TY - JOUR
T1 - Relation of Troponin I Levels Following Nonemergent Percutaneous Coronary Intervention to Short- and Long-Term Outcomes
AU - Feldman, Dmitriy N.
AU - Minutello, Robert M.
AU - Bergman, Geoffrey
AU - Moussa, Issam
AU - Wong, S. Chiu
PY - 2009/11/1
Y1 - 2009/11/1
N2 - 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.
AB - 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.
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U2 - 10.1016/j.amjcard.2009.06.032
DO - 10.1016/j.amjcard.2009.06.032
M3 - Article
C2 - 19840564
AN - SCOPUS:71749098583
SN - 0002-9149
VL - 104
SP - 1210
EP - 1215
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 9
ER -