Diastolic Ventricular Interaction

Abstract

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.