SummaryBackground: Plasma nitritehitrate (NOx) is a stable end product of the vasodilator nitric oxide (NO). However, there are few reports about plasma NOx levels in humans.Hypotlzrsis: The purpose of this study was to assess the availability of plasma NOx for evaluating basal endogenously-synthesized or endothelium-derived NO, and to examine whether NOx levels are lowered in patients with coronary artery disease (CAD) or its risk factors.Metlzods: Plasma NOx levels were measured using an automated system based on the Griess reaction. NOx levels for a 24-h period reproducibly became lowest at 6 A.M. in restricted healthy volunteers, and became stable in inpatient volunteers at 6 A.M. within 4 days after admission.Remlts: Based on these findings, NOx levels at 6 A.M. in inpatients can be considered as the basal levels. In 40 inpatients suspected of CAD (28 men, 12 women; mean age 60 f 1 1 years), the basal levels of NOx were not related to CAD and its risk factors, except for hypercholesteroleniia. The NOx level of patients with hypercholesterolemia was significantly lower than that ofpatients with normal cholesterol (n = 16,34 16 pmol/l vs. n = 24,49 k 23 pmoVI, p < 0.03). Furthermore, the NOx levels coirelated negatively with the total cholesterol and low-density lipoprotein cholesterol levels (r = -0.40, p < 0.01 ; r = -0.37, p < 0.003, respectively), but not with other lipid fraction levels.

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ndothelial dysfunction, which can be proved by demonstrating loss of acetylcholine-induced vasodilation, is an early event of atherosclerosis in human coronary arteries 1,2 and seems to accelerate the progression of the atherosclerotic process. 3 In clinical studies, selective loss of endothelium-dependent vasodilation in response to acetylcholine (ACh) has been observed in not only angiographically atherosclerotic coronary arteries, but also in normal coronary arteries of hypercholesterolemic patients. 4,5 Lipoprotein(a) (Lp(a)) has been associated with ischemic heart disease and myocardial infarction in many epidemiological studies [6][7][8][9][10] and is now considered to be an independent risk factor for cardiovascular diseases. Lp(a) is a lowdensity lipoprotein (LDL) -like particle, so it could be atherogenic and impair endothelial function as does LDL. 11 Recently, Sorensen et al have reported that flow-mediated dilation in femoral artery is inversely related to the Lp(a) level in children with familial hypercholesterolemia, suggesting a contribution by Lp(a) to endothelial dysfunction. 12 A study by Tsurumi et al also revealed that Lp(a) correlated well with endothelial dysfunction in the human coronary artery as well as serum LDL cholesterol. 13 Moreover, patients with diabetes mellitus (DM) showed endothelial dysfunction that was probably caused by hyperglycemia Circulation Journal Vol.66, March 2002and hypertriglyceridemia. [14][15][16] To confirm whether or not Lp(a) has an independent role in endothelial dysfunction, we examined normocholesterolemic and non-diabetic patients with angiographically normal coronary arteries. Methods Study PatientsThe study group consisted of 31 patients (without any angiographically segmental stenoses or irregularities in the coronary arteries), who underwent diagnostic cardiac catheterization for chest pain or abnormal results of a noninvasive stress test. The patients with hypercholesterolemia (serum LDL cholesterol ≥160 mg/dl), hypertriglyceridemia (serum triglyceride ≥400 mg/dl), previous myocardial infarction, valvular heart disease, cardiomyopathies or DM (fasting plasma glucose ≥126 mg/dl) were excluded. Table 1 shows the profile of the patients: there were 14 male and 17 female patients, aged 59.4±9.2 years; 10 were smokers and 10 had a history of elevated blood pressure that resulted in the initiation of antihypertensive therapy by primary physicians. Patients had only been treated with calcium antagonists, not with angiotensin converting enzyme inhibitors or angiotensin II receptor blockers. Because only normocholesterolemic and non-diabetic patients were selected, none had taken any lipid-lowering drugs, including HMG-CoA reductase inhibitors, or anti-diabetic drugs. All women were post menopausal, the result of bilateral oophorocystectomy in one patient (no. 9 in Table 1) and aging in the others. None of the women were receiving estrogen therapy. None of the patients had a family history of early coronary artery disease. The institutional Ethics Committee ap...