Evidence for Impaired Renin Activity in Postural Orthostatic Tachycardia Syndrome

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.

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“…Abnormal autonomic nervous system response to orthostatism, in addition to exaggerated levels of epinephrine and norepinephrine, contributes to the pathophysiological spectrum of mechanisms in OI that may be further accentuated by multiple factors such as excessive venous pooling in the lower extremities, volume dysregulations, autoimmunity and hyperadrenergic status [89]. Earlier reports emphasized a downregulation of renin activity and abnormal levels of angiotensin II in POTS patients [90][91][92][93]. This is further intensified in COVID-19 infection, as previous studies reported [94,95].…”

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“…Symptoms of dysautonomia include orthostatic or exertional intolerance (lightheadedness or syncope, palpitations, fatigue, cognitive impairment, blurred vision or muscle weakness/pain worse with standing or activity), GI symptoms, urinary symptoms, sicca, sweating abnormalities and temperature dysregulation. Validated questionnaires such as the Composite Autonomic Symptom Score (COMPASS-31) (124), the Survey of Autonomic Symptoms (SAS) (125), or the Malmo POTS Symptom Score (126) can be used to assess autonomic symptom burden. Symptoms of dysautonomia may be further investigated with more specialized testing, including the tilt table test with or without extracranial or transcranial doppler ultrasound, heart rate variability on deep breathing, Valsalva maneuver, Quantitative Sudomotor Axon Reflex Testing (QSART) and/or thermoregulatory sweat test (TST).…”

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