Abnormal baroreceptor-mediated vasodilation of the peripheral circulation in congestive heart failure secondary to idiopathic dilated cardiomyopathy.
BACKGROUND
Peripheral edema is a major clinical problem in congestive heart failure (CHF). The function of the edema-protective baroreceptor-mediated and local nervous vasoconstrictor reflexes of the lower leg during orthostasis in moderate and severe CHF has largely been unexplored.


RESULTS
Baroreceptor-mediated and local nervous regulation of subcutaneous blood flow of the lower leg was studied in healthy subjects and in patients with moderate and severe CHF secondary to idiopathic dilated cardiomyopathy. Blood flow was measured by the local 133Xe washout method in the supine position and during 45 degrees head-up tilt. When the central baroreceptor reflex alone was activated, the changes in subcutaneous blood flow of the heart failure patients in both groups were significantly different from those of the eleven control subjects: blood flow increased 48 +/- 26% in 10 severe and 3 +/- 24% in nine moderate CHF patients compared with the decrease in blood flow of -36 +/- 15% observed in 11 control subjects (p < 0.0001 for both). A highly significant direct association was demonstrated between changes in blood flow and New York Heart Association functional class (p = 0.007) and the left ventricular ejection fraction (p = 0.01). Activation of the baroreceptor and local venoarteriolar axon reflexes simultaneously increased blood flow significantly (30 +/- 9%) in 14 patients with severe CHF, compared with the decrease found in 14 control subjects (-53 +/- 9%) and in the group of 14 patients with moderate CHF (-17 +/- 25%) (p < 0.0001 for both).


CONCLUSIONS
Patients with CHF secondary to idiopathic dilated cardiomyopathy have an abnormal baroreceptor-mediated vasodilation in subcutaneous tissue of the lower leg during the upright position, which increases with the severity of the disease. The hemodynamic consequence is capillary hypertension and hyperemia in the leg during the upright position that may contribute to the development of edema and to the initiation of structural changes (microangiopathy) demonstrated in the microcirculation.
Wroblewski
H
H
Department of Medicine B, University Hospital, Rigshospitalet, Copenhagen, Denmark.
Kastrup
J
J
Mortensen
S A
SA
Haunsø
S
S
D000328:Adult; D001160:Arterioles / Q000294:innervation; D001369:Axons / Q000502:physiology; D001794:Blood Pressure; D002311:Cardiomyopathy, Dilated / Q000150:complications*; D005260:Female; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D007866:Leg / Q000098:blood supply; D008297:Male; D008875:Middle Aged; D011187:Posture; D011311:Pressoreceptors / Q000502:physiology*; D012018:Reflex / Q000502:physiology; D012039:Regional Blood Flow; D014655:Vascular Resistance; D014664:Vasodilation / Q000502:physiology*; D014680:Veins / Q000294:innervation