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C-reactive protein, infarct size, microvascular obstruction, and left-ventricular remodelling following acute
Stein Ørn1, Cord Manhenke, Thor Ueland
1Division of Cardiology, Stavanger University Hospital, PO 8400, 4068 Stavanger, Norway. drsteinorn@hotmail.com
Insights
Elevated C-reactive protein after percutaneous coronary intervention (PCI) for ST elevation myocardial infarction (MI) correlates with infarct size and left-ventricular remodelling. This suggests C-reactive protein plays a role in myocardial damage.
Area of Science:
- Cardiology
- Immunology
- Biomarkers
Background:
- ST elevation myocardial infarction (MI) requires timely revascularization.
- Left-ventricular (LV) remodelling and infarct size impact long-term prognosis.
- Inflammatory processes are implicated in myocardial injury post-MI.
Purpose of the Study:
- To assess the relationship between inflammatory mediators and infarct size/LV remodelling after primary percutaneous coronary intervention (PCI).
- To investigate the role of C-reactive protein (CRP) and other inflammatory markers in myocardial damage following MI.
Main Methods:
- Serial cardiac magnetic resonance (CMR) imaging for infarct size, microvascular obstruction (MO), and LV remodelling.
- Analysis of plasma inflammatory mediators (CRP, IL-6, TCC) before and after PCI.
- Recruitment of 42 patients with first-time MI and single-vessel occlusion.
Main Results:
- Plasma CRP, IL-6, and TCC increased post-PCI, peaking at 2 days.
- CRP levels at 2 days post-PCI correlated significantly with infarct size and LV remodelling at 2 months.
- Persistent MO was associated with higher CRP levels 2 days post-PCI.
Conclusions:
- The rapid increase in CRP post-PCI reflects inflammation in the infarcted area.
- CRP may serve as both a marker and mediator of myocardial damage via complement activation.
- Findings support CRP's role in assessing outcomes after MI revascularization.
Aims:
This study assessed the relationship between inflammatory mediators and indices of infarct size and left-ventricular (LV) remodelling following successful primary percutaneous coronary intervention (PCI) in patients with first time ST elevation myocardial infarction (MI).
Methods And Results:
Forty-two patients admitted with an occluded single vessel were recruited consecutively. Cardiac magnetic resonance was used for serial assessment (2 days, 1 week, 2 months) of infarct size, microvascular obstruction (MO), and LV remodelling. Inflammatory mediators were analysed before and after PCI. Our major findings were: (1) Following PCI, there was a marked increase in plasma levels of C-reactive protein, closely correlated with an increase in interleukin-6 and terminal complement complex, reaching maximum 2 days after PCI; (2) C-reactive protein 2 days after PCI was significantly correlated with infarct size and parameters of LV remodelling 2 months after PCI; (3) Patients with persistent MO had significantly higher C-reactive protein levels 2 days following PCI.
Conclusion:
We suggest that the rapid increase in C-reactive protein levels in this model of successful revascularization of a single, totally occluded vessel reflects the degree of inflammation within the infarcted area. Our findings support a role for C-reactive protein-mediated complement activation as both a marker and mediator of myocardial damage following MI. Clinical study no.: NCT 00465868.
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