Abstract 11329: Prospective Analysis of Vascular Resistance in Patients with Persistent Tachycardia and or Dyspnea on Exertion in the Post Acute Sequela of Covid-19 Syndrome

Abstract

Introduction: The cause of tachycardia and dyspnea on exertion (DOE) in the Post Acute Sequelae CoV-2 syndrome (PASC) has yet to be identified. While endothelial invasion of the virus is well documented, how that might explain PASC is unknown. Hypothesis: Covid induced changes in vascular signaling to autonomic regulatory centers can induce sinus tachycardia and DOE. Methods: In a prospective, observational study, we enrolled 18 PASC patients who reported DOE or inappropriate tachycardia. All patients had normal left ventricular function, CXR, Hgb and thyroid studies. None had preexisting autonomic dysfunction. Vascular resistance was assessed by echocardiographic measurement of aortic-vascular impedance (Zva)=(systolic BP + mean Ao valve gradient)/stroke volume index. Ambulatory heart rate monitoring and head-up tilt table testing (HUTT) were performed. Results: Consecutively enrolled patients (18) were studied (17 females, ages 27 to 64). None had a significant aortic valve gradient. Zva was elevated in 17 of 18 patients. Ambulatory monitoring revealed episodes of symptomatic sinus tachycardia. Higher average daily heart rates correlated significantly with higher Zva levels (fig1). The 14 patients with DOE trended to higher average Zva levels than the 4 patients without dyspnea (4.13 +- 0.85 vs 3.5 +- 0.24, P=0.14). Of the 17 patients who had HUTT, 16 demonstrated patterns of orthostatic intolerance consistent with excess sympathetic tone including both postural orthostatic tachycardia and neurogenic cardiac syncope. Conclusions: PASC associated sinus tachycardia and HUTT abnormalities result from excess sympathetic tone. Covid-19 vascular injury as evidenced by abnormal Zva values may result in abnormal vascular signaling to autonomic regulatory centers. Resultant increases in sympathetic output may produce inappropriate sinus tachycardia, vasomotor dysregulation and DOE via peripheral vasoconstriction.