Value of transthoracic echocardiography in therapy regimens evaluation in pulmonary embolism

Acute pulmonary embolism (APE) causes right ventricular dysfunction (RVD). APE patients with and without RVD can benefit from thrombolytic therapy or anticoagulants. In this study, we assessed the changes of right ventricular (RV) function on transthoracic echocardiography (TTE) after different therapy strategies among a broad spectrum of APE.

The present prospective randomized trial included 520 APE patients from 41 hospitals in China between June 2002 and November 2004. Patients were divided into two groups at presentation: group I (major APE)--52 patients with hemodynamic instability and 198 normotensive patients with RVD; group II (minor APE)--270 normotensive patients without RVD. The patients in group I were randomly divided into four subgroups according to different thrombolytic regimens: A--urokinase 12 h subgroup; B--urokinase 2 h subgroup; C--recombinant tissue-type plasminogen activator (rtPA) 50 mg subgroup and D--rtPA 100 mg subgroup; Different anticoagulants were randomly assigned to patients in group II: NA--heparin subgroup; NB--nadroparin subgroup. TTE were performed before the therapy, and 24 h, 14 days and 3 months after the therapy, respectively.

Mean age was 57.4 +/- 14.1 years and 323 patients (62.1%) were male. The indexes of RV function on TTE in group I were significantly improved compared with those in group II at each point (P < 0.05) and SPAP decreased after anticoagulants administration in group II. However, there was no difference among thrombolytic subgroups in group I and between the two anticoagulants subgroups in group II. The presence of RVD was much lower (34.0% vs. 100%, P < 0.001) 24 h after thrombolytic therapies than that before the therapy in group I, which documented that thrombolytic agents early reversed RVD in major APE patients. Even 3 months after the therapy, TRPG and SPAP were still higher in group I than those in group II.

TTE documented the identical effect of thrombolytic regimen of urokinase 12 h, urokinase 2 h, rtPA 50 mg and rtPA 100 mg in major APE which suggest rtPA 100 mg can supersede rtPA 50 mg in these patients. Heparin produced the similar results compared with nadroparin in minor APE. TTE can monitor the effect DC3 NAK of thrombolysis early and identify the patients with persistent pulmonary hypertension which possibly develop chronic thromboembolic pulmonary hypertension. Therefore, it can facilitate the management of APE.