COVID-19 can cause pulmonary hypertension, both during the acute phase of infection and in the months and years that follow. The connection involves direct damage to blood vessels in the lungs, widespread inflammation, and blood clots that form in the smallest arteries. A large longitudinal study tracking outcomes over four and a half years found that COVID-19 survivors, whether hospitalized or not, faced a roughly 40% higher risk of developing new pulmonary hypertension compared to matched individuals who never had the virus. The risk is real, but the full picture is more nuanced than that headline number suggests.
How Common Is It During Acute Infection?
During severe COVID-19 illness, elevated pressure in the pulmonary arteries shows up more often than you might expect. In one study of critically ill patients needing intensive care, about 39% met the echocardiographic criteria for acute pulmonary hypertension, and those patients had dramatically worse outcomes: their 21-day mortality rate was 46%, compared to 7% for ICU patients without elevated pulmonary pressures.1PubMed Central. Acute pulmonary hypertension and short-term outcomes in severe Covid-19 patients needing intensive care A review of earlier pandemic data found pulmonary hypertension in roughly 13% of COVID-19 patients overall, but the rate jumped to about 22% in severe cases versus just 2% in mild ones.2PubMed Central. An Update on Pulmonary Hypertension in Coronavirus Disease-19 (COVID-19) In both studies, elevated pulmonary artery pressure was a significant predictor of death.
These numbers come from the early pandemic period, when treatments were less refined and many patients arrived at the hospital in worse shape. Still, the pattern is clear: serious COVID-19 puts the lung vasculature under strain, and the severity of that strain tracks closely with how sick the patient is overall.
What Happens Inside the Lung Blood Vessels
The reason COVID-19 raises pressure in the pulmonary arteries is not a single mechanism but several overlapping ones, each reinforcing the others. The most fundamental is direct endothelial injury. The virus enters the cells lining pulmonary blood vessels, replicates inside them, and disrupts their membranes. An autopsy study published in the New England Journal of Medicine found severe endothelial damage in the lungs of COVID-19 patients, with intracellular virus visible in the vessel walls.3PubMed Central. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19 Once those cells are damaged, the vessels lose their ability to properly relax and dilate, which raises resistance to blood flow.
On top of that, the virus triggers a cascade of inflammatory signaling molecules. SARS-CoV-2 enters endothelial cells through the ACE2 receptor, and the resulting viral replication sets off a flood of pro-inflammatory cytokines that further damage the vessel lining and push the blood into a hypercoagulable state, meaning it clots too easily.4PubMed Central. Cardiopulmonary crosstalk in Long COVID: a systematic review of emerging evidence The microclots that form are particularly stubborn. Research has shown that inflammatory microvascular blood clots containing neutrophil extracellular traps, platelets, and fibrin accumulate in the lungs, kidneys, and heart during COVID-19 pneumonia.5PubMed Central. Immunothrombotic Dysregulation in COVID-19 Pneumonia Is Associated With Respiratory Failure and Coagulopathy
These processes work together. At least two distinct pathways drive clotting in COVID-19: a body-wide hypercoagulable state that causes larger clots and emboli, and local endothelial injury that sparks tiny clots forming right where they sit in the smallest lung vessels.6PubMed Central. Pulmonary Thrombosis and Thromboembolism in COVID-19 Those in-situ microclots physically block segments of the pulmonary vascular bed, and the remaining open vessels have to handle all the blood flow, which raises pressure. Meanwhile, the damaged and inflamed lung tissue struggles to absorb oxygen, and low oxygen itself causes pulmonary arteries to constrict, a reflex that further worsens the picture.
There is also a longer-term structural component. An autopsy study comparing lung tissue from 56 COVID-19 patients to samples from people who died of H1N1 influenza found that COVID-19 lungs showed thickened walls of small pulmonary arteries after about two weeks of disease, with smooth muscle overgrowth, scarring around the vessels, and the formation of new abnormal blood vessels.7PubMed Central. Histopathological Evaluation of Pulmonary Arterial Remodeling in COVID-19 This remodeling resembles what happens in chronic pulmonary hypertension from other causes, which raises the concern that some of these changes could persist after the infection clears. A case report of a chronically infected patient’s explanted lungs confirmed exactly that: the tissue showed moderate vascular remodeling with wall thickening consistent with pulmonary hypertension throughout both lungs.8PubMed Central. Pulmonary Hypertensive Changes Secondary to COVID-19 Pneumonia in a Chronically SARS-CoV-2-Infected Bilateral Lung Explant
Endothelin, a molecule produced by blood vessel walls that causes them to constrict and promotes cell growth, may also play a role. Researchers have suggested that the vasoconstrictive, pro-inflammatory, and pro-clotting actions of endothelin line up with the pattern of vascular changes seen in COVID-related pulmonary hypertension, which opens the door to endothelin-blocking drugs as a potential treatment strategy.
The Long-Term Risk After Recovery
One of the more concerning findings to emerge from pandemic research is that pulmonary hypertension does not always go away when the infection does, and it can appear for the first time months later. A 4.5-year longitudinal study tracked new diagnoses of pulmonary hypertension in COVID-19 survivors versus matched controls who never tested positive. Among people who had been hospitalized with COVID-19, the incidence of new pulmonary hypertension was about 11.9 per 1,000 person-years, compared to 8.5 among matched controls. Even among people who were never hospitalized for their infection, the rate was 3.6 per 1,000 person-years versus 2.5 among controls. After adjusting for confounders, the risk was roughly 41–42% higher in both groups.9ERJ Open Research. Elevated risk of first-time pulmonary hypertension among COVID-19 survivors: a 4.5-year longitudinal study
That finding is striking because it includes people who had mild infections managed entirely at home. It suggests the vascular damage is not limited to those who were critically ill. In a smaller study of 50 patients evaluated by echocardiography after recovering from COVID-19, only 30% had normal pulmonary artery pressure. Another 30% had elevated pressures with adequate oxygen levels, while 40% had both pulmonary hypertension and right ventricle dysfunction with low blood oxygen.10PubMed Central. Study of pulmonary hypertension in post-COVID-19 patients by transthoracic echocardiography That study looked at patients who had been symptomatic enough to seek follow-up care, so it likely overrepresents the sicker end of the spectrum. But the overall signal across studies is consistent: a meaningful fraction of COVID survivors develop measurable changes in pulmonary blood flow.
Researchers have noted that post-COVID survivors could be at risk for multiple forms of pulmonary hypertension, including types driven by direct pulmonary arterial changes, left heart disease, lung damage and chronic low oxygen, and unresolved blood clots in the pulmonary arteries.11PubMed Central. At a crossroads: coronavirus disease 2019 recovery and the risk of pulmonary vascular disease This means the “post-COVID pulmonary hypertension” label actually covers a range of conditions with different underlying causes, prognoses, and treatments.
Do These Changes Resolve Over Time?
This is one of the harder questions to answer because long-term follow-up data is still accumulating. A two-year prospective study of patients who survived severe COVID-19 found that at the 24-month mark, no patients had developed overt pulmonary hypertension or chronic thromboembolic disease. However, all patients showed a hyperdynamic state of the right ventricle, and about 20% had signs of increased resistance in the pulmonary blood vessels and higher workload on the right side of the heart.12PubMed Central. Two-year cardio-pulmonary follow-up after severe COVID-19: a prospective study That is cautiously encouraging: the most severe outcomes had not materialized, but subtle abnormalities persisted even two years out.
One specific worry early in the pandemic was that COVID-related blood clots in the lungs would lead to chronic thromboembolic pulmonary hypertension, a condition where old, organized clots permanently block parts of the pulmonary vascular bed. A large UK surveillance study found this fear was largely not borne out. By the second year of the pandemic, new diagnoses of this condition had returned to pre-pandemic levels. Of over 1,000 patients hospitalized with COVID-19 and screened afterward, only about 1% were flagged as high risk, and none received a confirmed diagnosis at the national specialist team review.13European Respiratory Journal. Chronic thromboembolic pulmonary hypertension is an uncommon complication of COVID-19 So while COVID-related blood clots are common during acute illness, they rarely organize into the kind of permanent obstruction that causes this particular form of chronic pulmonary hypertension.
The Toll on the Right Heart
Pulmonary hypertension does not just affect the lungs; it places enormous strain on the right ventricle, the chamber of the heart that pumps blood into the pulmonary arteries. When resistance in those arteries increases, the right ventricle has to work harder, and if the pressure stays elevated, it can weaken and fail. COVID-19 compounds this in two ways. First, the elevated pulmonary artery pressure directly increases the workload. Second, when acute respiratory distress syndrome develops and the patient needs mechanical ventilation, the ventilator itself further increases pressure in the pulmonary arteries, creating a vicious cycle.14Archives of Medical Science. Right ventricular dysfunction and pulmonary hypertension in COVID-19: a meta-analysis of prevalence and its association with clinical outcome
In one series of COVID-19 patients with acute respiratory distress syndrome, 41% developed acute cor pulmonale, a sudden failure of the right ventricle caused by high pulmonary pressures.15Journal of Cardiothoracic and Vascular Anesthesia. Usefulness of Right Ventricular Longitudinal Shortening Fraction to Detect Right Ventricular Dysfunction in Acute Cor Pulmonale Related to COVID-19 This is a life-threatening complication that requires immediate intervention. Even when it does not reach that extreme, right ventricular dysfunction in the setting of COVID-19 has consistently been linked to worse survival.
How Post-COVID Pulmonary Hypertension Is Detected
Echocardiography, an ultrasound of the heart, is the standard first-line screening tool. It can estimate pulmonary artery pressure non-invasively and identify right ventricle changes. But it has limits. When clinicians suspect pulmonary hypertension based on echocardiography, right heart catheterization remains the definitive test. One study of COVID-19 survivors who showed abnormalities on echocardiography confirmed that all had pre-capillary pulmonary hypertension on catheterization, with substantially elevated pulmonary artery pressures and high vascular resistance.16The Egyptian Journal of Bronchology. Evaluation of pulmonary hemodynamics via right heart catheterization in COVID-19 survivors This underscores that echocardiography is good for flagging the problem but invasive testing is still needed to confirm the diagnosis and characterize its severity.
Advanced imaging is also playing an increasing role. Dual-energy CT, a specialized scan that maps blood flow through the lungs, has proven useful for spotting perfusion abnormalities that standard CT scans miss. In one study of 79 patients assessed after COVID-19, lung perfusion was abnormal in about 87%, with a range of patterns including patchy defects, areas of reduced blood flow, and regions resembling pulmonary embolism.17PubMed Central. Pulmonary circulation abnormalities in post-acute COVID-19 syndrome: dual-energy CT angiographic findings in 79 patients An earlier study found that about a quarter of hospitalized COVID-19 patients had perfusion defects on dual-energy CT that did not overlap with the areas of lung damage visible on regular imaging, suggesting the vascular injury extends beyond the obviously inflamed tissue.18PubMed Central. Lung and kidney perfusion deficits diagnosed by dual-energy computed tomography in patients with COVID-19-related systemic microangiopathy At three months after hospitalization, another study found perfusion abnormalities in about two-thirds of patients, with the majority having patchy defects linked to residual lung changes.19EClinicalMedicine. Assessment of pulmonary arterial circulation 3 months after hospitalization for SARS-CoV-2 pneumonia
These perfusion abnormalities do not all represent established pulmonary hypertension. Many reflect microvascular damage and small clots that may or may not cause persistent pressure elevation. But they help explain why so many COVID survivors have lingering breathlessness even when standard chest X-rays and lung function tests look relatively normal. The vascular bed can be impaired in ways that only specialized imaging reveals.
When Someone Already Has Pulmonary Hypertension Before Getting COVID
People who have pulmonary hypertension before catching COVID-19 face a particularly dangerous situation. A real-world analysis found that patients with pulmonary arterial hypertension who contracted COVID-19 had a mortality rate of 16%, compared to 2% among similar pulmonary arterial hypertension patients who did not get infected. Hospitalization rates and the need for mechanical ventilation were also significantly higher.20Circulation. Abstract 15745: Health Outcomes in Pulmonary Arterial Hypertension Patients With COVID-19 Interestingly, when researchers compared pulmonary arterial hypertension patients who had COVID-19 against COVID-19 patients without pulmonary arterial hypertension, matched for disease severity, the outcomes were similar, suggesting that the excess risk is driven more by the severity of the COVID infection itself than by a unique vulnerability of the pulmonary hypertension condition.
A separate study found that pre-existing pulmonary hypertension was independently associated with higher in-hospital mortality from COVID-19, with adjusted odds roughly 1.6 to 2.1 times higher depending on the measurement used to define pulmonary hypertension.21PLOS ONE. Association between pre-existing Pulmonary Hypertension and COVID-19 related outcomes in inpatient and ambulatory care settings Among outpatients, COVID-19 itself was the dominant driver of bad outcomes regardless of whether someone had pulmonary hypertension. The takeaway for people with pre-existing pulmonary hypertension is straightforward: avoiding severe COVID-19 through vaccination and early treatment is especially important.
Treatment Options for COVID-Related Pulmonary Hypertension
Treating pulmonary hypertension that arises from COVID-19 depends on its underlying type and timing. During the acute phase, the focus is on managing the infection itself, supporting oxygenation, and preventing or treating blood clots. Anticoagulation became a standard part of COVID-19 management for hospitalized patients partly because of the recognized risk of pulmonary vascular clotting.
For the elevated pulmonary pressures specifically, one drug that has attracted attention is sildenafil, a vasodilator originally developed for pulmonary arterial hypertension (before becoming better known by its other brand name). In a clinical trial of patients with severe COVID-19 and pulmonary hypertension, sildenafil was associated with a five-fold lower risk of death, a four-fold lower risk of needing intubation, and roughly four fewer days in the ICU compared to placebo.22PubMed Central. Efficacy of Sildenafil in Patients with Severe COVID-19 and Pulmonary Arterial Hypertension These results were dramatic but came from a relatively small study, so they should be treated as promising rather than definitive. A review of the drug’s potential mechanisms in COVID-related pulmonary hypertension noted that beyond dilating blood vessels, it may reduce inflammatory signaling, inhibit harmful cell transitions in the pulmonary artery walls, and help prevent clot formation.23PubMed Central. Covid-19-induced pulmonary hypertension in children, and the use of phosphodiesterase-5 inhibitors
For patients who develop persistent pulmonary hypertension months after recovery, management follows the general approach used for pulmonary hypertension from any cause: identify and treat the underlying driver (residual clots, ongoing inflammation, left heart disease, chronic lung damage), use targeted vasodilator therapy when appropriate, and monitor for progressive right heart strain. The challenge is that post-COVID cases can involve multiple overlapping mechanisms, making them harder to categorize and treat than a typical case that fits neatly into one clinical group.
Pediatric Cases
Children were largely spared from severe acute COVID-19, but pulmonary hypertension has been documented even in the youngest patients. A reported case described a term newborn who developed persistent pulmonary hypertension along with features of multisystem inflammatory syndrome in childhood between 12 and 14 days of life.24PubMed. COVID-19-Related Potential Multisystem Inflammatory Syndrome in Childhood in a Neonate Presenting as Persistent Pulmonary Hypertension of the Newborn Multisystem inflammatory syndrome in children, the delayed hyperinflammatory condition that typically appeared weeks after infection, could affect the heart and lungs in ways that temporarily or persistently elevated pulmonary pressures. The evidence base in pediatric patients is much thinner than in adults, built largely on case reports and small series rather than large cohort studies. Researchers have noted that phosphodiesterase-5 inhibitors like sildenafil, already used in pediatric pulmonary hypertension from other causes, could theoretically address COVID-induced pulmonary hypertension in children through similar mechanisms as in adults, though controlled trial data in this population is essentially absent.
The rarity of severe pulmonary vascular complications in children reflects the generally milder course of COVID-19 in younger age groups, but it also means that when pulmonary hypertension does develop in a child after COVID, it can catch clinicians off guard. Pediatric cardiologists and pulmonologists familiar with the phenomenon have advocated for echocardiographic screening in children who show unexplained exercise intolerance or persistent respiratory symptoms after infection.