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.

BACKGROUND:Baroreflex dysfunction is common in chronic heart failure and contributes to the associated sympathoexcitation. Baroreceptor activity normally decreases during volume unloading, causing an increase in sympathetic outflow and resulting in forearm vasoconstriction. Some heart failure patients develop attenuated vasoconstriction or paradoxical vasodilation. The mechanism for this is unknown. We have recently demonstrated diastolic ventricular interaction in some patients with chronic heart failure as evidenced by increases in left ventricular (LV) end-diastolic volume in association with decreases in right ventricular (RV) volume during volume unloading. We reasoned that such an increase in LV volume, by increasing LV mechanoreceptor activity, would decrease sympathetic outflow and could therefore explain the abnormal vascular responses seen in such patients.METHODS AND RESULTS:We assessed changes in forearm vascular resistance (FVR) during application of -20 and -30 mm Hg lower-body negative pressure (LBNP) in 24 patients with chronic heart failure and 16 control subjects. Changes in LV and RV end-diastolic volumes were assessed during -30 mm Hg LBNP in all heart failure patients. Diastolic ventricular interaction was demonstrated in 12 patients as evidenced by increases in LV end-diastolic volume in association with decreases in RV end-diastolic volume during LBNP. Changes in FVR during LBNP (-20 and -30 mm Hg) were markedly attenuated in these 12 patients (-1.6+/-11.2 and -0.9+/-12.5 U) compared with both the remaining patients (11.9+/-10.0 and 17.0+/-12.3 U) and the control subjects (16.5+/-9.5 and 23.1+/-13.9 U) (P<.01 for both comparisons at each level of LBNP). FVR decreased in 5 of these 12 patients during -30 mm Hg LBNP, a response seen in none of the remaining patients (P=.01).CONCLUSIONS:Diastolic ventricular interaction in patients with chronic heart failure is associated with attenuated forearm vasoconstriction or paradoxical vasodilation during LBNP. This may explain the apparent derangement in baroreflex control of sympathetic outflow during acute volume unloading in heart failure.