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Date of Award

Spring 2024

Degree Name

Master of Medical Science (Physician Assistant)

Department

Physician Assistant; College of Health Sciences

First Advisor

Sophie Farley, MMS, PA-C

Abstract

The SARS-CoV-2 virus responsible for the COVID-19 pandemic has unique features, including a specific affinity for epithelial cells of pulmonary vasculature. Damage to vessels occurs by hypoxia, inflammation, and complement activation. In addition to these microvascular changes, pulmonary, cardiac, and systemic consequences increase the risk of developing pulmonary hypertension following an acute SARS-CoV-2 infection. Nonspecific signs and symptoms, multifaceted etiologies, and various diagnostic modalities for pulmonary hypertension make diagnosing the disease difficult. A mean pulmonary arterial pressure >20 mmHg measured by right heart catheterization remains the gold standard for definitive diagnosis. Further research is needed to develop appropriate screening criteria and guided diagnostic approaches to identify post-COVID-19 infection pulmonary hypertension.

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Post-Acute COVID-19 Sequela: Pulmonary Hypertension

The SARS-CoV-2 virus responsible for the COVID-19 pandemic has unique features, including a specific affinity for epithelial cells of pulmonary vasculature. Damage to vessels occurs by hypoxia, inflammation, and complement activation. In addition to these microvascular changes, pulmonary, cardiac, and systemic consequences increase the risk of developing pulmonary hypertension following an acute SARS-CoV-2 infection. Nonspecific signs and symptoms, multifaceted etiologies, and various diagnostic modalities for pulmonary hypertension make diagnosing the disease difficult. A mean pulmonary arterial pressure >20 mmHg measured by right heart catheterization remains the gold standard for definitive diagnosis. Further research is needed to develop appropriate screening criteria and guided diagnostic approaches to identify post-COVID-19 infection pulmonary hypertension.