title: Left ventricular dysfunction induced by nonsevere idiopathic pulmonary arterial hypertension: a pressure-volume relationship study.
abstract: BACKGROUND
  Severe increase in right ventricular pressure can compromise left ventricular (LV) function because of impaired interventricular interaction and aggravate the symptoms.
  
  
  OBJECTIVE
  To elucidate how nonsevere idiopathic pulmonary arterial hypertension (IPAH) influences LV function because of impaired interventricular interaction.
  
  
  METHODS
  Invasive pressure-volume (PV) loop analysis obtained by conductance catheterization was performed at rest and during atrial pacing in patients with mild IPAH (n = 10) compared with patients with isolated LV diastolic dysfunction (DD) (n = 10) and control subjects without heart failure symptoms (n = 9).
  
  
  RESULTS
  Patients with nonsevere IPAH (pulmonary artery pressure mean 29 ± 5 mm Hg) and patients with DD showed preserved systolic (ejection fraction 63 ± 12% and 62 ± 9%) and impaired LV diastolic function at rest (LV stiffness 0.027 ± 0.012 ml(-1) and 0.029 ± 0.014 ml(-1)). During pacing at 120 per minute patients with IPAH and DD decreased their stroke volume (-25% and -30%; P < 0.05) and failed to increase cardiac output significantly. Opposite to patients with DD and control subjects, temporary preload reduction during inferior vena cava occlusion initially induced an expansion of LV end-diastolic volume in IPAH (+7%; P < 0.05), whereas end-diastolic pressure continuously dropped. This resulted in an initial downward shift to the right of the PV loop indicating better LV filling, which was associated with a temporary improvement of cardiac output (+11%; P < 0.05) in the patients with IPAH, but not in patients with DD and control subjects.
  
  
  CONCLUSIONS
  Mild idiopathic pulmonary arterial pressure impairs LV diastolic compliance even in the absence of the intrinsic LV disease and contributes to the reduced cardiac performance at stress.
authors.affiliation: Department of Cardiology and Pneumology, Charité-Universitätsmedizin Berlin, CBF, Hindenburgdamm 30, 12200 Berlin, Germany.
authors.forename: Mario
authors.initials: M
authors.lastname: Kasner
authors.forename: Dirk
authors.initials: D
authors.lastname: Westermann
authors.forename: Paul
authors.initials: P
authors.lastname: Steendijk
authors.forename: Stephan
authors.initials: S
authors.lastname: Dröse
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Poller
authors.forename: Heinz-Peter
authors.initials: HP
authors.lastname: Schultheiss
authors.forename: Carsten
authors.initials: C
authors.lastname: Tschöpe
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery / Q000503:physiopathology; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology