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Discussing Covid-19 and hypertension

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Discussing Covid-19 and hypertension

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.
A recent paper discusses blood pressure and Covid-19. 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.
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, 27.4pc had hypertension. In comparison, 13.7pc 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:
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 patho-physiological 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.

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