title: Exaggerated hypertensive response to exercise in patients with diastolic heart failure.
abstract: Systolic load elevation during exercise prolongs left ventricular (LV) relaxation, compromises filling, and raises end-diastolic pressure, leading to reduced exercise tolerance. The aim of this study was to test the hypothesis that the hypertensive response to exercise is exaggerated in patients with diastolic heart failure (DHF). Echocardiograms and treadmill testing were performed in patients with DHF (n=20) and age-matched hypertension with LV hypertrophy (HTN; n=20). The Minnesota Living with Heart Failure Questionnaire was used to estimate quality of life (QOL). There were no differences in resting blood pressure or echocardiographic parameters between the groups. The maximum exercise time was significantly shorter in the DHF group than in the HTN group (6.0+/-3.0 vs. 12.5+/-2.5 min), and the peak systolic blood pressure during exercise was significantly higher in the DHF group (212+/-18 vs. 189+/-16 mmHg, p<0.05). After 4 weeks of treatment with candesartan, an angiotensin II receptor blocker (8 mg/d), peak systolic blood pressure during exercise decreased to 191+/-13 mmHg, maximum exercise time increased (10.4+/-3.0 min; p<0.05), and QOL improved in patients with DHF, while there was no change in patients with HTN, despite the similar resting blood pressure. In patients with DHF, systolic blood pressure markedly increased during exercise, and this was accompanied by impaired exercise tolerance and a decreased QOL, both of which were partly suppressed by blocking angiotensin II.
authors.affiliation: Department of Cardiology, Mie University Graduate School of Medicine, Tsu, Japan.
authors.forename: Shinya
authors.initials: S
authors.lastname: Kato
authors.forename: Katsuya
authors.initials: K
authors.lastname: Onishi
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamanaka
authors.forename: Takeshi
authors.initials: T
authors.lastname: Takamura
authors.forename: Kaoru
authors.initials: K
authors.lastname: Dohi
authors.forename: Norikazu
authors.initials: N
authors.lastname: Yamada
authors.forename: Hideo
authors.initials: H
authors.lastname: Wada
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nobori
authors.forename: Masaaki
authors.initials: M
authors.lastname: Ito
mesh_terms: D000368:Aged; D000804:Angiotensin II / Q000097:blood; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D001562:Benzimidazoles / Q000627:therapeutic use; D001713:Biphenyl Compounds; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004452:Echocardiography; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D054144:Heart Failure, Diastolic / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000503:physiopathology; D008297:Male; D011788:Quality of Life; D013777:Tetrazoles / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D013777:Tetrazoles; D000804:Angiotensin II; C081643:candesartan