Abstract

Abnormal reflex control of the peripheral microvasculature during orthostasis in congestive heart failure (CHF) and after heart transplantation (HT) may cause failure of microvascular homeostasis and peripheral edema. We explored the effect of passive head-up tilt on lower leg capillary filtration measured by strain-gauge plethysmography in 24 patients with CHF, in 20 patients after HT (12 patients with preserved native right atrium, 8 patients without native right atrium), and in 18 controls. We hypothesized that an impaired peripheral microvascular reflex during orthostasis in CHF and HT might allow increased arterial hydrostatic pressure to increase pressure at the capillary level. To identify an impact of changes in arterial hydrostatic pressure, capillary fluid filtration was expressed per mm Hg arterial hydrostatic pressure (capillary filtration coefficient arterial pressure [CFC AP]) and was measured (1) during elevated venous pressure alone (50 mm Hg venous stasis in supine position), and (2) during elevated hydrostatic pressure at both the venous and arterial side of the vascular tree (head-up tilt with a vertical distance from the right atrium to the strain-gauge of 68 cm of water [50 mmHg]). Elevated venous pressure alone resulted in the highest CFC AP in controls (0.79 ± 0.28 ml/min · 100 ml mm Hg · 10 −3 ± SD) versus those with CHF (0.44 ± 0.23, p <0.0001) and those after HT (0.54 ± 0.22, p <0.01). However, during head-up tilt, CFC AP was similar in all 3 groups, because CFC AP decreased in controls (to 0.49 ± 0.22, p <0.0001), in contrast to unchanged CFC AP in those with CHF (0.43 ± 0.24) and in those with HT (0.50 ± 0.21). HT patients with complete removal of the native right atrium had higher CFC AP (0.62 ± 0.17) during head-up tilt than patients with preserved native right atrium (0.36 ± 0.16, p <0.005). In conclusion, patients with CHF and those after HT have increased capillary filtration to a lesser degree than controls during elevated venous pressure alone. However, during orthostasis this apparent edema-protective mechanism vanishes, probably because of compromised microvascular reflex control. During daily upright activities, this may be one important factor in the edema pathogenesis. The phenomenon is particularly distinct in HT patients without preserved native right atrium.

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