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.