Abstract

Postprandial hypotension (PPH) is defined as a sudden and substantial decrease (>20 mmHg or >10 mmHg) in blood pressure (BP) within two hours post meal intake; This condition is highly prevalent in neurogenic orthostatic hypotension (nOH) and is associated with pre-syncopal symptoms and postprandial syncope. We studied factors contributing to PPH in nOH. Patients were admitted at the Vanderbilt clinical research center and placed on a sodium-controlled diet. Autonomic function testing, including continuous recording of BP and heart rate (HR) during head up tilt, sinus arrhythmia, and Valsalva Maneuver, was performed. Subjects took a high-carbohydrate meal (~500 Kcal). Hemodynamic parameters were monitored every 5 mins for 30 minutes before and up to 120 minutes afterwards. Results: We recruited 13 patients with peripheral autonomic failure (Parkinson’s Disease), 62% males, 73±9.08 y.o. and 13 with central autonomic failure (Multiple System Atrophy), 69% males, 62±8.23 y.o. All subjects had a substantial SBP (-42.9 ±27.90 mmHg) and DBP (-20.8 ±15.2 mmHg) decrease within 3 mins of standing, without compensatory HR increase (11.64 ± 5.97 bpm). The orthostatic increase in HR adjusted by decrease in SBP was abnormal (0.4±0.43, normal>0.5), sinus arrhythmia ratio was abnormal (1.05±0.04, normal>1.2). Pressor response in Valsalva Maneuver showed impaired sympathetic vasoconstriction. Postprandial hemodynamic changes were analyzed with area under the curve (AUC) and at 30-min timepoint post meal, which was the nadir. PD had a larger DBP increase (907±214.83 mmHg vs.1209±277.68 mmHg MSA, P=0.016), MSA had a higher HR increase (1102±236 mmHg vs. 1318±199.82 mmHg, P=0.029). No difference was found in AUC SBP, however at 30-min post-meal, SBP was lower in PD (-25±24.19 mmHg vs. -3.3±15.05 mmHg MSA, P=0.026). Only supine SBP predicted the postprandial decrease in SBP at 30 min (r=-0.5, P=0.04). Conclusion: PPH is more severe in peripheral autonomic failure; supine BP was associated with PPH.

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