Why the study?
Does orthostatic stress induce abnormal peripheral vasodilation in patients with severe heart failure compared to healthy controls?
Does orthostatic stress induce abnormal peripheral vasodilation in patients with severe heart failure compared to healthy controls?
Patients with severe heart failure exhibit sustained paradoxical peripheral vasodilation during orthostatic stress, suggesting a pathophysiological mechanism contributing to lower extremity edema.
Answers are grounded in this paper and cite their sources.
May promote edema in severe HF; hypothesis-generating and requires prospective confirmation before clinical consideration.
Baroreceptor-induced peripheral reflex vasoconstriction during upright posture is an important edema-prevention mechanism in humans. Congestive heart failure (CHF) has been associated with blunted baroreceptor control of regional blood flow during short-term head-up tilt. The effect of prolonged unloading of baroreceptors on subcutaneous blood flow of the calf was investigated in 12 healthy subjects and in 13 patients with severe idiopathic dilated cardiomyopathy (New York Heart Association functional class III or IV). The subjects were studied both supine and sitting for 3-h periods. When sitting, subcutaneous vascular resistance decreased -26 +/- 19% in CHF patients and increased 90 +/- 69% in control subjects (P < 0.0001). The corresponding subcutaneous blood flow increased 43 +/- 29% in patients with CHF compared with the decrease of -42 +/- 17% in control subjects (P < 0.0001). I conclude that patients with CHF secondary to idiopathic dilated cardiomyopathy have an abnormal baroreceptor-mediated peripheral vasodilation during orthostatic stress that is sustained for hours. This extended paradoxical vasodilation may participate as an additional pathophysiological mechanism contributing to lower extremity edema in patients with CHF.
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Henrik Wroblewski (1994) studied this question.
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