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Relationships between regional myocardial wall stress and bioenergetics in hearts with left ventricular hypertrophy

机译:左心室肥厚心脏局部心肌壁压力与生物能的关系

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摘要

This study utilized porcine models of postinfarction LV remodeling (MI: n=8) and concentric LVH secondary to aortic banding (AoB: n=8) to examine the relationships between regional myocardial contractile function (tagged MRI), wall stress (MRI and LV pressure), and bioenergetics (P-31 MR spectroscopy). Physiological assessments were conducted at a 4 week time point after myocardial infarction or aortic banding surgery. Comparisons were made with size matched normal animals (normal: n=8). Both myocardial infarction and aortic banding instigated significant LV hypertrophy. Ejection fraction was not significantly altered in the AoB group, but significantly decreased in the MI group (p<0.01 vs. normal and AoB). Systolic and diastolic wall stresses were approximately two times greater than normal in the infarct region and border zone. Wall stress in the AoB group was not significantly different from normal hearts. The infarct border zone demonstrated profound bioenergetic abnormalities, especially in the subendocardium, where the ratio of phosphocreatine to adenosine triphosphate (PCr/ATP) decreased from 1.98 ± 0.16 (normal) to 1.06 ± 0.30 (MI, p<0.01). The systolic radial thickening fraction and the circumferential shortening fraction in the anterior wall were severely reduced (MI, p<0.01 vs Normal). The radial thickening fraction and circumferential shortening fraction in the AoB group were not significantly different from normal. The severely elevated wall stress in the infarct border zone was associated with a significant increase in chemical energy demand and abnormal myocardial energy metabolism. Such severe metabolic perturbations cannot support normal cardiac function, which may explain the observed regional contractile abnormalities in the infarct border zone.
机译:本研究利用梗死后左室重塑(MI:n = 8)和继发于主动脉束带的同心LVH(AoB:n = 8)的猪模型来研究局部心肌收缩功能(标记MRI),壁应力(MRI和LV)之间的关系。压力)和生物能学(P-31 MR光谱)。在心肌梗塞或主动脉束带手术后4周的时间点进行生理评估。用大小匹配的正常动物进行比较(正常:n = 8)。心肌梗塞和主动脉束带均导致明显的LV肥大。 AoB组的射血分数没有明显改变,而MI组则明显降低(与正常和AoB相比,p <0.01)。在梗塞区域和边界区域,收缩壁和舒张壁的压力大约是正常压力的两倍。 AoB组的壁应力与正常心脏无明显差异。梗塞边缘区表现出深远的生物能异常,特别是在心内膜下层,其中磷酸肌酸与三磷酸腺苷的比例(PCr / ATP)从1.98±0.16(正常)降低至1.06±0.30(MI,p <0.01)。前壁的收缩期径向增厚分数和周向收缩分数大大降低(MI,与正常相比,p <0.01)。 AoB组的径向增厚率和圆周缩短率与正常值无明显差异。梗死边界区壁压力的严重升高与化学能需求的显着增加和心肌能量代谢异常有关。这种严重的代谢紊乱不能支持正常的心脏功能,这可以解释在梗塞边界区域观察到的局部收缩异常。

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