Diastolic Blood Pressure Rise During Valsalva as a Surrogate for Sympathetic Activation to Identify Functional Hyperadrenergic Postural Tachycardia Syndrome

Purpose Muscle sympathetic nerve activity (MSNA) is valuable for POTS management, but microneurography is clinically impractical. We investigated whether the Valsalva phase 2 diastolic blood pressure rise (DBP _{VM2l_rise} ) could be a surrogate for MSNA during the Valsalva and be used to identify hyperadrenergic POTS. Methods We included 21 POTS females and 22 healthy females to perform Valsalva and microneurography. MSNA spike rate was obtained using stationary wavelet transformation. The DBP _{VM2l_rise} cut point for hyperadrenergic POTS was optimized by the golden section search with its correlation to phase 2 MSNA spike rate as an objective function. We defined peripheral sympathetic neurovascular transduction (psNVT) as a ratio of DBP _{VM2l_rise} to early phase 2 MSNA increase. We compared Valsalva responses between the identified hyperadrenergic and non-hyperadrenergic POTS. Results The DBP _{VM2l_rise} strongly correlated with the Valsalva phase 2 MSNA spike rate percentage change from baseline in healthy (r = 0.874, p < 0.001). The DBP _{VM2l_rise} equal 15 mmHg optimally separated POTS into 7 hyperadrenergic (≥ 15 mmHg, r = 0.902, p = 0.014) and 14 non-hyperadrenergic (< 15 mmHg, r = 0.629, p = 0.021). Although similar MSNA spike rate, the hyperadrenergic group had higher baseline systolic blood pressure (118 ± 10vs105 ± 12 mmHg, p = 0.026), shorter pressure recovery time (1.15 ± 0.75vs2.59 ± 1.17 s, p = 0.005), and higher psNVT (2.60 ± 1.02vs0.58 ± 0.46 mmHg/spike∙s ^− 1 , p < 0.001) than the non-hyperadrenergic POTS. Conclusion DBP _{VM2l_rise} ≥ 15 mmHg could be a marker of hyperadrenergic response to subtype POTS. We defined this subset of POTS as functional hyperadrenergic POTS since they displayed hyperadrenergic phenotypes despite similar level of MSNA to other POTS. The higher psNVT of the hyperadrenergic group suggested a novel pathophysiology of enhanced neurovascular coupling.