4.7 Article

C-reactive protein, infarct size, microvascular obstruction, and left-ventricular remodelling following acute myocardial infarction

Journal

EUROPEAN HEART JOURNAL
Volume 30, Issue 10, Pages 1180-1186

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehp070

Keywords

Inflammation; C-reactive protein; Interleukin-6; Terminal complement complex; Acute myocardial infarction; Remodelling; Primary percutaneous intervention; Cardiac magnetic resonance

Funding

  1. Helse Vest [911017]
  2. Norwegian Association of Heart and Lung Patients, Helse og Rehabilitering [2003/2/0211]
  3. Norwegian Council on Cardiovascular Disease
  4. Family Blix Foundation

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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). 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. 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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