title: Value of transthoracic echocardiography in therapy regimens evaluation in pulmonary embolism.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors: Department of Respiratory Medicine, Shandong Provincial Hospital, Shandong University, Jinan, China.
authors: Ling
authors: L
authors: Zhu
authors: Chen
authors: C
authors: Wang
authors: Yuanhua
authors: Y
authors: Yang
authors: Yafeng
authors: Y
authors: Wu
authors: Zhenguo
authors: Z
authors: Zhai
authors: Huaping
authors: H
authors: Dai
authors: Baosen
authors: B
authors: Pang
authors: Zhaohui
authors: Z
authors: Tong
mesh_terms: D000328:Adult; D000368:Aged; D004305:Dose-Response Relationship, Drug; D004452:Echocardiography; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017762:Nadroparin / Q000627:therapeutic use; D011655:Pulmonary Embolism / Q000000981:diagnostic imaging* / Q000188:drug therapy*; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage; D014568:Urokinase-Type Plasminogen Activator / Q000008:administration & dosage; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging*
chemical_list: D005343:Fibrinolytic Agents; D017762:Nadroparin; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator
references: Lancet. 1988 Aug 6;2(8606):293-8
references: 2899718
references: J Am Coll Cardiol. 1997 Nov 1;30(5):1172-3
references: 9350910
references: Ann Intern Med. 2002 May 7;136(9):691-700
references: 11992305
references: Am Heart J. 1995 Dec;130(6):1276-82
references: 7484782
references: Circulation. 2000 Jul 11;102(2):211-7
references: 10889133
references: Am Heart J. 1994 May;127(5):1371-5
references: 8172067
references: Am Heart J. 1997 Sep;134(3):479-87
references: 9327706
references: Circulation. 1997 Aug 5;96(3):716-8
references: 9264472
references: N Engl J Med. 2002 Oct 10;347(15):1143-50
references: 12374874
references: Circulation. 1997 Aug 5;96(3):882-8
references: 9264496
references: Am J Cardiol. 1996 Jun 1;77(14):1252-4
references: 8651110
references: J Am Coll Cardiol. 1997 Nov 1;30(5):1165-71
references: 9350909
references: J Am Coll Cardiol. 1987 Nov;10 (5):971-8
references: 2959713
references: Circulation. 2000 Jun 20;101(24):2817-22
references: 10859287
references: Lancet. 1993 Feb 27;341(8844):507-11
references: 8094768
references: Heart. 1997 Apr;77(4):346-9
references: 9155614
references: Mayo Clin Proc. 2001 Nov;76(11):1102-10
references: 11702898
references: Arch Intern Med. 1998 Mar 23;158(6):585-93
references: 9521222
references: Arch Intern Med. 1991 May;151(5):933-8
references: 2025141
references: Am J Cardiol. 2003 Jul 1;92 (1):116-9
references: 12842266
references: Circulation. 2005 Sep 13;112(11):1573-9
references: 16144990
references: Chest. 2004 Apr;125(4):1539-45
references: 15078772
references: Am J Cardiol. 1999 Mar 1;83(5):804-6, A10
references: 10080447
references: Lancet. 1999 Apr 24;353(9162):1386-9
references: 10227218