Coronary artery disease
Relation of Troponin I Levels Following Nonemergent Percutaneous Coronary Intervention to Short- and Long-Term Outcomes

https://doi.org/10.1016/j.amjcard.2009.06.032Get rights and content

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.

Section snippets

Methods

All patients undergoing PCI at the New York Presbyterian Hospital, Weill Cornell Medical College (New York, New York) are enrolled in the Cornell Angioplasty Registry. A standard case-report form delineating comprehensive patient demographics, preintervention clinical status, procedural findings, and in-hospital complications is completed for each PCI performed. Immediate and in-hospital events are recorded. Patient follow-up is obtained by publicly available mortality data through the Social

Results

There were 3,611 PCIs performed in 2,504 consecutive patients undergoing urgent or elective PCI during the defined period. Of these, 693 patients had increased baseline cTnI, 227 had increased baseline CK-MB, and 496 had increased CK-MB level after PCI. The remaining 1,601 patients were included in the final analysis. There were 831 patients (51.9%) with increased cTnI levels (median 0.20 ng/ml, mean ± SD 0.55 ± 1.7 ng/ml) after PCI. The distribution of patients with increased cTnI levels

Discussion

This study represents a contemporary evaluation of short- and long-term outcomes in patients with normal cTnI and CK-MB before PCI and normal CK-MB levels after nonemergent PCI. There are several major findings in the present study of patients with normal baseline cTnI: (1) an isolated increase in cTnI after PCI occurs very commonly in ∼50% of patients; (2) patients with an isolated increase in cTnI after elective PCI are at very low risk for adverse in-hospital cardiac events; (3) an increase

Acknowledgment

We acknowledge several limitations in this study. First, our analysis was derived from a single high-volume tertiary care center population. Second, although data in the present study were collected prospectively, this is a retrospective analysis and is subject to the limitations of such analyses. Third, independent core angiographic laboratory analysis of baseline and postprocedural angiograms was not performed, which may have provided additional procedural information about predictors of cTnI

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