There is little information about the relation between mild cardiac troponin I (cTn-I)
increase after coronary interventions and late outcome. We therefore focused on the
long-term outcome and the clinical, morphologic, and procedural correlates of elevation
of cTn-I compared with cardiac troponin T, creatine kinase (CK), CK-MB activity and
mass, and myoglobin in 105 patients with successful elective percutaneous transluminal
coronary angioplasty (PTCA) for stable or unstable angina. Patients with myocardial
infarction and those with unstable angina who had a detectable increase in serum markers
before PTCA were excluded. Markers were measured before and after the procedure and
for 2 days. Patients were followed up to record recurrent angina, myocardial infarction,
cardiac death, repeat PTCA, or elective coronary artery bypass graft surgery. Procedure
success was achieved in all cases. Elevation in cTn-I (> or =0.1 microg/L) was observed
in 23 of 105 patients (22%) (median peak: 0.25 microg/L); 18% had cardiac troponin
T (cTn-T) release (> or = 0.1 microg/L, median peak 0.21); 11.4% CK-MB mass (> or
=5 microg/L), and 7.6% myoglobin (> or =90 microg/L) release. Five and 2 patients
had elevated CK and CK-MB activity, respectively. Fourteen of 18 patients with cTn-T
elevation had a corresponding elevation in cTn-I (kappa 0.68; p = 0.001). Patients
positive for cTn-I had more unstable angina (p = 0.042) and heparin before PTCA (p
= 0.046), and had longest total time (p = 0.004) and single inflation (p = 0.01).
By multivariate logistic regression, predictors of postprocedure cTnI elevation were
maximum time of each inflation (odds ratio 9.2; p = 0.0012), type B lesions (odds
ratio 6.6; p = 0.013), unstable angina (p = 0.041), and age > or =60 years (p = 0.032).
Clinical follow-up was available in 103 patients (98%) (mean 19+/-10 months). Kaplan-Meier
survival analysis showed that cTn-I elevation was not an important correlate of cardiac
events (p = 0.34, by log-rank analysis). The incidence of recurrent angina, myocardial
infarction, cardiac death, and repeat revascularization after 12 months was not different
in patients positive or negative for cTn-I. We conclude that cTn-I elevation after
successful PTCA is not associated with significantly worse late clinical outcome.
Levels of cTn-I allow a much higher diagnostic accuracy in detecting minor myocardial
injury after PTCA compared with other markers, but there is no association with periprocedural
myocardial cell injury and late outcome when cTn-I and other markers are considered.