Pulmonary embolism: Relation between the degree of right ventricle overload and the extent of perfusion defects

Abstract

Background Inasmuch as the presence of right ventricle (RV) overload in patients with pulmonary embolism (PE) is associated with a bad prognosis, evaluation of RV function in PE is of importance. This study was done to establish if the degree of RV overload can be predicted from the extent of perfusion defects (PDf). Methods One hundred twenty-one consecutive patients with PE diagnosed by lung scintigraphy (LS) were examined by echocardiography Doppler (ED) immediately after diagnosis. PDf were graded visually in categories (LS score 1 = ≤20%, 2 = >20% of total lung area) and on a continuous scale (normal perfusion = 0, no perfusion = 1). The reproducibility of both methods was tested. RV wall motion was assessed on a four-point scale (0 = normal to 3 = severely hypokinetic). The distance from LV posterior wall to RV anterior wall and dimensions of RV and LV were measured. Pulmonary artery systolic pressure (PAsP) was calculated by using the maximum velocity of tricuspid regurgitation. Results There were 51 patients with LS score 1 and 70 (58%) with score 2. In comparison with patients with LS score 1, those with score 2 more often had RV hypokinesis 2+ or 3+ (n = 49 vs n = 16) (p < 0.001), larger RV (34 ± 6 mm [22 to 48] vs 29 ± 5 [17 to 38]) (SD [range]) (p < 0.001) and higher PAsP (51 ± 13 mm Hg [21 to 83] vs 42 ± 14 [20 to 81]) (p < 0.001). The variability in both groups was large. With continuous scaling, PDf averaged 0.3. This was also the value that best discriminated RV hypokinesis 2+ or 3+ in a receiver operating characteristic curve. However, the variability for this scan scoring method was SD 0.073, giving a 95% confidence limit of ±0.15. Conclusion There is a significant correlation between RV overload and PDf, but the variability is large; therefore, an estimate of the size of perfusion defects in LS cannot replace ED in the assessment of PAsP and the degree of RV overload in PE. (Am Heart J 1998;135:868-74.)