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Kavithra Karalasingham
University of Calgary
Kavithra Karalasingham, a graduate student at the University of Calgary, investigated whether blood volume (BV) loading improves cardiac function in Postural Orthostatic Tachycardia Syndrome (POTS). Using cardiac magnetic resonance (CMR), POTS patients were assessed during orthostatic stress (volume-unloaded via lower body negative pressure) and after saline infusion (volume-loaded). Results showed that volume loading significantly increased end diastolic volume, stroke volume, and cardiac output, restoring these measures to levels comparable with healthy controls, while ejection fraction and end systolic volume remained unchanged. Overall, the findings suggest that increasing blood volume can reverse hemodynamic impairments in POTS, supporting volume loading as a potential therapeutic strategy to improve cardiac function and reduce orthostatic intolerance. Kavithra will present this research at the at the 14th Congress of the International Society for Autonomic Neuroscience in Bologna, Italy in September.
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ABSTRACT
Purpose: Postural Orthostatic Tachycardia Syndrome (POTS) is characterized by an excessive increase in heart rate (≥30bpm) in response to upright posture. When POTS patients stand, blood pools in their lower extremities, resulting in reduced blood volume (BV) returning to their heart. Reduced BV contributes to orthostatic intolerance in POTS. Increasing BV in POTS may improve cardiac function and relieve orthostatic intolerance and rescue the POTS phenotype.
Methods: Patients with POTS (n=9, 32±10years, F=9) completed a cardiac magnetic resonance (CMR) scan in a volume-unloaded phase, where patients underwent orthostatic stress using a lower body negative pressure chamber. Patients with POTS then repeated the CMR scan in a volume-loaded phase using normal saline infusion (1L). Healthy controls (HC) (n=3, 30±11years, F=3) completed the CMR scan in baseline conditions. We assessed if volume-loading improves cardiac function in POTS by comparing 1) POTS saline and POTS unloaded, and 2) POTS saline and HC baseline. Wilcoxon rank-sum and Mann-Whitney tests were used. Continuous data (mean±SD), LV end diastolic volume (EDV), end systolic volume (ESV), ejection fraction (EF), stroke volume (SV), and cardiac output (CO) were analyzed using the software, cvi42.
Results: BV loading improved EDV (111±20mL vs. 135±16mL; p=0.03), SV (69±11mL vs. 88±13mL; p=0.03), CO (4.9±0.5L/min vs. 6.1±1.0L/min; p=0.02) but did not affect ESV (p=0.2) or EF (p=0.07) compared to orthostatic stress. During volume loading in POTS, EDV (135±16mL vs. 139±13mL; p=0.5), SV (88±13mL vs. 83±10; p=0.5), CO (6.1±1.0L/min vs. 4.9±0.14; p=0.2) were not different from HC.
Conclusion: Volume-loading rescues the hemodynamic abnormalities in POTS, and may be a novel treatment strategy to improve cardiac function in POTS.
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