title: Pulmonary vascular response patterns during exercise in left ventricular systolic dysfunction predict exercise capacity and outcomes.
abstract: BACKGROUND
  Elevated resting pulmonary arterial pressure (PAP) in patients with left ventricular systolic dysfunction (LVSD) purports a poor prognosis. However, PAP response patterns to exercise in LVSD and their relationship to functional capacity and outcomes have not been characterized.
  
  
  RESULTS
  Sixty consecutive patients with LVSD (age 60±12 years, left ventricular ejection fraction 0.31±0.07, mean±SD) and 19 controls underwent maximum incremental cardiopulmonary exercise testing with simultaneous hemodynamic monitoring. During low-level exercise (30 W), LVSD subjects, compared with controls, had greater augmentation in mean PAPs (15±1 versus 5±1 mm Hg), transpulmonary gradients (5±1 versus 1±1 mm Hg), and effective pulmonary artery elastance (0.05±0.02 versus -0.03±0.01 mm Hg/mL, P<0.0001 for all). A linear increment in PAP relative to work (0.28±0.12 mm Hg/W) was observed in 65% of LVSD patients, which exceeded that observed in controls (0.07±0.02 mm Hg/W, P<0.0001). Exercise capacity and survival was worse in patients with a PAP/watt slope above the median than in patients with a lower slope. In the remaining 35% of LVSD patients, exercise induced a steep initial increment in PAP (0.41±0.16 mm Hg/W) followed by a plateau. The plateau pattern, compared with a linear pattern, was associated with reduced peak Vo(2) (10.6±2.6 versus 13.1±4.0 mL · kg(-1) · min(-1), P=0.005), lower right ventricular stroke work index augmentation with exercise (5.7±3.8 versus 9.7±5.0 g/m(2), P=0.002), and increased mortality (hazard ratio 8.1, 95% CI 2.7 to 23.8, P<0.001).
  
  
  CONCLUSIONS
  A steep increment in PAP during exercise and failure to augment PAP throughout exercise are associated with decreased exercise capacity and survival in patients with LVSD, and may therefore represent therapeutic targets.
  
  
  BACKGROUND
  URL: http://www.clinicaltrials.gov. Unique identifier: NCT00309790.
authors.affiliation: Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, 02114, USA. glewis@partners.org
authors.forename: Gregory D
authors.initials: GD
authors.lastname: Lewis
authors.forename: Ryan M
authors.initials: RM
authors.lastname: Murphy
authors.forename: Ravi V
authors.initials: RV
authors.lastname: Shah
authors.forename: Paul P
authors.initials: PP
authors.lastname: Pappagianopoulos
authors.forename: Rajeev
authors.initials: R
authors.lastname: Malhotra
authors.forename: Kenneth D
authors.initials: KD
authors.lastname: Bloch
authors.forename: David M
authors.initials: DM
authors.lastname: Systrom
authors.forename: Marc J
authors.initials: MJ
authors.lastname: Semigran
mesh_terms: D000368:Aged; D005080:Exercise Test; D017079:Exercise Tolerance; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011651:Pulmonary Artery / Q000503:physiopathology*; D011652:Pulmonary Circulation / Q000502:physiology; D011667:Pulmonary Veins / Q000503:physiopathology*; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*