With the coronavirus (COVID-19)
pandemic posing an immediate and novel risk to patients with cardiovascular conditions
, cardiologists have been tasked with the additional duty of learning as much as possible about the virus while still performing their day-to-day duties.
Thanks to the tireless efforts of researchers and clinicians, the amount of data available surrounding COVID-19 and its impact on patients is constantly expanding. Yet, as is often the case, much of this information just brings about new questions.
Research indicates SARS-CoV-2 binds to ACE2 receptors in the lungs and both hypertension and underlying cardiovascular disease have been linked to increased mortality after contracting the disease—yet, the mechanism behind how COVID-19 impacts cardiovascular function and leads to increased mortality is largely unknown.
For more on how cardiologists are having to adapt to the pandemic, HCPLive®
contacted Manesh Patel, MD, professor of medicine at Duke University School of Medicine, to take part in a Q&A about COVID-19.
HCPLive: How concerned are cardiologists for their patients?
Unfortunately, the outbreak is causing everyone to learn as much as they can about the virus. Obviously, the spike protein on the virus binds to the ACE2 receptor in the lung tissue and that has led people to believe that ACE inhibitors—or angiotensin receptor inhibitors—might, in some way, make the patients do worse. We strongly don't think that's the case. We're going to learn more as we go and all of the societies have come out and said, "Please keep your patients on those therapies so that their hearts are strong as this comes through".
I think the second message for all of us would be to practice social isolation as much as possible for our patients and being ready at the health system level. From a cardiovascular standpoint, what we're seeing in the description of these patients that have fairly sick courses are that they will have some cold or viral illness—this includes lower respiratory cough, some GI symptoms, a fever—that then leads to shortness of breath and several days of hospitalization with some ventilation. Unfortunately, when they start to get better, some of these patients can have a circulatory collapse with fulminant myocarditis or a low EF type of asystolic arrest. Those descriptions that have been out in the Lancet, JAMA, and other journals have started to give us an idea of what's coming.
As cardiovascular specialists, we're triaging our patients from our clinics to our catheter labs to our ICU wards so that we can better understand how to manage them as they come in but, again, we need to balance that with the public health need of limiting exposure to our patients. We're balancing a risk for each of our patients—the risk of them having a cardiovascular event moving forward versus the risk of them getting exposed to COVID-19 from coming to the health system. So, I think those are the things we're thinking about today as we think about the disease.
HCPLive: Other than hypertension, are there any specific CV risk factors that have a noticeably higher mortality rate from COVID-19?
I do not. I see that there's a widespread of different comorbidities people are identifying. In these affected populations, there's a different prevalence of these conditions that we're talking about. What's most concerning is that the case fatality rate, no matter how you slice it, is 10 times that of flu.
Aside from age, which does seem to have a link, there are different theories about why COVID-19 is affecting different people at different rates. Certainly, I'm worried some about the comorbidities you've described, but I suspect age and some potential prior immune reaction to viruses like the coronavirus might be sensitizing people. That seems like one of the possible theories.
Obviously, the more comorbidities patients have—especially pulmonary comorbidities and the cardiovascular ones that are associated with them—make them at higher risk. I think that's our central concern in most of our patients.
HCPLive: What does the fact that SARS-CoV-2 binds to ACE2 tell us about its specific impact on cardiovascular health?
A lot of people are asking that question and we're thinking about ways in which we would study that and test therapies against it. We haven't had a huge amount of it yet in North Carolina, but I think a lot of groups are carefully banding together to make sure that we capture clinical information on our patients, their medicines, and their comorbidities. Biologically, it looks like they get a cytokine storm and some of that might be getting driven by the things we've described. So that might be some biology we can help with.