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C-reactive protein and coronary artery disease.
Jpn Heart J. 2002 Nov; 43(6):607-19.JH

Abstract

Evidence suggests that inflammation plays a key role in the pathogenesis of atherosclerosis. The chronic inflammatory process can develop to an acute clinical event by the induction of plaque rupture and therefore cause acute coronary syndromes. The aim of this study was to determine the serum levels of the circulating acute-phase reactant C-reactive protein (CRP), which is a sensitive indicator of inflammation, in patients with chronic stable coronary artery disease (CAD) and acute coronary syndromes (ACS). We studied 56 subjects: 1) 25 consecutive patients (18 men, 7 women; mean age, 68.5 +/- 14.3 years, range, 40-86) with unstable angina (UA) or acute myocardial infarction (AMI); 2) 31 consecutive patients (25 men, 6 women; mean age 64 +/- 12.7; range, 47-83, years) with signs and symptoms of clinically stable CAD. High-sensitivity-C-reactive protein (hs-CRP) levels were determined with a commercially available enzyme-linked immunoassay method. In patients with unstable angina and AMI before reperfusion therapy, CRP levels were not significantly different to those in patients with stable CAD (5.96 +/- 2.26 versus 4.35 +/- 2.6 mg/L; P = 0.12), but tended to be higher in patients with unstable angina and AMI. Baseline CRP levels in the subgroup of patients with AMI (6.49 +/- 2.28 mg/L) were significantly higher than levels in patients with stable CAD (4.35 +/- 2.6 mg/L; P = 0.02). CRP levels in patients with unstable angina and AMI were measured four times during a 72-hour period (0, 12, 24, and 72 hours). The lowest value was observed at baseline and differed significantly from values measured at any other time of the observation period (P < 0.001; 5.96 +/- 2.26; 9.5 +/- 9.04, 18.25 +/- 11.02; 20.25 +/- 10.61). CRP levels after 12, 24, and 72 hours were also significantly different to the initial values for patients with stable CAD (P < 0.01). There was no correlation between CRP and creatine kinase (CK), CK-MB isoenzyme, or troponin I positivity as markers for the extent of the myocardial injury during the observation period. Baseline levels of serum CRP tended to be higher in patients with unstable angina or AMI but were not significantly different from levels in patients with chronic stable CAD. In the subgroup of patients with AMI, baseline CRP levels were significantly higher than the levels in patients with stable CAD. CRP as a marker of inflammation is significantly increased in patients with AMI and unstable angina shortly after the onset of symptoms (after a period of 12 hours), supporting the hypothesis of an activation of inflammatory mechanisms in patients with an acute coronary syndrome or AMI.

Authors+Show Affiliations

Department of Internal Medicine II/Cardiology and Intensive Care, General Hospital Wels, Grieslirchnerstrasse 42, A-4600 Wels, Austria.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12558125

Citation

Auer, Johann, et al. "C-reactive Protein and Coronary Artery Disease." Japanese Heart Journal, vol. 43, no. 6, 2002, pp. 607-19.
Auer J, Berent R, Lassnig E, et al. C-reactive protein and coronary artery disease. Jpn Heart J. 2002;43(6):607-19.
Auer, J., Berent, R., Lassnig, E., & Eber, B. (2002). C-reactive protein and coronary artery disease. Japanese Heart Journal, 43(6), 607-19.
Auer J, et al. C-reactive Protein and Coronary Artery Disease. Jpn Heart J. 2002;43(6):607-19. PubMed PMID: 12558125.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - C-reactive protein and coronary artery disease. AU - Auer,Johann, AU - Berent,Robert, AU - Lassnig,Elisabeth, AU - Eber,Bernd, PY - 2003/2/1/pubmed PY - 2003/2/21/medline PY - 2003/2/1/entrez SP - 607 EP - 19 JF - Japanese heart journal JO - Jpn Heart J VL - 43 IS - 6 N2 - Evidence suggests that inflammation plays a key role in the pathogenesis of atherosclerosis. The chronic inflammatory process can develop to an acute clinical event by the induction of plaque rupture and therefore cause acute coronary syndromes. The aim of this study was to determine the serum levels of the circulating acute-phase reactant C-reactive protein (CRP), which is a sensitive indicator of inflammation, in patients with chronic stable coronary artery disease (CAD) and acute coronary syndromes (ACS). We studied 56 subjects: 1) 25 consecutive patients (18 men, 7 women; mean age, 68.5 +/- 14.3 years, range, 40-86) with unstable angina (UA) or acute myocardial infarction (AMI); 2) 31 consecutive patients (25 men, 6 women; mean age 64 +/- 12.7; range, 47-83, years) with signs and symptoms of clinically stable CAD. High-sensitivity-C-reactive protein (hs-CRP) levels were determined with a commercially available enzyme-linked immunoassay method. In patients with unstable angina and AMI before reperfusion therapy, CRP levels were not significantly different to those in patients with stable CAD (5.96 +/- 2.26 versus 4.35 +/- 2.6 mg/L; P = 0.12), but tended to be higher in patients with unstable angina and AMI. Baseline CRP levels in the subgroup of patients with AMI (6.49 +/- 2.28 mg/L) were significantly higher than levels in patients with stable CAD (4.35 +/- 2.6 mg/L; P = 0.02). CRP levels in patients with unstable angina and AMI were measured four times during a 72-hour period (0, 12, 24, and 72 hours). The lowest value was observed at baseline and differed significantly from values measured at any other time of the observation period (P < 0.001; 5.96 +/- 2.26; 9.5 +/- 9.04, 18.25 +/- 11.02; 20.25 +/- 10.61). CRP levels after 12, 24, and 72 hours were also significantly different to the initial values for patients with stable CAD (P < 0.01). There was no correlation between CRP and creatine kinase (CK), CK-MB isoenzyme, or troponin I positivity as markers for the extent of the myocardial injury during the observation period. Baseline levels of serum CRP tended to be higher in patients with unstable angina or AMI but were not significantly different from levels in patients with chronic stable CAD. In the subgroup of patients with AMI, baseline CRP levels were significantly higher than the levels in patients with stable CAD. CRP as a marker of inflammation is significantly increased in patients with AMI and unstable angina shortly after the onset of symptoms (after a period of 12 hours), supporting the hypothesis of an activation of inflammatory mechanisms in patients with an acute coronary syndrome or AMI. SN - 0021-4868 UR - https://www.unboundmedicine.com/medline/citation/12558125/C_reactive_protein_and_coronary_artery_disease_ L2 - http://joi.jlc.jst.go.jp/JST.JSTAGE/jhj/43.607?from=PubMed DB - PRIME DP - Unbound Medicine ER -