title: Supine-exercise-induced oxygen supply to the right myocardium is attenuated in patients with severe idiopathic pulmonary arterial hypertension.
abstract: BACKGROUND
  Impaired right ventricular (RV) myocardial blood flow (MBF) has been associated with RV dysfunction and fatal RV failure in idiopathic pulmonary hypertension during stress. MBF and O(2) extraction from myocardial capillaries (O(2) extraction fraction (OEF)) influence myocardial O(2) supply.
  
  
  OBJECTIVE
  To determine how the baseline RV OEF affects the amount of MBF increase induced by supine exercise, the authors hypothesise that higher baseline OEF (H-OEF) results in limited O(2) extraction during exercise and that MBF must therefore be increased to obtain sufficient O(2).
  
  
  METHODS
  In 18 patients with idiopathic pulmonary hypertension, baseline OEF, resting MBF and exercise-induced MBF at 40% of maximal cardiopulmonary exercise testing load were measured using positron emission tomography and [(15)O]O(2), [(15)O]H(2)O and [(15)O]CO.
  
  
  RESULTS
  For the whole population, exercise increased RV MBF from 0.68±0.16 to 1.13 ± 0.38 ml/min/g (p < 0.0001). The MBF exercise-to-rest ratio (reserve) was 1.7 ± 0.7. The median baseline OEF was 0.73 at which the patient population was split into H-OEF and lower baseline OEF (L-OEF). Baseline MBF values (0.61 ± 0.11 and 0.74 ± 0.17 ml/min/g, respectively) were similar, and exercise induced a significant MBF increase in both groups (p = 0.0001). However, exercise-induced increase in MBF was significantly less in the H-OEF group than in the L-OEF group (0.97 ± 0.30 and 1.30 ± 0.39 ml/min/g, respectively, p < 0.05). Moreover, H-OEF patients had lower baseline stroke volume and cardiac output than the L-OEF group (52 ± 19 ml and 4.0 ± 1.1 l/min vs 78 ± 18 ml and 5.5 ± 0.9 l/min, respectively, both p < 0.05).
  
  
  CONCLUSIONS
  H-OEF patients were hemodynamically poorer and showed a lower exercise-induced MBF increase compared to L-OEF patients, suggesting exercise-induced O(2) supply limitation.
authors: Department of Pulmonology, Institute of Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands.
authors: Yeun Ying
authors: YY
authors: Wong
authors: Pieter G
authors: PG
authors: Raijmakers
authors: Paul
authors: P
authors: Knaapen
authors: Mark
authors: M
authors: Lubberink
authors: Gerrina
authors: G
authors: Ruiter
authors: J Tim
authors: JT
authors: Marcus
authors: Anco
authors: A
authors: Boonstra
authors: Adriaan A
authors: AA
authors: Lammertsma
authors: Nico
authors: N
authors: Westerhof
authors: Willem J
authors: WJ
authors: van der Laarse
authors: Anton
authors: A
authors: Vonk-Noordegraaf
mesh_terms: D006328:Cardiac Catheterization; D003326:Coronary Circulation / Q000502:physiology*; D018450:Disease Progression; D015444:Exercise / Q000502:physiology*; D065627:Familial Primary Pulmonary Hypertension; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology*; D012189:Retrospective Studies; D012720:Severity of Illness Index; D014055:Tomography, Emission-Computed; D018497:Ventricular Dysfunction, Right / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D010100:Oxygen