Abstract P263: Symptomatic Post-Acute SARS-CoV-2-Infection Hypertension Syndrome

Abstract

Introduction: The Post-COVID Cardiology Clinic at Washington University evaluates and treats patients with ongoing cardiovascular symptoms following acute COVID-19 infection. One clinical manifestation seen in the clinic is an increase in blood pressure, with associated symptoms like chest pain. Our investigation aims to describe the increase in blood pressure seen in symptomatic patients presenting to the Post-COVID Cardiology Clinic. Methods: The study employed a retrospective cohort design of consecutive adult patients who presented between September 2020 to May 2021 with cardiovascular symptoms following COVID-19 infection. Demographic information, symptoms, vital signs, and follow-up visit data were collected for the patients. To determine a baseline blood pressure, two blood pressure readings from office visits prior to COVID-19 infection were averaged. The blood pressure values were compared between baseline and cardiology office visits using a non-parametric Wilcoxon test for paired data. Results: One-hundred patients were included in the cohort (mean age 46.4 years (SD 46.4); 81% (81) female). At the initial visit, there was a significant increase in systolic (median 128 mmHg) and diastolic (median 83.5 mmHg) blood pressure from baseline (systolic median 121.5, p=0.029; diastolic median 76, p<0.001). All patients with an increase in blood pressure reported symptoms like chest pain. In the subset of 36 (36%) patients that have followed up, 35 (97%) patients were prescribed a new anti-hypertensive or required an increased dose of a prior anti-hypertensive at their initial visit. Blood pressures at follow-up were not significantly different from baseline (median systolic delta= 1.0mmHg, diastolic delta= -1.0mmHg; p>0.05), and 83% (30) reported improvement in symptoms. Conclusions: Patients presenting with cardiovascular symptoms post-acute COVID-19 show increased blood pressure when compared to blood pressure prior to infection. During subsequent follow-up appointments, patients showed improvement in their blood pressure and symptoms. While the pathophysiology has yet to be determined, it is likely related to the effects of a proinflammatory state, endothelial dysfunction, dysautonomia, or altered effects of the RAAS.