Can C reactive protein or troponins T and I predict outcome in patients with intractable unstable angina?
- aDepartment of Cardiology, Royal Brompton Hospital, London SW3, UK, bDepartment of Chemical Pathology, Royal Brompton Hospital
- Dr N Curzen, Department of Cardiology, The London Chest Hospital, Bonner Road, London E2 9JX, UK.
- Accepted 16 February 1998
Abstract
Objective To determine whether a single blood test for the measurement of C reactive protein, or troponin I or T concentrations could be used to stratify patients with intractable unstable angina awaiting transfer for coronary angiography by correlating these values with coronary anatomy and transient myocardial ischaemia.
Design Prospective study.
Setting Tertiary cardiac unit.
Patients All patients admitted to their local hospital with ischaemic chest pain, uncontrolled by medical treatment, in whom acute myocardial infarction had been excluded by serial measurement of creatine kinase and lack of Q waves on ECG.
Intervention Coronary angiography and ST segment monitoring for 24 hours.
Main outcome measures Concentrations of C reactive protein, troponins T and I, coronary anatomy, presence of transient myocardial ischaemia.
Results Median C reactive protein, troponin I, and troponin T concentrations were 17.1 mg/dl (4.8 to 203.9), 0.05 μg/l (0 to 7.8), and 0.0 μg/l (0 to 2.51), respectively. Seven patients (10%) had normal coronaries and 14, 20, and 31 had one, two, or three vessel coronary disease, respectively. Nineteen (26%) had transient myocardial ischaemia, 33 (46%) had complex lesion morphology, and six (8%) had intracoronary thrombus. Of the three markers, troponin T alone was higher in patients with multivessel disease (p < 0.05) and in those with transient myocardial ischaemia (p < 0.05), but there was no significant relation between C reactive protein, troponin T or I and lesion morphology or thrombus.
Conclusions In patients transferred to a tertiary centre with intractable chest pain, C reactive protein and troponin I are not predictive of transient myocardial ischaemia or lesion morphology, both of which are surrogate markers of outcome. Troponin T is, however, raised in patients with multivessel disease or transient myocardial ischaemia. These serum protein assays cannot be used to stratify the risk of patients with unstable angina who are awaiting transfer to the tertiary centre.
