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Prognostic implications of C-reactive protein and troponin following percutaneous coronary intervention
Jaroslav Hubacek1, Rashpal S Basran, Fiona M Shrive
1Department of Cardiovascular Sciences and Libin Cardiovascular Institute, University of Calgary, Calgary, Alberta.
Insights
Elevated C-reactive protein (CRP) and acute coronary syndrome predict troponin T (TnT) rise after PCI. However, this TnT rise does not indicate long-term adverse events following uncomplicated PCI.
Area of Science:
- Cardiology
- Biomarkers
- Interventional Cardiology
Background:
- C-reactive protein (CRP) is an inflammation marker implicated in atherosclerosis.
- The link between CRP and troponin T (TnT) elevation post-percutaneous coronary intervention (PCI) is not well-defined.
- Long-term outcomes of TnT increase after PCI require further investigation.
Purpose of the Study:
- To investigate the association between CRP levels and TnT elevation following PCI.
- To assess the long-term prognostic significance of TnT rise after PCI.
Main Methods:
- 1208 patients undergoing successful non-emergent PCI were studied.
- Baseline CRP and TnT levels were measured before and after PCI.
- Two-year follow-up data were collected to evaluate long-term outcomes.
Main Results:
- 20% of patients experienced a significant TnT rise post-PCI.
- Predictors of TnT rise included acute coronary syndrome, no statin use, elevated CRP, and longer stent length.
- Periprocedural TnT rise was not linked to adverse events at two-year follow-up.
Conclusions:
- Myocardial necrosis (indicated by TnT rise) is common after PCI, especially in patients with recent myocardial infarction.
- Statin therapy was associated with a blunted TnT response.
- Uncomplicated PCI with periprocedural TnT rise did not result in long-term adverse sequelae.
Background:
C-reactive protein (CRP), a marker of inflammation, plays a role in the pathophysiology of atherosclerotic events. The relationship between CRP levels and myocardial necrosis assessed by troponin T (TnT) in patients undergoing percutaneous coronary intervention (PCI) has not been established. In addition, the long-term significance of TnT rise following PCI is not clear.
Objectives:
To examine the relationship between CRP and the rise in TnT levels, and evaluate the long-term prognostic implications of TnT rise following PCI.
Methods:
A total of 1208 patients underwent successful nonemergent PCI. Baseline demographic characteristics, CRP and TnT levels were prospectively collected before and 12 h to 18 h following PCI. Long-term follow-up data over two years were available.
Results:
Among the patients studied (mean age 62 years), 64% presented with acute coronary syndrome. A PCI procedure was associated with a significant increase in TnT levels (higher than 0.1 microg/L) in 238 patients (20%). Multivariate logistic regression identified presentation with acute coronary syndrome or myocardial infarction, no statin use at the time of the procedure, increased CRP and increasing length of stent as independent predictors of TnT rise following PCI. Periprocedural TnT rise was not associated with adverse events in follow-up examinations (OR 1.09, 95% CI 0.73 to 1.65).
Conclusions:
Myocardial necrosis commonly occurred in otherwise successful PCI and was particularly prevalent in the proinflammatory milieu of a recent myocardial infarction. This response was blunted with statin therapy. However, there was no long-term adverse sequelae of these troponin rises following otherwise uncomplicated PCI.
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