Chronic treatment with propranolol does not alter sympathetic and cardiovagal baroreflex sensitivity in the Postural Orthostatic Tachycardia Syndrome

Abstract

Patients with Postural Orthostatic Tachycardia Syndrome (POTS) have marked increases in heart rate (HR) during orthostasis, while β‐blocker is commonly used to reduce tachycardia. We tested the hypothesis that chronic β‐blocker treatment alters baroreflex sensitivity in POTS. Eighteen POTS patients (age 16–44) were treated with placebo (n=10) or propranolol (n=8, 80 mg qd) for 1 mo. Sympathetic baroreflex sensitivity was quantified by 1) linear correlation between muscle sympathetic nerve activity (MSNA) and stroke volume supine and during a graded upright tilt, and 2) relating sympathetic bursts to the fall of diastolic blood pressure (BP) during Valsalva (VAL). Cardiovagal baroreflex sensitivity was assessed during early phase II (decreasing BP) and phase IV (increasing BP) of VAL. Patients’ quality of life was evaluated using SF‐36 form. Propranolol decreased upright HR but had limited impacts on MSNA. Sympathetic baroreflex sensitivity remained unchanged after propranolol treatment [−1.04±0.40 bursts/min/mL pre vs −0.99±0.33 post, P=0.78; −0.97±0.30 bursts/20s/mmHg pre vs −1.01±0.33 post, P=0.69). Cardiovagal baroreflex sensitivity during decreasing BP (5.05±3.58 ms/mmHg pre vs 5.75±2.03 post, P=0.44) and during increasing BP (14.23±7.59 ms/mmHg vs 13.05±4.43; P=0.92) of VAL was comparable before and after propranolol treatment. Patients’ quality of life remained unchanged after treatment. Placebo had no effects on any variables measured. These results suggest that chronic propranolol treatment decreased tachycardia but did not alter baroreflex sensitivity in POTS patients. Patients’ quality of life was not improved by propranolol. More effective therapies to improve not only symptoms but also patients’ overall well‐being are needed.