Terp K, Kim W Y, Ulrich M, Frokiaer J, Baandrup U, Rehling M, Bagger J P, Hasenkam J M
Department of Cardiothoracic and Vascular Surgery, Institute for Experimental Clinical Research, Skejby Sygehus, Aarhus, Denmark.
Heart Vessels. 1998;13(3):132-41. doi: 10.1007/BF01747830.
In ischemic heart disease, left ventricular function is affected by a diffuse and segmental loss of myocardium. The decline in the incidence of myocardial infarction and improved early revascularization in acute transmural ischemia predict a change in the natural history of ischemic heart disease. It is now believed that, minor ischemic episodes, which are known to induce multifocal myocardial degeneration, will predominate in the near future. The objective of the present study was to develop a clinically relevant experimental model for investigation of the pathophysiological significance of diffuse ischemic myocardial lesions. Cardiac performance was gradually depressed by selective intracoronary microembolization in 13 pigs. Left ventricular function was quantitated by ejection fraction (EF), pulmonary pressure, cardiac output, and derivatives of left ventricular pressure. Left ventricular volume was estimated by epicardial echocardiography, using a new, unbiased stereological volume estimator. A chronic substudy was performed in order to characterize the histological changes and to evaluate the feasibility of establishing a chronic preparation of the model. Embolization induced acute left ventricular dysfunction; left ventricular pressure change decreased from 966+/-274 to 637+/-146 mmHg/s, and early diastolic relaxation from 1403+/-515 to 824+/-344 mmHg/s, respectively. Ejection fraction decreased by 45%+/-5% and cardiac output by 29%+/-11%. End-diastolic volume increased significantly, from 66.1+/-13.2 to 77.0+/-19.4 cm3, and end-systolic volume increased from 35.9+/-13.9 to 52.3+/-7.6 cm3. No change in heart rate or left ventricular filling pressure was observed. Diffuse ischemic myocardial injury was identified after a mean follow-up of 40 days. Intracoronary microembolization induces acute left ventricular dysfunction due to microinfarcts. Increased left ventricular end-diastolic volume is the initial compensatory response to the acute impairment of cardiac performance in nontransmural myocardial ischemia. This model is suitable for the evaluation of the hemodynamic changes secondary to acute and chronic diffuse loss of functional myocardium.
在缺血性心脏病中，左心室功能受到心肌弥漫性和节段性丧失的影响。心肌梗死发病率的下降以及急性透壁性缺血中早期血运重建的改善预示着缺血性心脏病自然病程的改变。现在人们认为，已知会诱发多灶性心肌变性的轻微缺血发作在不久的将来将占主导地位。本研究的目的是建立一个临床相关的实验模型，以研究弥漫性缺血性心肌病变的病理生理意义。通过对13头猪进行选择性冠状动脉内微栓塞，心脏功能逐渐受到抑制。通过射血分数（EF）、肺动脉压、心输出量和左心室压力导数来定量左心室功能。使用一种新的、无偏倚的体视学体积估计器，通过心外膜超声心动图估计左心室体积。进行了一项慢性子研究，以表征组织学变化并评估建立该模型慢性制剂的可行性。栓塞导致急性左心室功能障碍；左心室压力变化分别从966±274降至637±146 mmHg/s，早期舒张期松弛从1403±515降至824±344 mmHg/s。射血分数下降45%±5%，心输出量下降29%±11%。舒张末期容积显著增加，从66.1±13.2增加到77.0±19.4 cm³，收缩末期容积从35.9±13.9增加到52.3±7.6 cm³。未观察到心率或左心室充盈压的变化。平均随访40天后发现弥漫性缺血性心肌损伤。冠状动脉内微栓塞由于微梗死导致急性左心室功能障碍。左心室舒张末期容积增加是对非透壁性心肌缺血中心脏功能急性损害的初始代偿反应。该模型适用于评估继发于功能性心肌急性和慢性弥漫性丧失的血流动力学变化。
