The SARS-CoV-2 virus, which causes COVID-19, has been linked to long-term cardiovascular and pulmonary complications. A serious concern is the development or worsening of pulmonary hypertension (PH), a condition characterized by high blood pressure in the arteries of the lungs. Although COVID-19 is primarily a respiratory illness, the virus’s ability to affect the body’s vascular system suggests a plausible link to this severe lung condition. Understanding how SARS-CoV-2 impacts the pulmonary vasculature is necessary to identify at-risk individuals and develop effective long-term treatment strategies.
Understanding Pulmonary Hypertension
Pulmonary hypertension (PH) is defined by elevated blood pressure within the pulmonary arteries, which carry deoxygenated blood from the right side of the heart to the lungs. This high pressure forces the right ventricle to work harder. Over time, this sustained overexertion causes the right ventricle muscle to weaken and fail, leading to severe health consequences.
Restricted blood flow through the lungs impairs the body’s ability to exchange oxygen and carbon dioxide. Common symptoms resulting from reduced cardiac function include shortness of breath, particularly during physical activity, and persistent fatigue. As the condition progresses, patients may also experience chest pain, dizziness, or swelling in the ankles and legs due to fluid buildup.
Mechanisms of Vascular Damage by SARS-CoV-2
The SARS-CoV-2 virus harms pulmonary blood vessels, creating conditions for high blood pressure in the lungs. The virus enters cells by binding to the Angiotensin-Converting Enzyme 2 (ACE2) receptor, which is abundant on endothelial cells lining the blood vessels. This viral attack causes endothelial dysfunction, damaging the inner lining of the pulmonary arteries. This damage disrupts vascular tone regulation, leading to uncontrolled narrowing of the blood vessels and increased resistance to blood flow.
The body’s overwhelming inflammatory response, often called a “cytokine storm,” is characteristic of severe COVID-19. Chronic inflammation promotes the proliferation of smooth muscle cells within the pulmonary artery walls, a process called vascular remodeling. This remodeling causes the vessel walls to thicken and stiffen, narrowing the artery and permanently increasing the pressure required to push blood through. These structural changes resemble the pathology seen in established forms of pulmonary hypertension.
The hypercoagulable state induced by COVID-19 increases the risk of thrombosis, or blood clot formation, within the pulmonary vasculature. Numerous microclots and macroclots form within the lung vessels during the acute phase, leading to thrombotic microangiopathy. These persistent clots physically obstruct blood flow, directly contributing to elevated pulmonary artery pressure and setting the stage for a specific, long-term form of the disease.
Clinical Evidence Linking COVID-19 and PH Development
Clinical observations link COVID-19 infection to the development of PH. Echocardiography, a non-invasive heart ultrasound, detects signs of pulmonary hypertension in hospitalized COVID-19 patients. Studies report that echocardiographic signs of PH were present in approximately 12% to 13% of individuals admitted to the hospital with the viral illness.
The incidence of this complication is higher in patients who experienced severe forms of the disease, particularly those requiring intensive care. Case series suggest a prevalence of acute pulmonary vascular disease as high as 20% in patients admitted to the Intensive Care Unit (ICU). This link between disease severity and PH markers indicates that the extent of lung and vascular injury correlates with the risk of developing the condition.
Long-term follow-up studies of COVID-19 survivors have identified new-onset PH months after recovery from the acute illness. One study found that the incidence of PH in patients with persistent symptoms was as high as 70%, suggesting a substantial long-term sequela. These findings underscore the need for sustained monitoring of individuals who have recovered from severe COVID-19.
Distinguishing Types of Post-COVID Pulmonary Hypertension
Pulmonary hypertension is categorized into five groups based on the underlying cause. COVID-19 primarily contributes to two of these classifications. One common form seen post-COVID is Group 3 PH, which is PH due to lung diseases or low oxygen levels. This type develops in patients who suffered extensive lung damage, such as pulmonary fibrosis and reduced oxygen transfer capacity, resulting from severe COVID-19 pneumonia and Acute Respiratory Distress Syndrome (ARDS).
Group 4 PH, known as Chronic Thromboembolic Pulmonary Hypertension (CTEPH), results from unresolved blood clots in the lungs. Given the high rate of thrombotic events during acute COVID-19, a small percentage of survivors may develop CTEPH when blood clots fail to dissolve completely and scar the pulmonary arteries. This progression from acute pulmonary embolism to a chronic condition is a well-established pathway, and the hypercoagulability associated with SARS-CoV-2 makes this outcome possible.
Some cases of post-COVID PH fall under Group 5, which encompasses PH caused by multifactorial or unclear mechanisms, such as systemic inflammation or direct viral effects not linked to lung disease or chronic clots. Determining the specific group is essential because the treatment approach varies significantly between classifications.
Screening and Management Considerations
Screening for PH is a consideration for high-risk groups following recovery from COVID-19. Individuals who experienced severe illness, including those with prolonged hospital stays, mechanical ventilation, or persistent breathing difficulties, warrant closer surveillance. The most common initial screening tool is a transthoracic echocardiogram, which provides a noninvasive estimate of pulmonary artery pressure and right heart function.
If screening tests indicate an elevated likelihood of PH, a more definitive test, such as right heart catheterization, may be necessary to confirm the diagnosis and determine its severity. Management goals for post-COVID PH include reducing symptoms, preventing the progression of right heart failure, and improving quality of life. Treatment often involves pulmonary vasodilators, which help relax and open the narrowed blood vessels in the lungs. For patients diagnosed with CTEPH (Group 4), specialized treatment, including targeted surgery or medication, is required to address the persistent clot burden.