1982HeartOpen access

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

Frederick C. de Beer, C R Hind, Keith A.A. Fox, R. Marshall Allan, A Maseri, Mark B. Pepys

Open full text 358 citations

Abstract

Serum C-reactive protein (CRP) and creatine kinase (CK) MB levels were measured prospectively in patients with definite myocardial infarction, patients with spontaneous or exercise-induced 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.

Open-access reader

About this research paper

What this paper is about

Serum C-reactive protein (CRP) and creatine kinase (CK) MB levels were measured prospectively in patients with definite myocardial infarction, patients with spontaneous or exercise-induced 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.

Why it matters

OpenAlex reports 358 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Serum C-reactive protein (CRP) and creatine kinase (CK) MB levels were measured prospectively in patients with definite myocardial infarction, patients with spontaneous or exercise-induced 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.

Key concepts: Medicine, Myocardial infarction, C-reactive protein, Internal medicine, Chest pain, Infarction, Creatine kinase, Cardiology

Related papers

Back to paper searchBrowse research topicsOriginal source
Measurement of serum C-reactive protein concentration in myocardial ischaemia and infarction. — Research Paper | ScholarLens