Increased interleukin-1β levels are associated with left ventricular hypertrophy and remodelling following acute ST segment elevation myocardial infarction treated by primary percutaneous coronary intervention

被引:96
作者
Orn, S. [1 ]
Ueland, T. [2 ]
Manhenke, C. [3 ]
Sandanger, O. [2 ,4 ]
Godang, K. [5 ,6 ]
Yndestad, A. [2 ,4 ]
Mollnes, T. E. [5 ,6 ,7 ]
Dickstein, K. [3 ]
Aukrust, P. [2 ,7 ,8 ]
机构
[1] Stavanger Univ Hosp, Dept Cardiol, Div Cardiol, N-4068 Stavanger, Norway
[2] Univ Oslo, Rikshosp, Oslo Univ Hosp, Res Inst Internal Med, N-0027 Oslo, Norway
[3] Univ Bergen, Inst Internal Med, Bergen, Norway
[4] Univ Oslo, Ctr Heart Failure Res, Oslo, Norway
[5] Univ Oslo, Rikshosp, Oslo Univ Hosp, Dept Endocrinol, N-0027 Oslo, Norway
[6] Univ Oslo, Rikshosp, Oslo Univ Hosp, Inst Immunol, N-0027 Oslo, Norway
[7] Univ Oslo, Fac Med, Oslo, Norway
[8] Univ Oslo, Rikshosp, Oslo Univ Hosp, Sect Clin Immunol & Infect Dis, N-0027 Oslo, Norway
关键词
interleukin-1; left ventricular remodelling; myocardial infarction; noninfarcted zone; C-REACTIVE PROTEIN; PROGNOSTIC IMPLICATIONS; MATRIX; MASS; DISEASE;
D O I
10.1111/j.1365-2796.2012.02517.x
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
.phi rn S, Ueland T, Manhenke C, Sandanger phi, Godang K, Yndestad A, Mollnes TE, Dickstein K, Aukrust P (Stavanger University Hospital, Stavanger; Oslo University Hospital Rikshospitalet; University of Bergen, Bergen; University of Oslo; Oslo; Norway). Increased interleukin-1 beta levels are associated with left ventricular hypertrophy and remodelling following acute ST segment elevation myocardial infarction treated by primary percutaneous coronary intervention. J Intern Med 2012; 272: 267276. Objectives. To assess the relationship between interleukin (IL)-1-related molecules, infarct size and left ventricular (LV) remodelling following acute myocardial infarction (MI). Methods. Forty-two patients with first-time diagnosis of ST segment elevation MI (STEMI), with a single occluded vessel successfully revascularized by primary percutaneous coronary intervention (PCI), were recruited to this observational study conducted at a university teaching hospital and followed for 1 year. Main outcome measures. Plasma levels of IL-1 beta, IL-1 receptor antagonist (IL-1Ra), IL-18 and caspase-1 were analysed before and 2 days, 1 week and 2 months after PCI. Serial cardiac magnetic resonance imaging (CMR) was used for the assessment of infarct size and LV remodelling. CMR findings at 1 year was the primary outcome variable. Results. Univariate analysis showed that IL-1-related mediators were strongly (IL-1 beta), moderately (caspase-1) and weakly (IL-1Ra) associated with impaired myocardial function and noninfarct mass, but not infarct size, 1 year after reperfused STEMI. In multivariate analyses, troponin T predicted LV ejection fraction (LVEF), infarct size and LV end-diastolic (LVEDVi) and end-systolic volume index (LVESVi). However, significant additional variance was explained by IL-1 beta, IL-18 and caspase-1. IL-1 beta levels at 2 months, IL-18 at 2 days and pre-PCI caspase-1 were predictors of LVEF. Caspase-1 and in particular IL-1 beta at 2 days were the only predictors of noninfarct mass. IL-1 beta and IL-18 at 2 days were predictors of LVEDVi, whilst pre-PCI levels of IL-1 beta contributed to prediction of LVESVi. By contrast, pro-B-type natriuretic peptide, C-reactive protein, IL-6 and transforming growth factor-beta 1 (TGF-beta 1) had no or only a weak (TGF-beta 1) association with these CMR parameters in multivariate analyses. Conclusions. IL-1 beta levels after STEMI were strongly associated with impaired myocardial function and noninfarct LV mass after 1 year, suggesting a potential role for IL-1 beta as a predictor of maladaptive myocardial remodelling following reperfused MI.
引用
收藏
页码:267 / 276
页数:10
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