# Hyperadrenergic postural tachycardia syndrome associated with augmented neurovascular transduction

## TL;DR

This study identifies a new clinical marker for hyperadrenergic POTS, showing that increased neurovascular transduction helps distinguish this subtype from others.

## Contribution

Proposes DBPVM2l_rise as a non-invasive sympathetic marker and reveals enhanced neurovascular transduction in hyperadrenergic POTS.

## Key findings

- DBPVM2l_rise strongly correlates with MSNA spike rate in healthy individuals and POTS patients.
- Hyperadrenergic POTS patients show higher baseline blood pressure and faster pressure recovery compared to non-hyperadrenergic POTS.
- Enhanced peripheral sympathetic neurovascular transduction is a key feature of hyperadrenergic POTS.

## Abstract

Muscle sympathetic nerve activity (MSNA) is valuable for managing postural tachycardia syndrome (POTS), but microneurography is clinically impractical. We investigated whether the Valsalva phase 2 diastolic blood pressure rise (DBPVM2l_rise) serves as a sympathetic marker and proposed enhanced neurovascular transduction as a pathophysiological mechanism in hyperadrenergic POTS.

We included 21 POTS women and 22 healthy women to perform Valsalva and microneurography. MSNA spike rate was obtained using stationary wavelet transformation. The DBPVM2l_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 DBPVM2l_rise to early phase 2 MSNA increase. We compared Valsalva responses between the identified hyperadrenergic and non-hyperadrenergic POTS.

The DBPVM2l_rise strongly correlated with the Valsalva phase 2 MSNA spike rate percentage change from baseline in healthy (r = 0.874, p < 0.001). The DBPVM2l_rise cutoff criterion of 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 ± 10 vs 105 ± 12 mmHg, p = 0.026), shorter pressure recovery time (1.15 ± 0.75 vs 2.59 ± 1.17 s, p = 0.048), and higher psNVT (2.60 ± 1.02 vs 0.58 ± 0.46 mmHg/spike·s−1, p < 0.001) than the non-hyperadrenergic POTS.

DBPVM2l_rise ≥ 15 mmHg could be a sympathetic clinical marker and could identify hyperadrenergic POTS, characterized by enhanced neurovascular transduction despite comparable MSNA levels. This novel pathophysiological insight underscores the importance of sympathetic markers in POTS clinical management.

The online version contains supplementary material available at 10.1007/s10286-025-01183-z.