Key result
In patients with intractable unstable angina, troponin T concentrations were significantly higher in those with multivessel disease or transient myocardial ischaemia (p < 0.05).
Why the study?
Can C reactive protein, troponin I, or troponin T predict coronary anatomy and transient myocardial ischaemia in patients with intractable unstable angina?
Observational (n=72)
No
Can C reactive protein, troponin I, or troponin T predict coronary anatomy and transient myocardial ischaemia in patients with intractable unstable angina?
p-value: p=<0.05
In patients with intractable unstable angina, troponin T is associated with multivessel disease and transient ischemia, but single measurements of CRP, TnI, and TnT are insufficient to stratify risk for tertiary transfer.
Troponin T was associated with multivessel disease in unstable angina; single measurements leave predictive utility for transfer unresolved.
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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Curzen et al. (1998) conducted an observational in Intractable unstable angina (n=72). C reactive protein, troponin I, and troponin T concentrations was evaluated on Coronary anatomy and presence of transient myocardial ischaemia (p=<0.05). In patients with intractable unstable angina, troponin T concentrations were significantly higher in those with multivessel disease or transient myocardial ischaemia (p < 0.05).
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