title: Forearm vasoconstriction during dynamic leg exercise in patients with chronic heart failure.
abstract: Previous studies assessing vascular responses in nonexercising beds during exercise in patients with chronic heart failure (CHF) have yielded varying results. We proposed that the clinical and hemodynamic severity of heart failure may explain some of the variation. We reasoned that diastolic ventricular interaction (DVI), by limiting the ability of such patients to increase left ventricular (LV) volume and stroke volume during exercise, would attenuate baroreflex activation, resulting in increased sympathetic activation and hence exaggerated vasoconstriction. We hypothesized therefore that vasoconstriction in nonexercising beds would be exaggerated in patients with symptomatic and hemodynamically severe heart failure, particularly if associated with DVI. We measured forearm vascular resistance (FVR) during semierect cycle exercise in 22 CHF patients and 23 control subjects. DVI was assessed by measuring changes in ventricular volumes (radionuclide ventriculography) during volume unloading (-30 mm Hg lower-body negative pressure) in the heart failure patients and was inferred when LV end-diastolic volume paradoxically increased. Patients with symptoms of heart failure developed larger increases in FVR during exercise than did asymptomatic patients. There were significant correlations between the change in FVR during peak exercise and the resting mean pulmonary arterial pressure and pulmonary vascular resistance. CHF patients with DVI developed exaggerated increases in FVR (median [25th to 75th percentile]) compared with the remaining patients during low-workload exercise (138 [66 to 171] vs 6.4 [-4.3 to 28] units, P = 0.002) and during peak exercise (160 [90 to 384] vs 61 [-7.4 to 75] units, P < 0.02). Vasoconstriction in nonexercising beds is exaggerated in CHF patients with clinically and hemodynamically severe heart failure, particularly if associated with DVI. This may explain some of the reported variation in the degree of sympathetic activation that occurs during exercise in CHF patients.
authors.affiliation: Department of Medicine, University of Queensland, Brisbane, Australia.
authors.forename: J J
authors.initials: JJ
authors.lastname: Atherton
authors.forename: L G
authors.initials: LG
authors.lastname: Dryburgh
authors.forename: H L
authors.initials: HL
authors.lastname: Thomson
authors.forename: T D
authors.initials: TD
authors.lastname: Moore
authors.forename: K N
authors.initials: KN
authors.lastname: Wright
authors.forename: G W
authors.initials: GW
authors.lastname: Muehle
authors.forename: L E
authors.initials: LE
authors.lastname: Fitzpatrick
authors.forename: M P
authors.initials: MP
authors.lastname: Frenneaux
mesh_terms: D000704:Analysis of Variance; D015444:Exercise; D017079:Exercise Tolerance; D005260:Female; D005542:Forearm / Q000098:blood supply; D006333:Heart Failure / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D015635:Radionuclide Ventriculography; D018709:Statistics, Nonparametric; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014655:Vascular Resistance; D014661:Vasoconstriction; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology