Forearm vasoconstriction during dynamic leg exercise in patients with chronic heart failure

Citation
Jj. Atherton et al., Forearm vasoconstriction during dynamic leg exercise in patients with chronic heart failure, HEART VESS, 13(6), 1998, pp. 278-289
Citations number
50
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
HEART AND VESSELS
ISSN journal
09108327 → ACNP
Volume
13
Issue
6
Year of publication
1998
Pages
278 - 289
Database
ISI
SICI code
0910-8327(1998)13:6<278:FVDDLE>2.0.ZU;2-3
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 fa ilure may explain some of the variation. We reasoned that diastolic ventric ular interaction (DVI), by limiting the ability of such patients to increas e left ventricular (LV) volume and stroke volume during exercise, would att enuate baroreflex activation, resulting in increased sympathetic activation and hence exaggerated vasoconstriction. We hypothesized therefore that vas oconstriction in nonexercising beds would be exaggerated in patients with s ymptomatic and hemodynamically severe heart failure, particularly if associ ated with DVI. We measured forearm vascular resistance (FVR) during semierect cycle exerci se in 22 CHF patients and 23 control subjects. DVI was assessed by measurin g changes in ventricular volumes (radionuclide ventriculography) during vol ume unloading (-30 mm Hg lower-body negative pressure) in the heart failure patients and was inferred when LV end-diastolic volume paradoxically incre ased. Patients with symptoms of heart failure developed larger increases in FVR d uring exercise than did asymptomatic patients. There were significant corre lations between the change in FVR during peak exercise and the resting mean pulmonary arterial pressure and pulmonary vascular resistance. CHF patient s with DVI developed exaggerated increases in FVR (median [25th to 75th per centile]) 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 exe rcise (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 associ ated with DVI. This may explain some of the reported variation in the degre e of sympathetic activation that occurs during exercise in CHF patients.