Frequently Asked Questions
Link to the Paper
Thank you all very much for kind interest and the many messages and emails. To enable the answering your questions more efficiently, we produced this page with the answers that might help in the first instance. We will be regularly updating this page, as the new questions come in.
​Stay safe. Valentina and Eike

Main Messages

  1. There is a considerable ongoing myocardial inflammation in the heart muscle weeks after recovery from COVID19 illness. This finding is important because it may herald a considerable burden of heart failure in a few years down the line. 
  2. Early diagnosis is important because there is a good chance that early treatment could reduce the relentless course of inflammatory damage or even halt it. To prove this, we need clinical trials most urgently. 
  3. It matters to use cardiac MRI as a diagnostic test because not every tool is sensitive to detect myocardial inflammation. We need to use standardised and validated imaging tests (like Goethe-CVI® Approaches), not any CMR can deliver that.
  4. We need to make the efforts to make MRI machines available for cardiac indications because it prognostically matters most what happens with the heart.

Why are the findings important?​

Our findings are important because they may herald a considerable burden of heart failure in a few years down the line. Cardiac involvement may not be the most visible part of the acute illness, however, it is there in a considerable proportion of patients. While we do not yet have the direct evidence for late consequences yet, such as development of the heart failure, which can be directly attributed to COVID19, it is quite possible that in a few years, this burden will be enormous, based on what we know from other viral conditions that similarly affect the heart (cardiotropic vira, swine flu, etc).

​Did you expect such a high cardiac involvement?

​Once the first reports of severe autoimmune disease, the 'cytokine storm' and similar, were mentioned, we immediately understood that the heart would have also been involved, because myocarditis is essentially an autoimmune problem. The high prevalence and extent, however, surprised us.

​Do we need early diagnosis?

​Early diagnosis is important because there is a good chance that early treatment could reduce the relentless course of inflammatory damage or even halt it. However, myocarditis - as also shown in our patients - is a silent pathology (i.e. subclinical). In myocarditis heart problem does not present with classical heart chest pain, such as angina. Early diagnosis helps to explain patients why they are not fully recovering, possibly reduce high-level activity for some time and potentially to guide therapy (see below).

​Should we use regular imaging or lab tests?

​We certainly need to proactively look for the evidence of cardiac inflammation in patients with recent COVID19 infection. However, it matters profoundly how go about this. One way could be a troponin blood test. However, troponin is a test to diagnose acute complications of coronary artery disease such as a 'heart attack’. It has never been validated for the use in myocarditis, meaning, that the cut-off values for heart attack cannot be used for myocarditis. If we use the same cut-off values, we would likely send home a lot of patients that actually have a serious heart disease. Similarly, echocardiography, although widely available, is not a sensitive test for myocardial inflammation, because it simply cannot see inside the heart muscle. In myocarditis, more often than not, pumping function remains normal in early stages (as also shown in our patients). If impaired, how would one know this is not due to an old damage? We perform echo in parallel to cardiac MRI in all of our patients, so we know that there is a huge diagnostic gap between echo and MRI. Finally, in some countries, doctors would only rely on biopsies of the heart muscle to confirm the heart inflammation, which is an invasive test, performed in a catheter lab. It is expensive, not widely available, not standardised (no clear cut-offs that relate to prognosis) and, most importantly, not without complications. The evidence that biopsies help to improve treatment is also missing. 

​Do patients have cardiac symptoms?

​The absence of heart-specific symptoms is quite important to note. It is typical for inflammatory heart conditions to remain silent (subclinical) for many years, sometimes with unspecific symptoms and slightly reduced fitness, before they give themselves away, usually when heart is already significantly reduced in function or has accumulated large amounts of fibrosis and patients develop heart failure. In our view, the relatively 'clear onset of COVID19 illness’ provides an opportunity - which we often do not have with other conditions - to take a proactive action and to look for heart involvement early, i.e. within a few weeks from recovery.

​Is there active virus replication in myocardium?

​In our biopsies we found no evidence of viral particles. I.e. infection is the initial trigger the antigen-presentation, which is most commonly myoglobin.  Cardiac inflammation is then perpetuated by autoimmune process. in some people this is self-limiting, in some it leads to permanent inflammation -> inflammatory cardiomyopathy -> heart failure.  Virus particles have been demonstrated in acute cases and postmortem examinations, i.e. very severe cases.

​Did the patients have any risk factors, even in retrospect, for cardiac involvement of the virus?

​Paucity of risk factors, a few had asthma. They were generally fit and well and sporty – many of them caught the infection while on skiing vacation.

​How generalizable are your findings (how characteristic was your population)?

​They were ‘common people’ who got themselves tested (we identified them through testing center, not through hospital admission). Not cardiac patients.

​Can you recommend post-recovery therapies?

​Currently we have no evidence that CMR could guide us in terms of treatment. The standard heart failure therapy cannot be recommended as most patients will have normal - preserved ejection fraction. In short, we urgently need clinical studies to inform us about any potential therapies that could offer cardio protection and prevent development of the heart failure. 
 
It is important to note that doctors are currently not very good at taking proactive therapeutic action prior to the development of heart failure (also known as cardio-protection), simply because they do not know how to look for signs early enough. Many would also not know that cardiac MRI can help with that. The reason for this is that not many will have an easy access to cardiac MRI, and even less, would have the training to make a good use of its findings.

How about the athletes ?

​What drugs could be tested in clinical trials?
This is indeed an area of a great uncertainty. We cannot really comment on it from the perspective of our study, because we did not look into athletes specifically. However, we would like to refer you to  a recent paper in JAMA Cardiology, which provides some cautious guidance till we all learn more.
In clinical trials, we could test a number of existing medications as well as test a number of potential candidates. However, for all this to be implemented in practice, we need further studies most urgently and we are inviting any interested parties to join us in our efforts to get this done. In a few years’ time, we might be overwhelmed not only by seriousness of the acute illness, but also with its chronic complications, ie. heart failure.