Can C reactive protein or troponins T and I predict outcome in patients with intractable unstable angina?
N P Curzen1, D J Patel, M Kemp
1Department of Cardiology, Royal Brompton Hospital, London, UK.
Insights
C-reactive protein and troponin I do not predict outcomes in unstable angina patients. Troponin T levels correlate with multivessel disease and transient ischemia, but these blood tests cannot stratify risk for patients awaiting transfer.
Area of Science:
- Cardiology
- Biomarkers
- Ischemic Heart Disease
Background:
- Unstable angina requires risk stratification for optimal management.
- Accurate prediction of coronary anatomy and ischemia is crucial for patients awaiting transfer.
Purpose of the Study:
- To evaluate C-reactive protein, troponin I, and troponin T as predictors of coronary anatomy and transient myocardial ischemia in unstable angina patients.
- To determine if these biomarkers can stratify risk in patients with intractable chest pain.
Main Methods:
- Prospective study in a tertiary cardiac unit.
- Measured C-reactive protein, troponin I, and troponin T in patients with unstable angina.
- Correlated biomarker levels with coronary angiography findings and 24-hour ST segment monitoring.
Main Results:
- Troponin T levels were significantly higher in patients with multivessel disease and transient myocardial ischemia.
- C-reactive protein, troponin I, and troponin T did not correlate with lesion morphology or intracoronary thrombus.
- Seven patients had normal coronaries, while others showed varying degrees of coronary disease.
Conclusions:
- Troponin T may indicate multivessel disease or transient ischemia in unstable angina.
- C-reactive protein and troponin I are not reliable predictors of outcome in this patient group.
- Current serum protein assays are insufficient for risk stratification of unstable angina patients awaiting transfer.
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 microgram/l (0 to 7.8), and 0.0 microgram/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.
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