Low-dose propranolol and exercise capacity in postural tachycardia syndrome: a randomized study

Abstract

Objective: To determine the effect of low-dose propranolol on maximal exercise capacity in patients with postural tachycardia syndrome (POTS).

Methods: We compared the effect of placebo vs a single low dose of propranolol (20 mg) on peak oxygen consumption (VO2max), an established measure of exercise capacity, in 11 patients with POTS and 7 healthy subjects in a randomized, double-blind study. Subjects exercised on a semirecumbent bicycle, with increasing intervals of resistance to maximal effort.

Results: Maximal exercise capacity was similar between groups following placebo. Low-dose propranolol improved VO2max in patients with POTS (24.5 ± 0.7 placebo vs 27.6 ± 1.0 mL/min/kg propranolol; p = 0.024), but not healthy subjects. The increase in VO2max in POTS was associated with attenuated peak heart rate responses (142 ± 8 propranolol vs 165 ± 4 bpm placebo; p = 0.005) and improved stroke volume (81 ± 4 propranolol vs 67 ± 3 mL placebo; p = 0.013). In a separate cohort of POTS patients, neither high-dose propranolol (80 mg) nor metoprolol (100 mg) improved VO2max, despite similar lowering of heart rate.

Conclusions: These findings suggest that nonselective β-blockade with propranolol, when used at the low doses frequently used for treatment of POTS, may provide a modest beneficial effect to improve heart rate control and exercise capacity.

Classification of evidence: This study provides Class II evidence that a single low dose of propranolol (20 mg) as compared with placebo is useful in increasing maximum exercise capacity measured 1 hour after medication.

Figure 1. Enrollment, treatment allocation, and follow-up of study participants

POTS = postural tachycardia syndrome.

Figure 2. Low-dose propranolol improves exercise capacity in patients with POTS

The effect of placebo vs low-dose propranolol on maximal exercise capacity was determined in 7 healthy subjects and 11 patients with postural tachycardia syndrome (POTS). There was no effect of low-dose propranolol on peak oxygen consumption (VO₂max) in healthy subjects (A), despite a significant lowering of peak heart rate responses (C). In contrast, propranolol significantly improved VO₂max in the patients with POTS (B), and reduced peak heart rate to a similar level as in controls (D).

Figure 3. Hemodynamic changes in response to exercise testing

Hemodynamic changes in response to semirecumbent exercise testing were assessed at 0-W and at 75-W resistance in healthy subjects and patients with postural tachycardia syndrome (POTS) receiving placebo vs low-dose propranolol. Exercise produced significant increases in cardiac output in healthy subjects (A) and patients with POTS (B), which were not different following placebo vs propranolol. There was no effect of placebo or propranolol on stroke volume in healthy subjects (C). However, low-dose propranolol significantly increased stroke volume during exercise in patients with POTS (D).