DIASTOLIC VENTRICULAR INTERACTION - A POSSIBLE MECHANISM FOR ABNORMALVASCULAR-RESPONSES DURING VOLUME UNLOADING IN HEART-FAILURE

Background Baroreflex dysfunction is common in chronic heart failure a nd contributes to the associated sympathoexcitation. Baroreceptor acti vity normally decreases during volume unloading, causing an increase i n sympathetic outflow and resulting in forearm vasoconstriction. Some heart failure patients develop attenuated vasoconstriction or paradoxi cal vasodilation. The mechanism for this is unknown. We have recently demonstrated diastolic ventricular interaction in some patients with c hronic heart failure as evidenced by increases in left ventricular (LV ) end-diastolic volume in association with decreases in right ventricu lar (RV) volume during volume unloading. We reasoned that such an incr ease in LV volume, by increasing LV mechanoreceptor activity, would de crease sympathetic outflow and could therefore explain the abnormal va scular responses seen in such patients. Methods and Results We assesse d changes in forearm vascular resistance (FVR) during application of - 20 and -30 mm Hg lower-body negative pressure (LBNP) in 24 patients wi th chronic heart failure and 16 control subjects. Changes in LV and RV end-diastolic volumes were assessed during -30 mm Hg LBNP in all hear t failure patients. Diastolic ventricular interaction was demonstrated in 12 patients as evidenced by increases in LV end-diastolic volume i n association with decreases in RV end-diastolic volume during LBNP. C hanges 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 bo th the remaining patients (11.9+/-10.0 and 17.0+/-12.3 U) and the cont rol subjects (16.5+/-9.5 and 23.1+/-13.9 U) (P<.01 for both comparison s at each level of LBNP). FVR decreased in 5 of these 12 patients duri ng -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 vasoconst riction or paradoxical vasodilation during LBNP. This may explain the apparent derangement in baroreflex control of sympathetic outflow duri ng acute volume unloading in heart failure.