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J Clin Med
2023 Jul 13;12(14):4660.
doi: 10.3390/jcm12144660.
Evidence for Impaired Renin Activity in Postural Orthostatic Tachycardia Syndrome
Jasmina Medic Spahic ,
Ingrid Yao Mattisson ,
Viktor Hamrefors ,
Madeleine Johansson , Fabrizio Ricci ,
Jan Nilsson ,
Olle Melander ,
Richard Sutton ,
Artur Fedorowski
Affiliations
- 1 Department of Clinical Sciences, Lund University, 214 28 Malmö, Sweden.
- 2 Department of Internal Medicine, Skåne University Hospital, 214 28 Malmö, Sweden.
- 3 Department of Cardiology, Skåne University Hospital, 214 28 Malmö, Sweden.
- 4 Department of Neuroscience, Imaging and Clinical Sciences, "G.d'Annunzio" University of Chieti-Pescara, Via dei Vestini 33, 66100 Chieti, Italy.
- 5 Fondazione Villa Serena per la Ricerca, 65013 Città Sant'Angelo, Italy.
- 6 National Heart and Lung Institute, Imperial College, Hammersmith Hospital Campus Du Cane Road, London W12 0HS, UK.
- 7 Department of Cardiology, Karolinska University Hospital, Department of Medicine, Karolinska Institute, 171 77 Stockholm, Sweden.
Abstract
Background: Postural orthostatic tachycardia syndrome (POTS) is a heterogeneous condition predominantly affecting autonomic control of the cardiovascular system. Its extensive symptom diversity implies multi-organ involvement that interacts in ways still requiring full exploration. Current understanding of POTS pathophysiology suggests alterations in the renin-angiotensin-aldosterone system as a possible contributing factor. Therefore, we investigated the relationship between the activity of the renin-angiotensin-aldosterone system and hemodynamic parameters in a cohort of POTS patients and controls recruited at a tertiary referral center.
Methods: The case-control study included 46 patients with POTS (27 ± 9 years), and 48 healthy controls (30 ± 9 years) without orthostatic intolerance. Plasma renin activity, expressed as angiotensin I generation, and plasma aldosterone were measured by enzyme-linked immunosorbent assay and were correlated with hemodynamic parameters obtained during active standing tests.
Results: Renin activity was significantly downregulated in POTS patients compared to healthy individuals (median, 3406 ng/mL vs. 9949 ng/mL,
p < 0.001), whereas aldosterone concentration did not differ between POTS and healthy controls (median, 218 pmol/L vs. 218 pmol/L,
p = 0.26). A significant inverse correlation between renin activity and supine and orthostatic blood pressure levels was observed in healthy individuals (
p < 0.05 for all), but not in POTS patients.
Conclusions: Renin activity, but not aldosterone concentration, is downregulated in patients with POTS. Moreover, renin activity in POTS is dissociated from supine and standing blood pressure levels in contrast to healthy individuals. These findings suggest impaired renin function in POTS, which may direct future therapeutic approaches.
