Association between right ventricular function and perfusion abnormalities in hemodynamically stable patients with acute pulmonary embolism

Background/objectives: Patients presenting with acute pulmonary embolism associated with hemodynamic compromise exhibit right ventricular enlargement and dysfunction on transthoracic echocardiogram. However, the degree of echocardiographic abnormalities among hemodynamically stable patients without preexisting cardiopulmonary disease during the acute stage of pulmonary embolism, and following treatment, is unknown. Therefore, this study was designed to assess the extent of light ventricular abnormalities detected on transthoracic echocardiogram in patients following acute pulmonary embolism and during treatment with anticoagulation or vena caval interruption. The extent of pulmonary vascular obstruction and complication rate on follow-up were also assessed. Design/interventions: Sixty-four consecutive hemodynamically stable patients without preexisting known cardiopulmonary disorder presenting with acute pulmonary embolism and undergoing treatment with anticoagulation or inferior vena caval interruption were studied. All subjects underwent a two-dimensional transthoracic echocardiogram within 24 h of diagnosis. The degree of perfusion abnormality on lung scan was quantified. Twenty-six patients underwent follow-up echocardiogram and lung scant 6 weeks. The echocardiographic findings were compared with those obtained from a group of normal control subjects matched for gender and age. Results: Although the mean right ventricular end-diastolic areas did not differ (21.9+/-5.2 cm(2) vs 20.1+/-2.9 cm(2) for control subjects; p=not significant), the right ventricular end-systolic area was larger in comparison to our series of control subjects (14.6+/-5.1 cm(2) vs 11.7+/-2.0 cm(2); p=0.025). Fractional right ventricular area change was reduced in the patient group compared with the control subjects (34.3+/-9.0% vs 41.3+/-7.0%; p=0.003) The extent of light ventricular end-systolic area enlargement and decrease in fractional area change did not correlate with the degree of pulmonary vascular obstruction. Patients who were restudied at 6 weeks showed minimal improvement in echocardiographic findings, despite almost complete resolution of perfusion defects on lung scan. Conclusions: The extent of light ventricular dysfunction in hemodynamically stable, previously normal patients with acute pulmonary embolism does not reflect the extent of the perfusion abnormalities. Further, light ventricular enlargement and systolic dysfunction are present and persistent despite treatment with heparin and warfarin therapy or vena caval interruption.