- 作者：Duncan J. Campbell ; Jithendra B. Somaratne ; Alicia J. Jenkins ; David L. Prior ; Michael Yii ; James F. Kenny ; Andrew E. Newcomb ; Darren J. Kelly ; Mary Jane Black
- 关键词：Coronary microvasculature ; Myocardial infarction ; Capillary ; Arteriole ; Angiogenesis ; Advanced glycation end-product
- 刊名：International Journal of Cardiology
- 出版年：2013
- 出版时间：10 August, 2013
- 年：2013
- 卷：167
- 期：3
- 页码：1027-1037
- 全文大小：1274 K
Background
Myocardial microvascular dysfunction has been implicated in the pathogenesis of myocardial infarction (MI). We tested the hypothesis that patients with MI have lower microvasculature density in myocardium remote from the site of infarction than patients with similar extent of coronary artery disease (CAD) without MI and examined the relationship between myocardial capillary length density and plasma levels of angiogenesis-related biomarkers.Methods
We analyzed biopsies from non-ischemic left ventricular (LV) myocardium and measured plasma levels of angiogenesis-related biomarkers in patients undergoing coronary artery bypass graft surgery, 57 without previous MI (no-MI) and 27 with recent non-ST-segment-elevation MI (NSTEMI). Comparison was made with biopsies from 31 aortic stenosis (AS) patients and 6 patients with ¡°normal¡± LV without CAD.
Results
Myocardial microvascular density of NSTEMI patients was approximately half the density of no-MI patients, and similar to AS patients. Whereas the reduced microvascular density of AS patients was accounted for by their cardiomyocyte hypertrophy, this was not the case for NSTEMI patients, who had higher diffusion radius/cardiomyocyte width ratio than no-MI, ¡°normal¡± LV, and AS patients. NSTEMI patients had lower plasma levels of carboxymethyl lysine and low molecular weight fluorophores, higher vascular endothelial growth factor (VEGF) receptor-1/VEGF-A ratio, and higher endostatin and hepatocyte growth factor levels than no-MI patients.
Conclusions
Recent MI was associated with reduced microvasculature density in myocardium remote from the site of infarction and alteration in plasma levels of angiogenesis-related biomarkers.