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Postural Orthostatic Tachycardia Syndrome (POTS) is a clinical syndrome characterized by the presence of tachycardia in the absence of orthostatic hypotension; symptoms of orthostatic intolerance (presyncope and syncope) are present secondary to autonomic dysfunction (1). It is thought that one of the implications for POTS involves plasma volume disturbances leading to blood pooling. The Renin Angiotensin Aldosterone System (RAAS) is one system that assists in plasma volume regulation (2). In this study we hypothesized that these disturbances are brought about by an inactivation of RAAS. This was done by retrospectively reviewing the medical records of POTS patients. In these patients, diagnosis of POTS was established by an increase in Heart Rate of over 30 bpm within 10 minutes of tilt. Stroke Volume was used as a measure of volume disturbances; those POTS patients whose stroke volumes had not increased by the End of the Tilt as compared to their 6 minute supine baseline were considered to have an inactivation of RAAS. Our total sample of POTS patients numbered at 447, out of which 417 patients had lower stroke volumes at the end of their tilt table tests when compared to their baseline; this makes for 92.87% of our POTS Patient Sample. The average Stroke Volume at the 6 minute mark was calculated to be 74.67; the average stroke volume at the end of the tilt table test (30 minutes) was calculated to be 46.33 mL; . The results seen in this study show that more than 90% of our POTS Patient Sample there is no recovery of the stroke volume by the end of the tilt table test, this volume disturbance can be the result of decreased RAAS activation. This observation is supported by the difference found between average stroke volumes seen at 6 minute baseline and at 30 minutes of tilt. In normal individuals, we should see an increase in stroke volume at the end of the tilt as RAAS is activated. However, as patients with POTS are known to have lower plasma volumes (2), compounded with the inactivation of RAAS; the resulting hypovolemia will amplify the symptoms of POTS, increasing their severity. These patients should respond well to fludrocortisone, as there will be a correction of hemodynamic impairments (RAAS inactivation) leading to symptomatic relief (3). Further studies and analyses are needed to look into the levels of Renin and Aldosterone at Baseline & at Tilt, as well as the effects of fludrocortisone on such patients with RAAS inactivation. References:(1) Satish R. R., Circulation. 2013. June 11; 127(23): 2336-2342.(2) Satish R. R. et al., Circulation. 2005. March 2; 111(13): 1574-1582. (3) Freitas. J et al., Clin Auton Res. 2000. October; 10(5): 293-303. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.

Intro POTS is said to be a type of dysautonomia characterized by Tachycardia brought about by postural shifts in blood volume and circulation. This results in various Symptoms (Sx) including dizziness, lightheadedness, syncope, palpitations and tremulousness. POTS is often associated with EDS, a rare inherited connective tissue disorder pertaining to the production and processing of collagen. POTS causes abnormal increases in HR. If left untreated, pts can suffer from TIC indicated by an increasing Left Ventricle End Diastolic Diameter (LVEDD). Methods Electronic health records of 1300 POTS pts were reviewed retrospectively. Female pts with EDS between the ages of 20-40 who had imaging records of 3 or more echocardiograms in the past 5 yrs, with no more than 1 yr between consecutive echocardiograms were randomly selected. Our records identified 94 pts fulfilling this criteria. An assessment of the relation between associated Sx and corresponding Echocardiogram LVEDD values was made by observing pts reported Sx such as shortness of breath, chest pain, dizziness/lightheadedness, palpitations, and their overall feeling of well-being. Corresponding Functional Capacity (FC) values of each pt analyzed by reviewing Cardiopulmonary Exercise Stress Tests were also noted. Lastly, treatment modalities including drugs, exercise and I/V fluids were also monitored. A timeline with regards to changes in LVEDD was established to determine the effectiveness of various treatments. Results Of the 94 pts fulfilling the inclusion criteria: Mean age was 30 +/- 6.3 yrs. Mean LVEDD of pts reporting min Sx was 4.02 +/- 0.43. Mean LVEDD of pts reporting max Sx was 4.28 +/- 0.45. T-Test (p-value The average FC of pts experiencing min Sx was 69% while it was 63% for pts experiencing max Sx. T-Test (p-value = 0.006665) indicates that the mean of FC with least Sx is significantly higher than FC with maximum Sx. The average Decrease in FC per 0.1 cm Increase in LVEDD was 2.55% Pts with LVEDD of 4.04 +/- 0.48 were seen to have the highest FC >70%. Overall, 40 pts were seen to have >70% FC at LVEDD with the Lowest Sx. At >70% FC, 44 pts showed improvement with medication (Midodrine 20, Florinef 12, Beta Blockers 12), 25 pts with exercise and 11 on IV Fluids (including saline and/or albumin infusions). Conclusion Pts with POTS and EDS, tend to develop a worsening of Sx as LVEDD progressively increases resulting in a Tachycardia Induced Cardiomyopathy. However, aggressive management of Sx with medication and a dedicated exercise regimen can improve Sx, decrease LVEDD and cause reversal of the disease process. From the evidence collected, it can be recommended that POTS pts’ LVEDD values be maintained between 3.8 - 4.2 cm, as this range was seen to produce the least amount of Sx as well as a higher FC (>70%).