Is this a case of relapsed myocarditis, or myocarditis of a different etiology?

Recent reports may be overlooking a more concerning issue in relation to post-vaccine myocarditis outcomes.

I’ve seen growing discussion around this recent case report¹, which notes “relapse” of myocarditis in two male teens months after experiencing myocarditis right after receiving COVID vaccines.

I put relapse in quotation marks because I don’t think these case reports are clear indicators of a sudden occurrence of myocarditis.

In short, the case report highlight two male teens (15 and 16, respectively) who experienced myocarditis within days of receiving the second dose of a Pfizer/BioNTech vaccine.

The overall time course of myocarditis and supposed relapse are noted below:

From Amodio, et al. A timeline of events for the two adolescents featured in this case report, with the 1st patient shown on the left and the 2nd shown on the right.

The first patient was argued to be “healthy”, but I remind readers that I’ve grown more hesitant when studies make such comments due to how subjective health is measured in studies.

The second patient had a noted history of asymptomatic ventricular monomorphic extrasystoles, also called premature ventricular contractions, which is a benign condition in which the lower chambers of the heart may beat more frequently than normal, causing a sensation of the heart fluttering. This patient is also noted to be obese with a BMI of 31 (in contrast to patient 1 having a BMI of 18) at the point of hospitalization.

There’s a concerning number suggesting a BMI of 48 for patient 2 and 29 for patient 1 (Table 1), which may suggest that the patients gained weight by the time of their follow-up (my assumption, although it was noted that patient 2 was given clearance to participate in sports after follow-up).

I won’t highlight the clinical presentation and the follow-up, although in both cases it didn’t appear that both patients fully recovered as most mainstream outlets tend to report. Patient 1 still showed evidence of late gadolinium enhancement at the 6-month follow-up as well as persistent focal lesions.

Interestingly, both patients showed evidence of anti-endothelial autoantibodies, although there appears to be inconsistencies in this reporting. For instance, patient 1 was noted to have evidence of anti-endothelial autoantibodies during the first episode with no indication of autoantibodies during the second (note- they didn’t mention it, not that there was no evidence of autoantibodies). In contrast, patient 2 was noted to show evidence of both anti-heart and anti-endothelial autoantibodies during the 2nd episode with no remarks about the 1st episode. There isn’t any indication of what tests and which antibodies were checked for as well. It may be that clinical evaluations may have missed out on these tests, but it unfortunately suggests that there’s some information that’s missing.

In regards to these findings the authors make a comment that they are unsure what these autoantibodies may entail. They make the following comment which cited another article that seems to be gaining traction again:

These autoantibodies might be innocent bystanders resulting from myocardial inflammation and injury, or might reflect a certain immune–genetic background that predisposes to developing hyperimmunity and myocarditis upon any trigger. However very recent findings in post mRNA vaccine myocarditis did not show evidence of cardiac targeted autoantibodies in these patients suggesting that this mechanism is unlikely to act as main pathogenic trigger [18].

The study referenced is the Barmada, et al.² study I wrote about a while back in which I noted that I don’t consider the study to be a full refutation of autoimmunity hypotheses, so I’m a bit skeptical of this comment.

Is myocarditis post-COVID vaccination driven by inflammation and heart-damaging immune cells?

When looking specifically at the 2nd episodes there appears to be something interesting which most people seem to have overlooked. In this case, the authors note that both patients had evidence of human herpesvirus 7 (HHV7) present during the 2nd myocarditis presentations.

For patient 1:

Quantitative antigenic nasal swab for SAR-CoV2 resulted negative while the complete viral PCR evaluations, as previously described, showed residual copies for HHV7 (1124 copies/ml). On CMR new focal lesions along the LV wall with edema and LGE were observed. Altogether, these data were consistent with relapsing of acute myocarditis. Considering the myocarditis recurrence and HHV7 positivity, high dose intravenous immunoglobulins (IVIG) were administered along with angiotensin-converting enzyme (ACE) inhibitors with rapid improvement of clinical conditions and cardiac enzyme values.

Patient 2 was also noted to have evidence of HHV7 at the 1st clinical presentation:

The broad viral evaluations showed positivity for HHV7 (1750 copies/ml).

As well as the 2nd clinical presentation:

Nasal swab for SARS-CoV2 was negative. Serological and PCR virological screening demonstrated few copies of HHV7 (<500 copies/ml).

At first, this may not appear to mean much, and in a prior article on autopsy reports of myocarditis post-vaccination I mentioned that 1 of the autopsies noted the presence of human herpesvirus 6 (HHV6):

Autopsy reports of myocarditis following mRNA vaccinations

However, there appears to be evidence of human herpesvirus being associated with various forms of viral myocarditis.

For instance, an article published in 2006³ noted one strain of parvovirus as well as HHV6 as being large contributing factors in viral myocarditis.

Another article from 2017⁴ noted an outbreak of myocarditis among pediatric patients who were diagnosed in a small-town hospital, which appeared to correlate with HHV7 infections.

What all of this tells us that there may actually be some more to these cases of myocarditis that may not have been recognized beforehand.

There’s quite a few lines of thought we can follow, but here are a few that this case report has got me thinking about:

1. These two cases may not be examples of “myocarditis relapse”, but instead a case of a second episode of myocarditis triggered by an HHV infection. However, it’s quite possible that the first instance of myocarditis may have compromised the heart, in which case the greater risk of viral myocarditis may have led to these second episodes.

2. Given that patient 2 was noted to have a possible HHV7 infection at the time of the first presentation it’s possible that a concurrent viral infection at the time of vaccination may also contribute to myocarditis in some way, possibly due to the multiple burdens placed on the heart. This may explain the positive HHV6 PCR finding highlighted in one autopsy report by Schwab, et al.⁵ and may provide an explanation for myocarditis that has yet to be explored. Note that there’s growing evidence associating pediatric infection with HHV6 and cardiomyopathy.⁶

   1. Case reports of myocarditis may only check for infection with SARS-COV2 and not other viruses. If so, that would mean that underlying viral infections may be overlooked to a large degree.

The authors note this in regards to HHV infections:

As noted in previous studies. viral infections could act as a trigger in a predisposed individual. Our cases show a new diagnosed HHV7 infection during the second episode and a persisting viral replication respectively with the second patient presenting symptoms compatible with an ongoing upper airway viral infection. HHV-7 has been recently described in association with severe myocarditis as potential causative agent [19]. The presumptive viral etiology of the second episode of myocarditis supported the choice to administer IVIG as suggested by international guidelines in association with supportive care [20], [21]. Since HHV-7 infection generally occurs during childhood and up to 95% of adults are seropositive [22], it can be considered an endemic virus and we cannot establish if HHV-7 detection is incidental or represent the causative agent of myocarditis. However, the rapid reduction of HHV-7 copies after their initial detection is more in favor of an incidental finding in this case.

Given all of this the conclusion of “relapse” myocarditis here may be a bit improper. Unless these second episodes can be directly tied to the first it may not be appropriate to consider these relapses, but rather myocarditis caused by other factors that may be influenced by the episodes of vaccine-related myocarditis.

No matter which way it’s examined it’s rather obvious that messaging on myocarditis has tended to downplay the severity of myocarditis as just being transient in nature and leading to full recoveries.

What may be the case is that one incidence of myocarditis may increase the risk of further cases down the line. In that regard, the cases of vaccine-related myocarditis may increase the risk of myocarditis from other sources, including myocarditis from other viral sources.

There are several avenues that have yet to be explored, and even with limited data it’s a rather bold assumption for medical authorities to make in suggesting that the myocarditis these children experience won’t cause further problems in the future.

It’s also apparent that these children diagnosed with myocarditis are also dealt a heavy blow to their childhoods in which they may be limited to any sort of physical activity for months at a time. If the numbers from Table 1 are proper, it suggests that both adolescents showed a drastic increase in BMI by the time of follow-up or 2nd episode, which may also contribute to cardiovascular issues and worse health outcomes as well. So even if the vaccine-related myocarditis may not contribute to greater risk of myocarditis in the future these children may be harmed in one other way by inhibiting their ability to be children and be physically active.

So there’s a bit with these case reports that need further explaining. The authors don’t note whether these patients received a booster prior to the 2nd episodes. Nonetheless, this report at least suggests that greater surveillance should be done not for just myocarditis but any subsequent cases of myocarditis in the future.

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1. Amodio, D., Manno, E. C., Cotugno, N., Santilli, V., Franceschini, A., Perrone, M. A., Chinali, M., Drago, F., Cantarutti, N., Curione, D., Engler, R., Secinaro, A., & Palma, P. (2023). Relapsing myocarditis following initial recovery of post COVID-19 vaccination in two adolescent males - Case reports. Vaccine: X, 14, 100318. https://doi.org/10.1016/j.jvacx.2023.100318

2. Anis Barmada et al., Cytokinopathy with aberrant cytotoxic lymphocytes and profibrotic myeloid response in SARS-CoV-2 mRNA vaccine–associated myocarditis.Sci. Immunol.8,eadh3455(2023).DOI:10.1126/sciimmunol.adh3455

3. Mahrholdt, H., Wagner, A., Deluigi, C. C., Kispert, E., Hager, S., Meinhardt, G., Vogelsberg, H., Fritz, P., Dippon, J., Bock, C. T., Klingel, K., Kandolf, R., & Sechtem, U. (2006). Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation, 114(15), 1581–1590. https://doi.org/10.1161/CIRCULATIONAHA.105.606509

4. Rahmi Ozdemir and others, Report of a Myocarditis Outbreak among Pediatric Patients: Human Herpesvirus 7 as a Causative Agent?, Journal of Tropical Pediatrics, Volume 64, Issue 6, December 2018, Pages 468–471, https://doi.org/10.1093/tropej/fmx093

5. Schwab, C., Domke, L. M., Hartmann, L., Stenzinger, A., Longerich, T., & Schirmacher, P. (2023). Autopsy-based histopathological characterization of myocarditis after anti-SARS-CoV-2-vaccination. Clinical research in cardiology : official journal of the German Cardiac Society, 112(3), 431–440. https://doi.org/10.1007/s00392-022-02129-5

6. Reddy, S., Eliassen, E., Krueger, G. R., & Das, B. B. (2017). Human herpesvirus 6-induced inflammatory cardiomyopathy in immunocompetent children. Annals of pediatric cardiology, 10(3), 259–268. https://doi.org/10.4103/apc.APC_54_17