BOSTON — It was a controversy centered around a viral fact: COVID-19 gains entry into human cells by first attaching to something called an ACE-2 receptor.
"The ACE-2 receptor is a ubiquitous receptor," said Mandeep Mehra, MD, a cardiologist at Brigham and Women's Hospital. "So, in fact, it's found in the lung tissue. But it's found in almost every tissue and it's a key component of the cardiovascular system."
And there is a class of high blood pressure drugs known as ACE Inhibitors -- which, in some animal studies, were found to increase levels of ACE-2.
Ergo, a field day for COVID-19 in humans taking ACE Inhibitors?
In March, Cardiologist Greg Lewis of Massachusetts General Hospital told Boston 25 News he saw two problems with that conclusion. "In humans that has not been a consistent finding, number one. And number two, it's not even clear whether having more ACE 2 helps you or hurts you."
Though leading medical organizations urged restraint, worries over ACE Inhibitors and a related class of drugs, the Angiotensin Receptor Blockers (ARBs) persisted as the pandemic heated up.
“This led a lot of people to actually stop taking their medications,” Mehra said. “And for physicians to actually advise patients to switch these medications out to other anti-hypertensives. This was a huge, huge problem early on in the course of COVID-19.”
But that is one COVID-19 problem researchers can apparently scratch off the list.
A massive new study on the effects of COVID-19 on patients with heart disease found neither the ACE Inhibitors nor the Angiotensin Receptor Blockers predispose patients to worse infections. In fact, just the opposite may be true.
The study appears in the New England Journal of Medicine.
Researchers looked at hospital discharge records for nearly 9,000 COVID-19 patients from Asia, Europe and North America. The study found that it was underlying cardiac disease -- not cardiovascular drugs -- that was the marker for poor COVID-19 outcomes.
And that’s because while COVID-19 may enter through the lungs, it doesn’t necessarily stay there.
"In fact, it's a vascular virus," said Mehra, lead author of the study. "This virus uniquely also involves the blood vessels and it involves a protective layer of the cardiovascular system called the endothelial cell."
Mehra said endothelial cells are "very active" in such physiological processes as clotting, blood pressure maintenance and control of inflammation.
This explains, he says, why some severely ill COVID-19 patients are found to have developed numerous small blood clots. “The minute the endothelial cell starts to get disturbed there is in fact an upregulation (increased response) of the clotting cascade, there is a change in the way your blood pressure is regulated and there is a change in the entire body’s inflammatory structure.”
And that especially spells trouble for anyone who confronts COVID-19 with coronary artery disease, heart failure or some type of arrhythmia.
“These are patients going into the disease already with disturbed endothelial cell dysfunction. What that means is their reserve is extremely low,” Mehra said. “So any additional insult to their endothelial cell lining or to their vascular wall, is only going to propagate the disease. And we think that is probably the mechanism by which these patients are predisposed to having a worse outcome with COVID 19.”
How much of a COVID-19 risk factor is cardiac disease?
"Our data seems to suggest the risk conferred by cardiovascular illness is at almost the same level as you see with pre-existing lung disease," Mehra said.
For any patients or doctors still nervous about taking ACE Inhibitors or Angiotensin Receptor Blockers, Mehra was unequivocal:
“Nearly 9000 patients across 3 continents has completely debunked the issue (that) these medications or cardiovascular medications have anything to do with the negative observed outcomes with COVID-19.”
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