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Measurement of serum C-reactive protein concentration in myocardial ischaemia and infarction
Insights
Serum C-reactive protein (CRP) is a sensitive marker for myocardial infarction, peaking later than creatine kinase MB (CK MB). Elevated CRP levels in chest pain patients with normal CK MB suggest non-infarction pathology.
Area of Science:
- Biochemistry
- Cardiology
- Immunology
Background:
- Myocardial infarction diagnosis relies on cardiac biomarkers.
- Creatine kinase MB (CK MB) is a traditional marker, but its short half-life can limit detection.
- C-reactive protein (CRP) is an acute-phase reactant indicating inflammation and tissue injury.
Purpose of the Study:
- To prospectively evaluate serum C-reactive protein (CRP) and creatine kinase MB (CK MB) levels in patients with myocardial infarction (MI) and other causes of chest pain.
- To compare the temporal profiles of CRP and CK MB following MI.
- To assess the utility of CRP in differentiating MI from other conditions and in monitoring post-MI complications.
Main Methods:
- Prospective measurement of serum CRP and CK MB levels.
- Inclusion of patients with definite myocardial infarction, angina, coronary arteriography, and non-cardiac chest pain.
- Serial sampling to determine peak levels and time courses of biomarkers.
Main Results:
- All patients with myocardial infarction showed elevated CRP levels.
- A significant correlation existed between peak CRP and CK MB values.
- CRP peaked around 50 hours post-pain onset, significantly later than CK MB (around 15 hours).
- In uncomplicated MI cases, CRP normalized around seven days; in complicated cases, CRP remained elevated.
- Angina or coronary arteriography did not elevate CRP or CK MB.
- Raised CRP with normal CK MB indicated non-MI pathological processes.
Conclusions:
- CRP is a sensitive indicator of myocardial infarction, with a distinct temporal profile compared to CK MB.
- CRP monitoring aids in identifying non-MI causes of chest pain and detecting post-MI complications.
- CRP's sustained elevation suggests ongoing tissue injury or complications after myocardial infarction.
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.