Postprandial Hypotension in Parkinson's Disease and Multiple System Atrophy

Objective: We describe a case with Parkinson’s Disease (PD), neurogenic orthostatic hypotension (nOH) and profound postprandial hypotension (PPH) and reviewed our database to determine the degree of PPH in central (multiple system atrophy, MSA) versus peripheral (PD) autonomic failure due to alpha-synucleionopathies. Background: Postprandial hypotension (PPH) is a significant co-morbid condition, affecting patients with autonomic failure due to alpha-synucleionopathies. Our previous data showed no difference in PPH severity between pure autonomic failure patients and MSA. Design/Methods: Patient history and examination was obtained from patient and hospital records. 27 total cases were selected from patients seen in Vanderbilt Autonomic Dysfunction Center in the last 5 years, 7 men and 3 women with PD including index patient, 11 men and 6 women with MSA. Diagnosis based on data at hospitalization. PPH was measured sitting before and 120 minutes after a high carbohydrate breakfast. Results: Index patient is a 70 YO female with PD admitted for management of nOH and supine hypertension. Orthostatic vital signs were 192/101 supine, heart rate 74, and 149/92, hr 100 after 10 min standing (ΔSBP 43 mm hg). Postprandial pressures before and after meal were 165/99, hr 85 and 84/55, hr 109 50 min after (ΔSBP 81 mm hg). Data review showed PD patients (10 total) had significantly greater PPH than 17 MSA patients (ΔSBP 48 ± 24 mm vs. 21± 18 mm, p=0.002). nOH was non-significantly greater in PD vs MSA (ΔSBP 81±24 mm vs. 62± 28 mm, p=0.11). PD patients were older (79 vs 63, p=0.007) but of similar race and gender distribution. Conclusions: Postprandial hypotension can be greater than orthostatic hypotension in patients with PD. Patients with PD and nOH are more likely to develop postprandial hypotension compared to MSA patients, which may be due to less residual sympathetic tone. Postprandial hypotension should be considered in diagnostic evaluation and treatment. Disclosure: Dr. Peltier has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with CSL Behring, Lundbeck Pharmaceutical Companies, and Alnylam. Dr. Kimmet has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Lundbeck. Dr. Garland has nothing to disclose. Dr. Black has nothing to disclose. Dr. Diedrich has nothing to disclose. Dr. Shibao has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Lundbeck. Dr. Shibao has received research support from Lundbeck. Dr. Biaggioni has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Lundbeck, Theravance Biopharma. Dr. Biaggioni has received research support from Lundbeck (investigator-initiated grant) and Theravance Biopharma (Clinical Trial).