ELEVATION OF C-REACTIVE PROTEIN IN ACTIVE CORONARY-ARTERY DISEASE

被引:473
作者
BERK, BC [1 ]
WEINTRAUB, WS [1 ]
ALEXANDER, RW [1 ]
机构
[1] HARVARD UNIV, BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED, DIV CARDIOVASC, BOSTON, MA 02115 USA
关键词
D O I
10.1016/0002-9149(90)90079-G
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Unstable angina occurs most commonly in the setting of atherosclerotic coronary artery disease (CAD), but there is little information concerning the mechanisms responsible for the transition from clinically stable to unstable coronary atherosclerotic plaque. Recently, increased focal infiltration of inflammatory cells into the adventitia of coronary arteries of patients dying suddenly from CAD and activation of circulating neutrophils in patients with unstable angina have been observed. To characterize the presence of inflammation in "active" atherosclerotic lesions, the acute phase reactant C-reactive protein (CRP) was measured in 37 patients admitted to the coronary care unit with unstable angina, 30 patients admitted to the coronary care unit with nonischemic illnesses and 32 patients with stable CAD. CRP levels were significantly elevated (normal < 0.6 mg/dl) in 90% of the unstable angina group compared to 20% of the coronary care unit group and 13% of the stable angina group. The average CRP values were significantly different (p = 0.001) for the unstable angina group (2.2 ± 2.9 mg/dl) compared to the coronary care (0.9 ± 0.7 mg/dl) and stable angina (0.7 ± 0.2 mg/ dl) groups. There was a trend for unstable angina patients wtth ischemic ST-T-wave abnormalities to have higher CRP values (2.6 ± 3.4) than those without etectrocardiographic changes (1.3 ± 0.9, p = 0.1). The data demonstrate increased levels of an acute phase reactant in unstable angina. These findings suggest that an inflammatory component in "active" angina may contribute to the susceptibility of these patients to vasospasm and thrombosis. © 1990.
引用
收藏
页码:168 / 172
页数:5
相关论文
共 29 条
[1]   INTERLEUKIN-1 INHIBITS CONTRACTION OF VASCULAR SMOOTH-MUSCLE [J].
BEASLEY, D ;
COHEN, RA ;
LEVINSKY, NG .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 83 (01) :331-335
[2]   VASOCONSTRICTION - A NEW ACTIVITY FOR PLATELET-DERIVED GROWTH-FACTOR [J].
BERK, BC ;
ALEXANDER, RW ;
BROCK, TA ;
GIMBRONE, MA ;
WEBB, RC .
SCIENCE, 1986, 232 (4746) :87-90
[3]   INTERLEUKIN-1 (IL-1) INDUCES BIOSYNTHESIS AND CELL-SURFACE EXPRESSION OF PROCOAGULANT ACTIVITY IN HUMAN VASCULAR ENDOTHELIAL-CELLS [J].
BEVILACQUA, MP ;
POBER, JS ;
MAJEAU, GR ;
COTRAN, RS ;
GIMBRONE, MA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1984, 160 (02) :618-623
[4]  
DEBEER FC, 1982, BRIT HEART J, V47, P239
[5]   LEUKOCYTES AND THE RISK OF ISCHEMIC DISEASES [J].
ERNST, E ;
HAMMERSCHMIDT, DE ;
BAGGE, U ;
MATRAI, A ;
DORMANDY, JA .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1987, 257 (17) :2318-2324
[6]   UNSTABLE ANGINA WITH FATAL OUTCOME - DYNAMIC CORONARY THROMBOSIS LEADING TO INFARCTION AND OR SUDDEN-DEATH - AUTOPSY EVIDENCE OF RECURRENT MURAL THROMBOSIS WITH PERIPHERAL EMBOLIZATION CULMINATING IN TOTAL VASCULAR OCCLUSION [J].
FALK, E .
CIRCULATION, 1985, 71 (04) :699-708
[7]   LEUKOCYTE COUNT AS A PREDICTOR OF MYOCARDIAL-INFARCTION [J].
FRIEDMAN, GD ;
KLATSKY, AL ;
SIEGELAUB, AB .
NEW ENGLAND JOURNAL OF MEDICINE, 1974, 290 (23) :1275-1278
[8]  
GERRITY RG, 1981, AM J PATHOL, V103, P181
[9]  
GEWURZ H, 1982, ADV INTERNAL MED, V27, P345
[10]  
JONASSON L, 1988, LAB INVEST, V58, P310