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As you all know we are in the midst of the COVID-19 pandemic and whilst we know the virus predominantly affects the lungs there have been several reports that it can also damage the heart and a lot of people have written to me to ask to try and clarify what i understand about the virus and its effects on the heart.
The first thing to say that we only have limited data at the moment and our understanding of the virus, how it behaves and most importantly the long term consequences of being infected with the virus are extremely limited. This particular virus has only been in existence in humans for 5 months so our understanding of it is constantly evolving. What I tell you today may completely change tomorrow as more research is done. I can tell you what we know about it as things stand.
COVID-19 and heart damage
Several studies from China have suggested that patients with active COVID infection also have troponin elevations suggesting a degree of myocardial injury. The studies are mainly from hospitalised patients who by definition are sicker than patients who are not in hospital. In these hospitalised patients anywhere between 7-28% patients are found to have elevated troponin levels.
The likelihood of finding elevated Troponins is greater in those patients who are sicker and in general those who have die.
There was a study of 416 patients from china which found that 20% of patients had elevated troponin. Those patients were older. They had greater burden of comorbidities (diabetes, high blood pressure, already damaged hearts etc) and they had more severe lung disease and in general were much sicker. The mortality rates were super high -51% compared to only 4.5% in patients who did not have elevated troponins. In fact if the troponin was high when the patient was admitted then the risk of death during that admission was 4x higher.
So clearly very concerning data. However from these studies, it is not clear whether there was something about the virus that directly attacked the heart and therefore caused the injury of whether it was indirect effect of the virus and just the stress caused by the sick state that caused the already preexisting condition to flare up and complicate the patient’s disease course.
Why is this important to figure out? I suppose it is important to know this because if the virus directly attacks the heart in some way then it may cause adverse consequences in young otherwise healthy patients who have very minimal respiratory symptoms such as progressive heart failure or heart rhythm disturbances in which case one could make a case for testing everyone, doing these tests on everyone and if evidence of heart damage on echo is found then early initiation of treatment to stop heart function deteriorating can be started.
Let’s look at some mechanisms by which the virus could cause heart damage:
Viral myocarditis - in this scenario, the virus would directly enter the heart muscle and start causing inflammation and damage to the heart muscle.
Is this possible? Maybe - because the ACE2 receptors that exist in the lung which are known to be essential for the virus to get into the lung also exist in the heart.
Is there any evidence to confirm this? No. To confirm this you would have to take a bit of heart muscle and study it under a microscope to see if you could actually see the virus. Now not many people do this because it is a highly invasive test but in the exceptionally few patients in whom a biopsy has been done the virus was not visualised.
Hypoxia - Obviously the big problem with the virus is that it makes the lungs wet and very stiff and this means that there is difficulty in getting oxygen into the bloodstream. In addition the stress of the virus on the body will cause the heart to work harder so the demand is increased and the supply is reduced and therefore sheer lack of enough oxygen in the absence of any underlying heart disease could also cause heart damage.
Stress cardiomyopathy - we know from our patients that sometimes when the body is under extreme stress such infection then there is such a massive release of stress hormones that the heart can become almost a little stunned and there may be a rise in troponin and the heart can look very weak on an echocardiogram. The good news is that once the stressor has been removed the heart does tend to recover in a majority of patients.