Diastolic filling in acute left ventricular dysfunction: Role of the pericardium

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 < 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 < 0.01) as compared with baseline values. This increase was associated with a marked increase in left ventricular end-diastolic pressure (baseline, 8 ± 3 mm Hg; postembolization, 25 ± 6 mm Hg; p < 0.001) and in the time constant of left ventricular pressure decline. Opening the chest produced no changes, but opening the pericardium decreased the 1 3 and the 1 2 filling fraction (19.1 ± 9.2%, 35.9 ± 11.8%, respectively, p < 0.001) as compared with postembolizalion values. Opening the chest or pericardium produced no changes in left ventricular areas, area ejection fraction, time constant of pressure decline or end-diastolic pressures. Redistribution of diastolic filling to early in diastole occurs in the acutely dilated left ventricle with elevated filling pressures despite marked abnormalities of left ventricular relaxation and is mediated by pericardial restraint.