Mechanisms governing the postural response and baroreceptor abnormalities in chronic congestive heart failure: effects of acute and long-term converting-enzyme inhibition.

Abstract

SUMMARYWe assessed the hemodynamic and hormonal response to tilt and the baroreceptor response in 12 patients in sinus rhythm with severe chronic congestive heart failure. We also assessed the response to acute (n = 12) and chronic (n = 8) converting-enzyme inhibition with captopril. The control tilt was characterized by high cardiac filling pressures, absence of significant peripheral pooling and apparent absence of afferent stimuli for hemodynamic and hormonal response. After acute captopril, the hemodynamic response to tilt was improved, but not normalized. The chronic response was characterized by the absence of a reflex increase of systemic vascular resistance on tilt despite peripheral pooling. Five patients developed orthostatic hypotension, but responded to acute infusion of 0.9% sodium chloride. Efferent sympathetic activity (response to cold pressor) was abnormal during the control study, but indistinguishable from normal subjects by the time of chronic captopril therapy. This paralleled an improved responsiveness of plasma catecholamines during chronic tilt. The Valsalva maneuver remained abnormal. There was a distinct absence of the normally anticipated heart rate increase on tilt, suggesting a parasympathetic abnormality.IN BOTH normal and hypertensive persons, upright posture is associated with significant peripheral pooling. 14 Orthostatic hypotension does not occur because reflex increase of systemic resistance and heart rate compensate for the peripheral pooling. Activation of the renin-angiotensin system and compensatory change of sympathetic and parasympathetic tone are also important adjustments.2' 5-8 Abelmann and Fareeduddin9' 10 demonstrated that the hemodynamic response to tilt in chronic congestive heart failure is atypical; that is, there was no significant peripheral pooling in the upright posture. Hence, reflex stimulation of increased systemic vascular resistance and heart rate did not appear necessary to avert orthostatic hypotension. This atypical response was attributed to intense volume expansion and vasoconstriction, but the interactions of controlling mechanisms are not known. Studies in animal models and in humans have demonstrated abnormalities of sympathetic and parasympathetic control of heart rate in chronic congestive heart failure. 1-15Few data are available regarding the effects of vasodilator therapy on these abnorrnalities, although this mode of therapy is widely used.'6 Vasodilator therapy could significantly alter the vasoconstriction, volume alterations and hormonal response that normally accompany the assumption of upright posture. This may have some influence on the reported discrepancy between supine and dynamic assessment of hemodynamic improvement during chronic vasodilator therapy of severe congestive heart failure.17 In the present study we reevaluated the factors contributing to the tilt response and baroreceptor function in severe chronic congestive heart failure. We assessed the effects of acute and chronic vasodilator therapy on these responses using the...

Enalapril in African patients with congestive cardiac failure.

“…The maximum tachycardia during strain (phase II) was comparable with findings in normal volunteers, but the maximum bradycardia during overshoot (phase IV) was significantly lower in the cardiac patients (P < 0.001), compared with normals (Ajayi et al, 1986). This may be indicative of an abnormality in efferent parasympathetic cardiac control in heart failure as previously suggested (Cody et al, 1982).…”

Sodium and water balance in chronic congestive heart failure.

“…All 10 patients received both the 10 meq and 100 meq sodium diets. Hemodynamic measurements were obtained in the supine (-) and upright (t) positions, both before and after a 25- (7). Following catheter placement, a 1-h stabilization period ensued.…”

Evidence for a direct renal stimulating effect of prostaglandin E2 on renin release in patients with congestive heart failure.

“…Abnormal structure and function of these receptors have been demonstrated in experimental heart failure2 12 and appear to be normalized after reversal of heart failure. 13 The reflex sympathetic response to tilt has been shown to improve in patients with congestive failure after converting enzyme inhibition, 14 suggesting that the autonomic changes are not irreversible.…”