title: Experimental model of chronic global left ventricular dysfunction secondary to left coronary microembolization.
abstract: A model of chronic left ventricular dysfunction characterized by left ventricular dilation, elevated filling pressures and histologic changes has been lacking. In this study the use of coronary microsphere embolization-induced ischemia was explored as a method of producing chronic left ventricular dysfunction. Acute ischemic left ventricular dysfunction was induced in 13 mongrel dogs with 50 microns plastic microspheres until the peak positive first derivative of left ventricular pressure (dP/dt) decreased by 25% and the left ventricular end-diastolic pressure increased to greater than or equal to 12 mm Hg. After 8 weeks of observation, hemodynamic and echocardiographic variables were measured in each dog. Acute left ventricular dysfunction resulted in a dilated left ventricle with systolic dysfunction (area ejection fraction 24 +/- 6% vs. 57 +/- 9% initially, p less than 0.01) and elevated left ventricular filling pressures. Isovolumetric relaxation was prolonged and the peak rapid filling/atrial filling velocity and integral ratios were reduced. Eight weeks after embolization, there was an increased left ventricular size (end-diastolic area 15.1 +/- 2.1 cm2 at 8 weeks vs. 13.5 +/- 1.4 cm2 early after microsphere injection, p less than 0.05), unchanged end-systolic area, improved area ejection fraction and increased left ventricular mass. Left ventricular end-diastolic pressure increased and, despite continued abnormal relaxation, the peak rapid filling/atrial filling velocity and integral ratios increased to above baseline values, demonstrating a "restrictive" pattern. Gross and histologic examination revealed diffuse, patchy scarring associated with perivascular fibrosis. Thus, coronary microsphere embolization resulted in a model of chronic moderate left ventricular systolic dysfunction and abnormal diastolic function characterized by a "restrictive" filling pattern.
authors.affiliation: Division of Cardiology, Harper Hospital, Wayne State University, Detroit, Michigan 48201.
authors.forename: S J
authors.initials: SJ
authors.lastname: Lavine
authors.forename: P
authors.initials: P
authors.lastname: Prcevski
authors.forename: A C
authors.initials: AC
authors.lastname: Held
authors.forename: V
authors.initials: V
authors.lastname: Johnson
mesh_terms: D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D003327:Coronary Disease / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography; D004617:Embolism / Q000139:chemically induced / Q000150:complications*; D006333:Heart Failure / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D006439:Hemodynamics; D007269:Injections, Intra-Arterial; D008863:Microspheres; D016277:Ventricular Function, Left / Q000502:physiology*