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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.

Tests to look for heart damage

The first thing to say is what tools do we have to determine heart damage? There are predominantly 2 tools.

  1. A blood test called Troponin – which measures heart muscle breakdown products in the blood. This is a very sensitive marker meaning that if the troponin is normal then there is no acute heart muscle damage but if the troponin is elevated, it doesn’t necessarily tell you exactly why the heart muscle damage has happened and whilst in a population of patients, it is broadly safe to say that the higher the value of the troponin, the larger the amount of damage, it is very difficult to say that in an individual. I see people (not COVID patients) who can have a small rise with more damage than others who may have a larger rise.
  2. Echocardiography – which is an ultrasound based imaging technique which allows direct visualisation of the heart. When the heart is damaged to any large extent, that damaged bit of the heart will not contract like the rest of the heart and therefore it will be fairly easy to visualise. Echocardiography will not tell you if a few cells have been damaged but will pick up substantial damage and the larger the amount of damage the worse the outlook of the patient both in the short term and in the long term. It is also true to say that not all damage seen on the echocardiography is necessarily permanent and in some cases when the offending trigger is removed, at least some of the damaged muscle can regain function and this improvement may be visualised on the echocardiogram.


Of the two tests, troponins are very easy to do and echocardiography is a bit more difficult because it needs specialised machinery, specialised personnel and involves more exposure to the potentially infectious patient and therefore much of what we know about heart injury in COVID-19 patients comes from troponin measurement.

Troponin detects myocardial injury. Echocardiography detects injury which is so great that it has a measurable impact on how the pumping function of the heart and therefore picks up the presence of heart failure (i.e the heart is failing to pump out as much blood as it should)


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:

  1. 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.

  1. 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.
  2. 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.
  3. Acute plaque rupture – many older people have diseased heart arteries without knowing about it. You can have plaque within the heart vessels which may not be causing a narrowing or blockage and therefore is not obstructing blood flow and the patient can be completely asymptomatic. However at times of extreme stress and inflammation, these plaques can break off and the body thinks that there is an open wound where the plaque was and proceeds to form a blood clot to cover this wound and the blood clot inadvertantly blocks the vessel resulting in a sudden heart attack and possibly even sudden death.
  4. Cytokine storm – finally sometimes it may be that the cytokines, which are protective proteins produced by the infected body, can get out of control and start spreading beyond infected body parts and attacking healthy tissue.


So at this point, it seems that it is more likely that people who have an underlying heart disease that has been undetected are more likely to be the ones that sustain myocardial injury from the virus. There is little evidence to definitively suggest that the virus directly damages the heart in patients without underlying heart disease. The good news (if there is any good news) is that firstly if the damage is not enough to be seen on echo then in general the medium and long term prognosis is good. If the heart is indeed damaged on the echocardiogram then it may well improve once the patient recovers from the virus and finally some of the medications that we now use in heart failure are exceptionally good and may substantially help strengthen the heart over time. 

I hope you found this useful and would be most grateful if you’d consider sharing it with anyone you may feel may benefit. 

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