Altered venous capacitance as a cause of postprandial hypotension in multiple system atrophy

Abstract

Patients with multiple system atrophy (MSA) often have clinically significant postprandial hypotension (PPH). To elucidate the cause of insufficient cardiac preload augmentation that underlies PPH, we recorded calf venous capacitance (CVC) by strain-gauge plethysmography, in 17 MSA patients and eight healthy controls before and after oral glucose ingestion. Among 17 MSA patients, nine who showed a decrease in systolic blood pressure exceeding 20 mmHg and were diagnosed with PPH. MSA patients without PPH showed a significant decrease in CVC and a significant increase in cardiac output after oral glucose ingestion, as did controls; those with MSA exhibiting PPH showed a significant increase in CVC and no significant change in cardiac output. The change in CVC correlated positively with the decrease in systolic and diastolic blood pressure after glucose ingestion, and also correlated negatively with the increase in cardiac output. Physiologically, PPH is prevented by a decrease in venous capacitance, which increases circulating blood volume and cardiac output. In some MSA patients, failure of venous capacitance to decrease may induce PPH.

The effect of intraduodenal glucose on muscle sympathetic nerve activity in healthy young and older subjects

“…Hypothesis 4 (about cardiac output) is supported by the findings that in healthy young subjects, meal ingestion increases cardiac output [12,37] and that, with aging, the cardiovascular reserve capacity decreases [21]. Our study failed to reveal significant differences in CO between the healthy young and older subjects (Table 2), although at the nadir of the systolic blood pressure, stroke volume was significantly higher in the young group.…”

The potential prognostic role of cardiovascular autonomic failure in α‐synucleinopathies

“…In dysautonomic patients, impairment of sympathetic output and consequent failure of activating counterbalance mechanisms also produce PPH, which is commonly defined as a decrease in SBP ≥20 mmHg within 2 h after a meal . Preliminary cross‐sectional studies reported PPH in 48% of dysautonomic PD patients and 47% of MSA patients .…”

Acute Effects of Nutritive and Non-Nutritive Sweeteners on Postprandial Blood Pressure

“…The majority of studies investigating PPH have utilised an oral [11,12,13,16,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73], and/or ID glucose [14,18,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88] load that induces a substantial fall in BP. There have been a total of 58 studies related to effects of glucose on postprandial BP in a range of cohorts including health [11,12,14,16,18,39,40,41...…”