ArticleHypertension (Dallas, Tex. : 1979)2024
Hyperadrenergic Postural Tachycardia Syndrome: Clinical Biomarkers and Response to Guanfacine.
Article in Hypertension (Dallas, Tex. : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Hyperadrenergic and neuropathic features based on clinical autonomic testing in individuals with POTS: an observational cross-sectional study.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026Article
- Orthostatic Hypertension: Clinical Spectrum and Gaps in Knowledge.Current hypertension reports · 2026Review
- Hyperadrenergic postural tachycardia syndrome associated with augmented neurovascular transduction.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026Article
- Diastolic Blood Pressure Rise During Valsalva as a Surrogate for Sympathetic Activation to Identify Functional Hyperadrenergic Postural Tachycardia Syndrome.Research square · 2025Article
- Biomarkers over Time: From Visual Contrast Sensitivity to Transcriptomics in Differentiating Chronic Inflammatory Response Syndrome and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2025Review
- The Relation Between Cardiac Output and Cerebral Blood Flow in ME/CFS Patients with a POTS Response During a Tilt Test.Journal of clinical medicine · 2025Article
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Abstract
backgroundA subset of patients with postural tachycardia syndrome (POTS) are thought to have a primary hyperadrenergic cause. We assessed clinical biomarkers to identify those that would benefit from sympatholytic therapy.
methodsWe measured sympathetic function (supine muscle sympathetic nerve activity, upright plasma norepinephrine, and blood pressure responses to the Valsalva maneuver) in 28 patients with POTS (phenotyping cohort) to identify clinical biomarkers that are associated with responsiveness to the central sympatholytic guanfacine in a separate uncontrolled treatment cohort of 38 patients that had received guanfacine clinically for suspected hyperadrenergic POTS (HyperPOTS).
resultsIn the phenotyping cohort, an increase in diastolic blood pressure (DBP) >17 mm Hg during late phase 2 of the Valsalva maneuver identified patients with the highest quartile of resting muscle sympathetic nerve activity (HyperPOTS) with 71% sensitivity and 85% specificity. In the treatment cohort, patients with HyperPOTS, identified by this clinical biomarker, more often reported clinical improvement (85% versus 44% in nonhyperadrenergic;
conclusionsThese results are consistent with the concept that POTS is caused by a central sympathetic activation in a subset of patients, which can be identified clinically by an exaggerated DBP increase during phase 2 of the Valsalva maneuver and improved by central sympatholytic therapy. These results support further clinical trials to determine the safety and efficacy of guanfacine in patients with POTS enriched for the presence of this clinical biomarker.
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