The hemodynamic impact of diffuse myocardial ischemic lesions: an animal experimental model based on intracoronary microembolization

In ischemic heart disease, left ventricular function is affected by a diffu se and segmental loss of myocardium. The decline in the incidence of myocar dial infarction and improved early revascularization in acute transmural is chemia predict a change in the natural history of ischemic heart disease. I t is now believed that, minor ischemic episodes, which are known to induce multifocal myocardial degeneration, will predominate in the near future. Th e objective of the present study was to develop a clinically relevant exper imental model for investigation of the pathophysiological significance of d iffuse ischemic myocardial lesions. Cardiac performance was gradually depre ssed by selective intracoronary microembolization in 13 pigs. Left ventricu lar function was quantitated by ejection fraction (EF), pulmonary pressure, cardiac output, and derivatives of left ventricular pressure. Left ventric ular volume was estimated by epicardial echocardiography, using a new, unbi ased stereological volume estimator. A chronic substudy was performed in or der to characterize the histological changes and to evaluate the feasibilit y of establishing a chronic preparation of the model. Embolization induced acute left ventricular dysfunction; left ventricular pressure change decrea sed from 966 +/- 274 to 637 +/- 146 mmHg/s, and early diastolic relaxation from 1403 +/- 515 to 824 +/- 344 mmHg/s, respectively. Ejection fraction de creased bq 45% +/- 5% and cardiac output by 29% +/- 11%. End-diastolic volu me increased significantly, from 66.1 +/- 13.2 to 77.0 +/- 19.4 cm(3), and end-systolic volume increased from 35.9 +/- 13.9 to 52.3 +/- 7.6 cm(3). No change in heart rate or left ventricular filling pressure: was observed. Di ffuse ischemic myocardial injury was identified after a mean follow-up of 4 0 days. Intracoronary microembolization induces acute left ventricular dysf unction due to microinfarcts. Increased left ventricular end-diastolic volu me is the initial compensatory response to the acute impairment of cardiac performance in nontransmural myocardial ischemia. This model is suitable fo r the evaluation of the hemodynamic changes secondary to acute and chronic jiff use loss of functional myocardium.