Relation of troponin I levels following nonemergent percutaneous coronary intervention to short- and long-term outcomes.
Increases of creatine kinase (CK) and CK-MB cardiac enzymes after nonemergent percutaneous coronary intervention (PCI) have been associated with an increased risk of cardiovascular events during follow-up. However, there are limited data about the incidence and prognostic significance of an isolated increase of cardiac troponin I (cTnI) without an increase in CK-MB after PCI. The aim of this study was to evaluate the impact of an isolated cTnI increase on long-term survival in patients undergoing nonemergent PCI with normal CK-MB levels after PCI. Using the 2004/2005 Cornell Angioplasty Registry, we evaluated the clinical outcomes in 1,601 patients (undergoing elective or urgent PCI) with normal preprocedure cTnI and CK-MB and normal CK-MB levels after the procedure. Patients were divided into 2 groups based on the presence of cTnI increase after PCI. The mean follow-up period was 24.6 +/- 7.6 months. An increase in cTnI was observed in 831 patients (51.9%). Drug-eluting stents were used in 87% of patients and glycoprotein IIb/IIIa inhibitors were administered in 48% of patients. Incidence of in-hospital major adverse cardiovascular events was low, 0.1% versus 0% (p = 1.000), in patients with versus without cTnI increases, respectively. By 2 years of follow-up, Kaplan-Meier survival rates were 94.1% versus 96.4% (log-rank p = 0.020) in those with versus without cTnI increases, respectively. By multivariate Cox regression analysis, an increase in cTnI after PCI (hazard ratio 1.62, 95% confidence interval 1.01 to 2.59, p = 0.047) was an independent predictor of increased long-term mortality. In conclusion, an isolated increase in cTnI after nonemergent PCI is common, not associated with more frequent adverse in-hospital outcomes compared to patients with normal cTnI, and provides long-term prognostic information regarding mortality.
New York Presbyterian Hospital, Weill Cornell Medical College, New York, USA. dnf9001@med.cornell.edu
Dmitriy N
DN
Feldman
Robert M
RM
Minutello
Geoffrey
G
Bergman
Issam
I
Moussa
S Chiu
SC
Wong
D000368:Aged; D000787:Angina Pectoris / Q000453:epidemiology; D015906:Angioplasty, Balloon, Coronary; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000401:mortality* / Q000628:therapy*; D052279:Creatine Kinase, MB Form / Q000097:blood; D054855:Drug-Eluting Stents; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000453:epidemiology; D006801:Humans; D007902:Length of Stay; D008297:Male; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D011379:Prognosis; D012042:Registries; D019210:Troponin I / Q000097:blood*
D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019210:Troponin I; D052279:Creatine Kinase, MB Form