Hypertension, or high blood pressure, is highly prevalent in the United States and beyond. As the COVID-19 pandemic continues, researchers are keen to understand whether hypertension or the drugs that treat it might interact with the virus.

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A recent paper discusses blood pressure and COVID-19.

All data and statistics are based on publicly available data at the time of publication. Some information may be out of date.

To date, the novel coronavirus, SARS-CoV-2, has reached every continent on Earth other than Antarctica. The disease that it causes — COVID-19 — has led to the deaths of thousands of people.

Risk factors are of particular interest to both scientists and the public alike.

Over recent weeks, medical experts have published hundreds of papers examining every aspect of the disease. A recent commentary that appears in the American Journal of Hypertension looks at hypertension.

Overall, the authors conclude that, as it stands, there is no firm evidence that hypertension or blood pressure drugs will increase a person’s risk of contracting SARS-CoV-2. Similarly, current evidence does not support the theory that individuals with hypertension are more likely to experience worse symptoms of COVID-19 should they contract the virus.

Studies have demonstrated that certain existing conditions are associated with an increased risk of contracting SARS-CoV-2 and with more severe symptoms of COVID-19.

For instance, a study that investigated 41 patients in Wuhan, China, found that 32% had underlying health conditions — most commonly, diabetes, hypertension, and cardiovascular disease.

Another study, which appears in JAMA Internal Medicine, followed 201 people with COVID-19. Of these individuals, 84 developed acute respiratory distress syndrome (ARDS). Of the 84 who developed ARDS, 27.4% had hypertension. In comparison, 13.7% of those who did not develop ARDS had hypertension.

However, these associations between hypertension and COVID-19 are not necessarily causal. As the authors of the recent commentary explain:

“[H]ypertension is exceedingly frequent in the elderly, and older people appear to be at particular risk of being infected with SARS-CoV-2 virus and of experiencing severe forms and complications of COVID-19.”

In the JAMA study, the average age of individuals who developed ARDS was 58 years compared with 48 years in those who did not develop ARDS. In short, the questions surrounding hypertension and COVID-19 risk need further investigation.

For people with hypertension, doctors sometimes prescribe angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). These medications belong to a group of drugs called renin-angiotensin-aldosterone system (RAAS) antagonists.

These drugs inhibit the RAAS and interrupt activity at a receptor called ACE2. Scientists have shown that SARS-CoV-2 binds to ACE2 receptors to facilitate its entry into lung cells. This coincidence raises some intriguing questions.

There is some evidence that ACE inhibitors and ARBs increase the number of ACE2 receptors. As the authors explain, this “could theoretically increase the binding of SARS-CoV-2 to the lung and its pathophysiological effects, leading to greater lung injury.” In other words, if these drugs increase the number of entry points for the virus, they might cause more severe symptoms.

However, in opposition to this theory, some research indicates that ACE2 can protect against severe lung injury. Along similar lines, the authors of the recent commentary explain that, due to interactions with the RAAS, both ACE inhibitors and ARBs might “contribute to reduce inflammation systemically and particularly in the lung, heart, and kidney.”

If this is the case, the drugs “could diminish the potential for development of either acute respiratory distress syndrome, myocarditis, or acute kidney injury, which can occur in COVID-19 patients.”

In fact, some researchers have suggested ARBs as a potential treatment for COVID-19.

Other researchers have proposed soluble ACE2 as a therapy. As SARS-CoV-2 binds to ACE2 receptors, increased levels of circulating ACE2 might help “mop up” the virus, preventing it from reaching the lungs and other organs that bear the ACE2 receptor.

To date, however, researchers have not tested these approaches in people.

As it stands, official bodies recommend continuing medication for hypertension. For instance, the Heart Failure Society of America, the American College of Cardiology, and the American Heart Association recommend “continuation of RAAS antagonists for those patients who are currently prescribed such agents for indications for which these agents are known to be beneficial, such as heart failure, hypertension, or ischemic heart disease.”

Overall, many questions remain. As of yet, there is not enough evidence to conclude definitively that high blood pressure increases COVID-19 risk. As for hypertension medications, they might ward off SARS-CoV-2, make COVID-19 worse, or not influence the infection at all. The authors of the new commentary conclude:

“[T]here is, as yet, no evidence that hypertension is related to outcomes of COVID-19 or that ACE inhibitor or ARB use is harmful, or, for that matter, beneficial, during the COVID-19 pandemic.”

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