Most studies of what causes symptoms of COVID-19 to linger on after the virus has passed focused, with little success, on the heart muscle. Doctors at Houston Methodist Hospital instead looked at the heart arteries and hit on a promising idea.
KERA's Sam Baker talked about this with the study's co-author, Dr. Mouaz Al-Mallah, a professor of cardiology at the Houston Methodist DeBakey Heart and Vascular Center.
Why did you decide to look at arteries in studying long COVID?
Usually, when normal people exercise or move around, their heart needs more blood. The arteries dilate so you can get enough blood to the heart, so your heart can function and provide enough blood to the entire body and muscles.
We noted in this study that among those patients with prior COVID infection, there was a nearly 20% decrease in the amount of blood that is supplied to the heart muscle. This may potentially in part explain why these patients continue to have chest pain or shortness of breath. When their heart needs more blood there not getting it fully.
40 to 50% of these patients actually had this decreased blood flow to the heart. And we know from prior studies that this decrease in blood flow to the heart is not a benign condition and if persists, that is associated with a worse outcome.
This study pointed to endothelial cells as a sign of how COVID affects the heart. What are endothelial cells?
The cells that are possible for dilating your arteries when you are exercising. Your endothelial cells signal to the arteries that it’s time to dilate because Sam is exercising, and he needs more blood delivered to his heart. So, let’s relax and open the arteries so more blood is delivered.
You’re finding that COVID gets in the way?
Yes. We have some work from our basic science colleagues here at Houston Methodist that shows that COVID affects the endothelial cells and makes them less active.
So, we know from other disease states that patients with diabetes and other conditions have their endothelial cells not fully functional, and that’s why their arteries don’t dilate. And what we noted here is that these patients here with COVID have kind of this similar situation.
How or why would COVID do that?
There might be some biomarkers that it really is whether the virus is attacking these cells directly or not. We don’t have these assets yet.
Is there a specific type of COVID patient who develops this? Older patients, younger patients, maybe people with preexisting heart conditions? What have you seen so far?
We found this across the board. So that’s kind of probably more related to the infection itself rather than preexisting conditions these patients had.
What could damaged endothelial cells ultimately do to someone with long COVID or to someone period?
We know this condition from before the days of COVID. That’s called coronary microvascular dysfunction because there are a whole subset of patients who continue to have chest pain and shortness of breath. And these patients have no blockages in their arteries. It's just that endothelial cells are not working fine.
What is new in this study is that linking this and some patients report that initially it was linked more often to diabetes, high cholesterol, obesity, renal, kidney problems, things like that. But what we found here is that probably COVID is giving us something that is similar.
Since we know of this particular problem with damaged endothelial cells anyway. Is there a treatment for it?
Before the days of COVID, we primarily focused on statins, aspirin, and calcium channel blockers in some patients. That is not the definitive therapy.
And I would say risk factor modification is actually a very important and helpful treatment in these patients. Specifically controlling blood pressure, controlling sugar, controlling cholesterol, exercising, quitting smoking, and weight loss. All of these have been shown before to be very helpful in the treatment of this condition.
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