title: Diastolic filling in acute left ventricular dysfunction: role of the pericardium.
abstract: Patients with congestive heart failure and elevated left ventricular filling pressures demonstrate an abnormal pattern of diastolic filling that is characterized by a redistribution of diastolic filling to early diastole with reduced reliance on late diastolic filling. The diastolic filling pattern superficially resembles that which is seen with constrictive pericarditis. To examine potential mechanisms for these clinical findings, a model of ischemic left ventricular dysfunction was produced in seven dogs by repeated coronary microsphere embolization, producing a dilated left ventricle with reduced systolic function. Measurements of left ventricular systolic and end-diastolic pressures, rate of rise of left ventricular pressure (dP/dt) and echocardiographic end-diastolic and end-systolic areas were obtained at baseline, during intermediate embolization (moderate left ventricular systolic dysfunction, dilation and mild increases in left ventricular end-diastolic pressure), postembolization (further embolization resulting in severe left ventricular systolic dysfunction, dilation and marked increases in left ventricular end-diastolic pressure), after thoracotomy and after pericardiectomy. The filling fraction at 1/3 and 1/2 of diastole and the time constant of left ventricular pressure decline were also determined. Repetitive coronary microembolization caused progressive left ventricular dilation and decreasing systolic function, which did not change after opening the chest or pericardium. The filling fraction at 1/3 and 1/2 of diastole declined with intermediate embolization (12.0 +/- 5.6% and 23.1 +/- 10.8%, respectively) as compared with baseline values (29.0 +/- 11.9%, 42.9 +/- 15.6%, p less than 0.05). After embolization, there was an increase in the 1/3 and the 1/2 filling fraction (47.5 +/- 8.9%, 72.0 +/- 6.0%, respectively, p less than 0.01) as compared with baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Division of Cardiology, Harper Hospital, Wayne State University, Detroit, Michigan.
authors.forename: S J
authors.initials: SJ
authors.lastname: Lavine
authors.forename: C A
authors.initials: CA
authors.lastname: Campbell
authors.forename: R A
authors.initials: RA
authors.lastname: Kloner
authors.forename: S J
authors.initials: SJ
authors.lastname: Gunther
mesh_terms: D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology; D003971:Diastole; D004285:Dogs; D004452:Echocardiography; D004617:Embolism / Q000209:etiology / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology; D006331:Heart Diseases / Q000473:pathology / Q000503:physiopathology*; D006352:Heart Ventricles; D008863:Microspheres; D009206:Myocardium / Q000473:pathology; D010496:Pericardium / Q000503:physiopathology*; D013599:Systole; D014743:Videotape Recording