Deepak Bhatt, MD, MPH: Maybe we can pivot now to talk a little bit about cardiovascular-related issues. Cardiovascular biomarkers have played a big part in terms of patients admitted with coronavirus and COVID-19 [coronavirus disease 2019]. Troponins, D-dimers and BNP [brain natriuretic peptides] are often measured, for example. What do you think is the current state-of-the-art in terms of biomarker assessment in that inpatient, someone admitted with COVID-19 positivity?
C. Michael Gibson, MS, MD: Those are all good markers. I might add to the list, Deepak, troponin, a measure of myocardial injury. Many of these patients will have some form of myocardial injury. It's a bit unclear at this point, but our best line of sight into this is with autopsy studies. There is virus in the interstitium of the heart and in the inflammatory cells infiltrating the heart. So far, no study has shown viral particles inside the myocytes themselves.
When it comes to direct heart involvement, a lot of it is inflammatory. A lot of it may be the cytokine response, the cytokine storm. It does not appear to be a direct attack by the virus itself, at least so far from all the data I've seen. For the heart, we'll have to see how things play out with remdesivir and dexamethasone in limiting that myocardial injury from the cytokine storm.
The other issue, as you point out, is D-dimer. With inflammation in general, D-dimer goes up, but with this endotheliitis, infection of the endothelium by this virus, you're seeing a lot of activation of the clotting system because of that endothelial disruption. That's leading to a lot of clotting: about a third of people are developing clots, both big clots, pulmonary emboli, but also little clots, microthrombi in the coronary circulation. When it comes to the heart, yes, you can have some injury from the cytokine storm, but you can also have microthrombosis in the coronary system.
When you come into the ED [emergency department], when you and I are called about someone with ST elevation who's COVID-19 positive, is it myocarditis? Is it microthrombosis of the small vessels? Is it epicardial plaque rupture? Is it a type 2 MI [myocardial infarction] from fast heart rates and excess demand? It is still very complicated. You can get all these markers back, but you're not quite sure which of those pathways is the one that's causing it.
Deepak Bhatt, MD, MPH: Absolutely. It's a real case study in inflammation and thrombosis and their interplay. I would add to the list of things you mentioned Takotsubo or stress cardiomyopathy.
C. Michael Gibson, MS, MD: Absolutely.
Deepak Bhatt, MD, MPH: It’s described in these folks who are coming in COVID-19 positive. From an interventional cardiology perspective or emergency cardiology perspective, the spectrum of disease has been amazing. There are also some delayed presentations of people with acute coronary syndromes, not necessarily because they're COVID-19 positive, but because of COVID-19 positivity in the health care system and patients' concerns about going to the hospital and catching COVID-19.
Transcript Edited for Clarity