Abstract 13713: Coronary Endothelial Dysfunction and Microvascular Vasospasm in Patients With Postural Orthostatic Tachycardia Syndrome

Background: Postural Orthostatic Tachycardia Syndrome (POTS) is characterized by autonomic dysfunction-related symptoms such as orthostatic intolerance, palpitations, dizziness, and chest pain. The mechanisms driving chest pain in POTS are unclear.

Hypothesis: We hypothesized that coronary endothelial dysfunction (ED) and abnormal microvascular reactivity may be a contributor to chest pain in POTS.

Methods: Patients (n=6) were diagnosed with POTS or had significant tachycardia despite medical therapy out of 67 patients in our cohort. All patients reported persistent chest pain and were referred for coronary function testing (CFT) to test macro- and micro-vascular function. CFT was performed to test endothelium-dependent and non-endothelium dependent function using graded doses of intracoronary acetylcholine (ACH), and intravenous adenosine (ADO). Coronary Flow Reserve<2.0 and Index of Microvascular Resistance>25 diagnosed coronary microvascular dysfunction. Coronary artery diameter narrowing to ACH (100 mcg) was used to diagnose ED. Epicardial coronary spasm was defined as >90% constriction to ACH. Microvascular spasm was diagnosed by ACH provoked-chest pain and EKG changes in the absence of epicardial spasm.

Results: Mean age was 44.1 ± 15.2 years, 67% were female, and all tolerated CFT without complications. POTS symptoms, baseline medications, and CFT results are shown ( Table ). All had an abnormal response to ACH, indicating ED and microvascular spasm. Non-endothelium function was normal in all patients. Anti-anginal medications were changed based on CFT information, with improvement in chest pain with calcium channel blocker use.

Conclusion: In all 6 pts, CP was associated with ED and microvascular spasm. Mechanistic links between ED and POTS need further investigation. Given that ED is a prognostic marker associated with recurrent angina hospitalization and events, investigation of therapies that target ED in POTS may be warranted.