number of affected vessels) as well as the severity of stenosis (using the Gensini scoring system).
Compared with the control group, ischemic patients had significantly lower levels of NOx (52.8 ± 7.3 vs 15.8 ± 7.3, P < 0.000) with a significantly lower level of NOx in the MI group compared with the AP group (22.1 ± 3.4 vs 9 ± 2.3, P < 0.000). No significant correlation either with the extent or the severity of coronary artery disease was shown.
Furthermore, compared with nonsmokers, smokers with ischemic heart disease exhibited significantly lower levels of serum NOx (28.5 ± 14.2 vs 13.8 ± 10.3, P < 0.002). Other risk factors (dyslipidemia, hypertension, diabetes mellitus [DM]) in the ischemic group did not show any significant correlation with serum NOx level (P = 0.1, P = 0.09, P = 0.1, respectively).
In conclusion, although NO plays a major role in mediating coronary arterial dilation under healthy condition, it is substantially defective in coronary arterial disease, yet the poor correlation with DM and dyslipidemia (diseases primarily characterized by endothelial dysfunction) would point to impaired NO function rather than just defective production.