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1.
Korean Journal of Medicine ; : 535-541, 2003.
Article in Korean | WPRIM | ID: wpr-48803

ABSTRACT

BACKGROUND: There is increasing evidence that inflammation is an important determinant of the development of atherosclerosis and that oxidation of low-density lipoprotein (LDL) obviously plays an important role in the pathogenesis of atherosclerosis. We assessed the levels of oxidized LDL and inflammatory markers in patients with ischemic heart disease and normal group who has normal coronary angiograms. METHODS: Coronary angiography was performed in 142 patients. 107 patients of ischemic heart disease (stable angina pectoris 58, unstable angina pectoris 30, acute myocardial infarction 19) and 38 normal control subjects. We assessed the level of oxidized LDL and inflammatory markers, such as CRP, ESR, fibrinogen and leukocyte. RESULTS: CRP was 3.88+/-2.05 mg/dL in acute myocardial infarction group, and 0.29+/-0.15 mg/dL in normal control subject group (p<0.05). Fibrinogen was 541.6+/-45.1 mg/dL in acute myocardial infarction group, 321.4+/-25.6 mg/dL in normal control subject group (p<0.05). Leukocyte was 10942.1+/-737.6/mm3 in acute myocardial infarction group, 6394.3+/-235.1/mm3 in normal control subject group (p<0.05). Oxidized LDL was 23.0+/-4.0 EU/mL in acute myocardial infarction group, and 16.2+/-1.5 EU/mL in normal control subject group (p<0.05). CRP, ESR and fibrinogen values of the patients with stable angina pectoris and unstable angina pectoris were higher than that of normal control group, but there were no statistical significance. Oxidized LDL (ox-LDL) and Leukocyte value of the patients with unstable angina pectoris, acute myocardial infarction was significantly higher than that of the patients with stable angina pectoris and normal control subjects (p<0.05). CRP, ESR and fibrinogen values of the patients with acute myocardial infarction were also higher than that of normal control subjects. CONCLUSION: This study demonstrate that CRP, fibrinogen and oxidized LDL, leukocyte values of acute myocardial infarction group were significantly higher than that of control group and stable, unstable angina pectoris group. Oxidized LDL and Leucokyte values were also significantly elevated in unstable angina group, but CRP values were not in unstable angina group.


Subject(s)
Humans , Angina Pectoris , Angina, Stable , Angina, Unstable , Atherosclerosis , Coronary Angiography , Fibrinogen , Inflammation , Leukocytes , Lipoproteins , Myocardial Infarction , Myocardial Ischemia
2.
Korean Circulation Journal ; : 1267-1273, 2001.
Article in Korean | WPRIM | ID: wpr-102904

ABSTRACT

BACKGROUND AND OBJECTIVES: Nicorandil has pharmacologic effects similar to nitroglycerin and potassium in respect to the channel opening action in vascular smooth muscle cells. We examined hemodynamic changes in patients following nicorandil infusion. We investigated the action mechanism of nicorandil, and whether nicorandil affects hemodynamic changes in patients receiving antianginal medication. SUBJECTS AND METHODS: A total of 17 patients (11 normal control group, 6 coronary artery disease group) undergoing cardiac catheterization for investigation of chest pain participated in this study. During cardiac catheterization, nicorandil was infused into the pulmonary artery at a dose of 80 microgram/kg over a period of 1 min. Hemodynamic parameters were measured before and at 5, 10 and 20 minutes after nicorandil infusion. RESULTS: Five minutes after nicorandil infusion, the maximal changes in preload and afterload hemodynamic parameters were observed in both the coronary artery disease and control group. Changes of preload parameters were sustained longer than those of afterload parameters, and were maintained until 20 minutes after the infusion. Afterload parameters (heart rate and cardiac output), were slowly normalized five minutes after the infusion. In the coronary artery disease group with antianginal medication, additive hemodynamic changes were also seen after the infusion, although the degree of changes were small. CONCLUSION: Following nicorandil infusion, both the preload and afterload hemodynamic parameters decreased, and the preload parameters showed a larger decrease for a longer period than the afterload parameters. In the coronary artery disease group with antianginal medication, additive hemodynamic changes were also seen following nicorandil infusion.


Subject(s)
Humans , Angina Pectoris , Cardiac Catheterization , Cardiac Catheters , Chest Pain , Coronary Artery Disease , Coronary Vessels , Hemodynamics , Muscle, Smooth, Vascular , Nicorandil , Nitroglycerin , Potassium , Pulmonary Artery
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