title: Long-term effects of acute pulmonary embolism on echocardiographic Doppler indices and functional capacity.
abstract: OBJECTIVE
  Hemodynamic and functional consequences of acute pulmonary embolism (APE) are believed to be reversible with antithrombotic treatment. To verify this hypothesis, we reassessed our patients at least 1 year after an episode of APE.
  
  
  METHODS
  We compared echo Doppler indices and 6-min walking test parameters (6-MWT) of 36 patients (13 men, 23 women, age 66 +/- 11 years), studied on average 3.1 +/- 2.2 years after an acute episode of pharmacologically treated massive or submassive APE, with data of 30 age-matched subjects (12 men, 18 women, age 67 +/- 12 years).
  
  
  RESULTS
  At least 1 year after APE, right ventricular (RV) diameter remained increased in patients compared with controls (27 +/- 2 vs. 23 +/- 2 mm, p<0.001). Also, acceleration time of pulmonary ejection (AcT) was markedly shorter (97 +/- 19 vs. 123 +/- 19 ms, p<0.001) and the diameter of the pulmonary trunk was significantly larger in patients than in controls (21 +/- 2.6 vs. 18 +/- 2.2, p<0.001). Although the mean value of the tricuspid valve peak systolic gradient (TVPG) in the APE group at follow-up was similar to that in controls, TVPG>30 mmHg was recorded in three patients with APE (8.3%). There was no difference in the distance of 6-MWT between both groups; however, the mean desaturation after 6-MWT was higher in the APE group than in controls (3.04 +/- 2.08 vs. 1.45 +/- 0.69%, p=0.0005).
  
  
  CONCLUSIONS
  Pharmacologic treatment of acute pulmonary embolism does not prevent mild persistent changes in morphology and function of the cardiovascular system. Despite normalization of pulmonary artery systolic pressure and similar exercise capacity, survivors of APE present signs suggesting RV dysfunction and/or its disturbed coupling to the pulmonary arterial bed, as well as ventilation to perfusion mismatch at exertion persisting long after the acute embolic episode.
authors.affiliation: Department of Internal Medicine and Cardiology, Medical University of Warsaw, Poland. mciurzyn@amwaw.edu.pl
authors.forename: M
authors.initials: M
authors.lastname: Ciurzyński
authors.forename: M
authors.initials: M
authors.lastname: Kurzyna
authors.forename: A
authors.initials: A
authors.lastname: Bochowicz
authors.forename: B
authors.initials: B
authors.lastname: Lichodziejewska
authors.forename: D
authors.initials: D
authors.lastname: Liszewska-Pfejfer
authors.forename: P
authors.initials: P
authors.lastname: Pruszczyk
authors.forename: A
authors.initials: A
authors.lastname: Torbicki
mesh_terms: D000208:Acute Disease; D000368:Aged; D000925:Anticoagulants / Q000627:therapeutic use; D001794:Blood Pressure / Q000502:physiology; D018450:Disease Progression; D015150:Echocardiography, Doppler; D005080:Exercise Test; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D005500:Follow-Up Studies; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D011655:Pulmonary Embolism / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000503:physiopathology; D012189:Retrospective Studies; D013300:Streptokinase / Q000627:therapeutic use; D013997:Time Factors; D014261:Tricuspid Valve / Q000000981:diagnostic imaging / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D017725:Ventricular Pressure / Q000502:physiology
chemical_list: D000925:Anticoagulants; D005343:Fibrinolytic Agents; D006493:Heparin; D013300:Streptokinase