Q&A with... Dr Rob Bell

We caught up with Dr Rob Bell, Cardiology Specialist Registrar at UCLH, Senior Research Fellow at UCL and a co-author of the paper published in the European Heart Journal last month which found that around half of those hospitalised with Covid-19 and who show raised levels of a protein called troponin have suffered some damage to their heart, according to a new study.

What was the motivation for the study?

During the first wave of COVID-19, we saw huge numbers of patients being admitted. That this was a respiratory disease was obvious, but there were other problems being identified, such as thrombosis and also cardiac abnormalities. Some of these cardiac abnormalities were related to the lung disease – the heart has to work harder to push blood through a lung circulation that has been damaged by the virus, or has been blocked by clot (pulmonary embolus) – but I was concerned that we really did not understand the mechanisms of cardiac injury, and whether the blood results – that in over 80% of cases results pointed to a cardiac injury of some description – was something that could be attributed to lung disease or whether there was something also occurring in the heart itself.

Why did you look at patients with elevated troponin?

Troponin is a protein that is only expressed by heart cells. If you find this protein in the blood, it means that the heart cells have become leaky and have allowed the release of troponin. We use this protein measure as a marker of heart attack – but it was obvious that the vast majority of patients being admitted with COVID were not having heart attacks. The question thus arises – what exactly is the troponin in the blood actually telling us? Another potential cause for troponin leak is inflammation of the heart – so called “myocarditis” – but how much of the leak was related to myocarditis or to other mechanisms of heart injury was unknown.

In this study, we wanted to see what a raised troponin meant in these patients – so we undertook to perform a cardiac MRI in as many patients who had an elevated troponin as possible. We did this in collaboration with Barts and the imaging facility in Chenies Mews (Roger Williams Building). Inevitably, because we could only do this scan in patients who had recovered (patients on intensive care were frequently too ill to move for any kind of scan), this meant we could not scan those who did not survive, or those who were too frail or infirm who would not be able to attend hospital for a scan.

The study found that over half the patients had demonstrable cardiac pathology 3-6 months post discharge – how do you interpret and think about this result?

What this study represents is a “first step”. It tells us that an elevated troponin is not a meaningless result – in over half of the people who have an elevated troponin, there is something not right about the heart – be that coronary disease (we were making a new diagnosis in two thirds of patients where coronary disease was not previously known about) or inflammation of the heart.

How these observations impact upon people’s survival with COVID is yet to be determined (and is surprisingly difficult) – but it does highlight a need to pay much more attention to the heart in this disease and to apply known treatments that may benefit patient outcomes.

Interestingly, aspirin, a cornerstone of the management of coronary disease, and colchicine, a cornerstone of the management of cardiac inflammation, are both being studied in the RECOVERY study – so it will be interesting to see whether non-discriminant administration of these drugs helps the whole COVID population, but it may be that a more targeted approach with these medicines may be even more beneficial.

Is there anything else you think important for patients or clinicians to know as a result of the study?

An elevated troponin means that there is a 1 in 2 chance of having some form of underlying cardiac pathology. 1 in 4 this will be related to coronary artery disease – and in two thirds of these, this is a new diagnosis. These patients should be optimised in terms of cardiovascular risk to prevent further future ischaemic events.

1 in 4 patients will have evidence of myocardial inflammation. Fortunately, this invariably appears mild, but can result in persisting chest pain. What this means in terms of future cardiovascular problems is unknown, but other forms of myocarditis is prone to relapses of inflammation and this is something that we do need to look out for.

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