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

Abstract

SUMMARY Serum C-reactive protein (CRP) and creatine kinase (CK) MB levels were measured prospectively in patients with definite myocardial infarction, patients with spontaneous or exerciseinduced angina, subjects undergoing coronary arteriography, and patients with non-cardiac chest pain. All individuals with infarction developed raised CRP levels and there was a significant correlation between the peak CRP and CK MB values. The CRP, however, peaked around 50 hours after the onset of pain at a time when the CK MB, which peaked after about 15 hours, had already returned to normal. In 20 patients who recovered uneventfully, CRP levels fell, returning to normal about seven days after infarction in four cases who were followed to this point. In eight complicated cases, including four who died within the first 10 days, the CRP level remained high. Angina alone or coronary arteriography did not cause a rise in the CRP or CK MB concentrations. Increased CRP production is a non-specific response to tissue injury and raised CRP levels in cases of chest pain with a normal CK MB indicated a pathological process other than myocardial infarction. Regular monitoring of CRP levels may also assist in early recognition of intercurrent complications occurring after myocardial infarction.Differential diagnosis of myocardial infarction from other causes of chest pain is a common clinical problem. Even when the diagnosis is established there are many difficult questions such as: recognition of myocardial necrosis in patients with known ischaemic heart disease, recognition of intercurrent complications in the post-infarct period, prognosis in the immediate post-infarct period, and assessment of convalescent infarct patients for discharge from the coronary care unit to the ward, and from ward to home.C

C-Reactive Protein: Eighty Years from Discovery to Emergence as a Major Risk Marker for Cardiovascular Disease

“…Notable among these reports were data from Frederick de Beer, Brad Berk, and Wayne Alexander (16,17 ), who described increased CRP concentrations among patients with "active" coronary disease, as well as highly influential studies from Attilio Maseri, Giovanna Liuzzo, Luigi Biasucci, and Frits Haverkate (18,19 ), in which increased concentrations of CRP were again observed among those with unstable angina or chronic atherothrombotic disease. Because concentrations of CRP increase after myocardial ischemia, however, these studies of individuals with known vascular disease were not informative regarding the key question of whether CRP concentrations are increased in advance of disease expression.…”

C‐reactive protein as a marker for active coronary artery disease in patients with chest pain in the emergency room

“…8 Earlier studies have examined CRP concentrations during the course of acute myocardial infarction. 9 These studies were followed by several angiographic series and by cross-sectional and case-control studies, suggesting that CRP concentrations correlated directly with the presence and severity of coronary, cerebral, and peripheral arterial atherosclerosis. [10][11][12] In addition, various studies examined CRP concentrations among patients with angina pectoris.…”

C-Reactive Protein and Asymmetric Dimethylarginine: Markers or Mediators in Cardiovascular Disorders?

“…C-reactive protein had been characterised as an acute phase protein. One of the first reports of CRP as a cardiovascular risk factor came from observations that circulating concentrations of CRP were increased following myocardial infarction [5]. This was followed by a study of a cohort of patients with unstable angina where higher concentrations of CRP correlated with poor outcome [6].…”