Local Heat Stress in Autonomic Failure Patients With Supine Hypertension

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Primary autonomic failure is a neurodegenerative condition characterized by severe impairment of the autonomic nervous system. The clinical hallmark of autonomic failure is disabling orthostatic hypotension, but at least half of patients are also hypertensive while lying down. This supine hypertensi...

Primary autonomic failure is a neurodegenerative condition characterized by severe impairment of the autonomic nervous system. The clinical hallmark of autonomic failure is disabling orthostatic hypotension, but at least half of patients are also hypertensive while lying down. This supine hypertension can be severe and associated with end-organ damage and worsening of orthostatic hypotension due to increased pressure natriuresis. It also complicates the management of these patients by limiting the use of daytime pressor agents for the treatment of orthostatic hypotension. It is well known that heat exposure (e.g. hot weather or a hot bath or shower) produces an acute and temporary worsening of orthostatic hypotension in autonomic failure patients. However, the mechanisms underlying this phenomenon are completely unexplored. Factors that may predispose autonomic failure patients to the acute lowering blood pressure effects of heat stress include 1) impaired heat dissipation due to inability to sweat, 2) preserved heat-mediated skin vasodilation, and 3) blunted sympathetic hemodynamic responses to maintain blood pressure. In this study, we test the hypothesis that moderate levels of local (abdominal) passive heat stress will lower blood pressure in autonomic failure patients with supine hypertension. To test this hypothesis, we propose this pilot study with the following specific aims: To evaluate the acute blood pressure effects of local passive heat stress in autonomic failure patients with supine hypertension, we will compare changes in BP between controlled local heat stress (~44ºC) using a commercial heating pad that covers the abdomen and part of the torso, and a control (non-heating) study day using the same heating pad but turned off. To evaluate the mechanisms underlying BP changes during local heat stress, we will compare changes in hemodynamic parameters (cardiac output, stroke volume and peripheral vascular resistance), segmental fluid shifts (measured by segmental bioimpedance), skin blood flow and skin temperature between the heat and non-heating study days.

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