Elevation of C-reactive protein in “active” coronary artery disease

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Abstract

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.

References (29)

  • N Stratford et al.

    Inflammatory infiltrates in human coronary atherosclerosis

    Atherosclerosis

    (1986)
  • A Maseri et al.

    Pathogenetic mechanisms underlying the clinical events associated with atherosclerotic heart disease

    Circulation

    (1980)
  • E Falk

    Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death

    Circulation

    (1985)
  • JB Mandelson et al.

    Intracoronary thrombus in nontransmural myocardial infarction and unstable angina pectoris

    Am J Cardiol

    (1983)
  • RG Gerrity

    The role of the monocyte in atherogenesis

    Am J Pathol

    (1981)
  • K Kohchi et al.

    Significance of adventitial inflammation of the coronary artery in patients with unstable angina: results at autopsy

    Circulation

    (1985)
  • A Pomerance

    Peri-arterial mast cells in coronary atheroma and thrombosis

    J Pathol Bact

    (1958)
  • MP Bevilacqua et al.

    Interleukin 1 (IL-1) induces biosynthesis and surface expression of procoagulant activity in human vascular endothelial cells

    J Exp Med

    (1984)
  • D Beasley et al.

    Interleukin 1 inhibits contraction of vascular smooth muscle

    J Clin Invest

    (1989)
  • PS Libby et al.

    Interleukin-1: a mitogen for human vascular smooth muscle cells that induces the release of growth-inhibitory prostanoids

    J Clin Invest

    (1988)
  • H Gewurz et al.

    C-reactive protein and the acute phase response

    Adv Intern Med

    (1982)
  • HD Lewis et al.

    Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina

    N Engl J Med

    (1983)
  • Beckman Instruction Manual 015-245559. ICS (TM) C-reactive protein reagent. Bera, California: Beckman Instruments,...
  • FC deBeer et al.

    Measurement of serum C-reactive protein concentration in myocardial ischaemia and infarction

    Br Heart J

    (1982)
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    This study was supported in part by grants HL22602 and HL07049 from the National Institutes of Health, Bethesda, Maryland.

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