title: Force- and relaxation-frequency relations in patients with diastolic heart failure.
abstract: BACKGROUND
  Chronotropic effects on myocardial contractility (the positive force-frequency relation) and relaxation (the positive relaxation-frequency relation) are impaired in patients with congestive heart failure and depressed left ventricular (LV) ejection fraction (systolic heart failure [SHF]). However, the force- and relaxation-frequency relation and LV-arterial coupling in patients with diastolic heart failure (DHF) has not been fully investigated.
  
  
  RESULTS
  To examine inotropic and lusitropic responsiveness to atrial pacing, LV pressure-volume relations were measured using a conductance catheter and microtip manometer in patients with DHF (n = 18) and SHF (n = 11). In patients with SHF, an increase in heart rate by 40 beat/min did not affect LV end-systolic elastance (Ees), which reflects LV contractility, or the time constant of LV relaxation. By contrast, in patients with DHF, an increase in heart rate by 40 beat/min significantly enhanced Ees (2.1 vs 2.9 mm Hg/mL, P < .05) but not the time constant. Furthermore, LV-arterial coupling, quantified as Ees/arterial elastance, was impaired during pacing in patients with DHF (1.1 vs 0.8, P < .05) as well as SHF.
  
  
  CONCLUSIONS
  In patients with DHF, the force-frequency relation was preserved, but the relaxation-frequency relation was impaired. Furthermore, LV-arterial coupling was impaired as heart rate increased, which may be related to the impaired LV function. These results suggest that the impaired relaxation-frequency relation and exacerbated LV-arterial coupling during tachycardia may be an important therapeutic target in patients with DHF.
authors.affiliation: The First Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamanaka
authors.forename: Katsuya
authors.initials: K
authors.lastname: Onishi
authors.forename: Masaki
authors.initials: M
authors.lastname: Tanabe
authors.forename: Kaoru
authors.initials: K
authors.lastname: Dohi
authors.forename: Kaoru
authors.initials: K
authors.lastname: Funabiki-Yamanaka
authors.forename: Naoki
authors.initials: N
authors.lastname: Fujimoto
authors.forename: Tairo
authors.initials: T
authors.lastname: Kurita
authors.forename: Takashi
authors.initials: T
authors.lastname: Tanigawa
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kitamura
authors.forename: Masaaki
authors.initials: M
authors.lastname: Ito
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nobori
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nakano
mesh_terms: D000328:Adult; D000368:Aged; D002304:Cardiac Pacing, Artificial; D003971:Diastole / Q000502:physiology; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D013610:Tachycardia / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*