title: Ventricular-Arterial Coupling and Exercise-Induced Pulmonary Hypertension During Low-Level Exercise in Heart Failure With Preserved or Reduced Ejection Fraction.
abstract: BACKGROUND
  Exercise-induced pulmonary hypertension (EIPH) may develop even at low workloads in heart failure (HF) patients. Ventricular-arterial stiffening plays an important role in the pathophysiology of HF with preserved ejection fraction (HFpEF). This study aimed to compare the response of ventricular-arterial coupling and PH during low-level exercise between HFpEF and HF with reduced EF (HFrEF).
  
  
  RESULTS
  Echocardiography was performed at rest and during 10 W of bicycle exercise in HFpEF (n = 37) and HFrEF (n = 43). Load-independent contractility (end-systolic elastance [Ees], preload recruitable stroke work [PRSW], and peak power index [PWRI]), arterial afterload (arterial elastance [Ea]), and ventricular-arterial interaction (Ea/Ees) were measured with the use of a noninvasive single-beat technique. EIPH was defined as an estimated pulmonary arterial systolic pressure (PASP) of ≥50 mm Hg at 10 W of exercise. PASP was significantly increased during 10 W of exercise in both HF types, and ~50% of HFpEF patients developed EIPH. Arterial afterload was increased significantly during exercise in both groups. HFrEF and HFpEF patients showed a significant increase in LV contractility assessed by Ees, PRSW, and PWRI during exercise. Although Ea/Ees ratio decreased significantly in HFrEF, reduction in Ea/Ees was attenuated because of blunted Ees increases in patients with HFpEF compared with HFrEF.
  
  
  CONCLUSIONS
  Even at low-level exercise, ~50% of HFpEF patients developed EIPH. Reduction in Ea/Ees was attenuated owing to less Ees increase in HFpEF compared with HFrEF. Further studies are needed to elucidate the association between ventricular-arterial coupling and EIPH in HFpEF.
authors.affiliation: Department of Medicine and Biological Science, Gunma University Graduate School of Medicine, Maebashi, Japan. Electronic address: lady2o814@gmail.com.
authors.forename: Masaru
authors.initials: M
authors.lastname: Obokata
authors.affiliation: Second Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
authors.forename: Yasufumi
authors.initials: Y
authors.lastname: Nagata
authors.affiliation: Department of Cardiovascular Surgery, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Kado
authors.affiliation: Department of Medicine and Biological Science, Gunma University Graduate School of Medicine, Maebashi, Japan.
authors.forename: Masahiko
authors.initials: M
authors.lastname: Kurabayashi
authors.affiliation: Second Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Otsuji
authors.affiliation: Department of Laboratory and Transfusion Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
authors.forename: Masaaki
authors.initials: M
authors.lastname: Takeuchi
mesh_terms: D000368:Aged; D004452:Echocardiography; D015444:Exercise / Q000502:physiology; D005080:Exercise Test / Q000009:adverse effects*; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D012189:Retrospective Studies; D013318:Stroke Volume / Q000502:physiology*; D059289:Vascular Stiffness / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology*
keywords: Arterial afterload; exercise; heart failure; ventricular-arterial coupling