These are well reviewed elsewhere,2 and can be summarized as follows: (1) Quite distinct “types” of acute and chronic myocarditis are evident from clinical, histological, and pathogenesis perspectives; “myocarditis” is as nonspecific a diagnosis as is “hepatitis.” (2) Even when suspected, it is difficult to reliably detect and stratify myocardial inflammation into types of myocarditis in ways that are clinically relevant, accurate, cost‐effective, and safe; this is particularly so when there is chronic low‐grade disease. (3) We have a poorly developed understanding of root causes and effector mechanisms, features that determine prognosis and therapy (see Moving Forward: Cutting the Knot) (4) Perhaps unsurprisingly, we do not have well‐evidenced therapies; providing supportive management when needed is self‐evident, but apparently contradictory choices are often made between immunosuppression and antiviral agents (including immunopromoters).

Therefore, there is a Catch‐22 of sorts: We are not good at detection/stratification and therefore have not developed and tested therapies for well‐defined types of myocarditis; we do not have good treatments, and therefore do not routinely pursue more granular diagnoses. Notably, although cardiac magnetic resonance (CMR) imaging has transformed our ability to detect acute myocardial inflammation, CMR and other imaging modalities rarely identify root causes or effector mechanisms, and have poor sensitivity for differentiating chronic progressive disease from noninflammatory cardiomyopathies.3
Moving Forward: Cutting the Knot

To move beyond this impasse requires us to address the ”scanty understanding of root causes and effector mechanisms” as they relate to “different types of acute and chronic” myocarditis. For example, although viral agents (most commonly viruses) are often causally implicated, there are noninfectious causes (toxins, drugs, malignancy, autoimmunity, RNA vaccines, etc.) as well as nonviral microbial causes. Human and animal studies supply substantial evidence that, in susceptible hosts, acute and/or chronic heart‐specific autoimmunity can be triggered by self‐limiting viral infections.4 Infection is not necessary for this, however: heart‐specific autoimmunity can develop when myocardial antigens are presented to the immune system in an appropriate place and inflammatory context (eg, inoculation of susceptible mouse strains with myosin heavy chain plus vaccine adjuvant). This gives rise to an intriguing hypothesis that other causes of acute, chronic, or recurrent myocardial injury can promote cardiac autoimmunity in susceptible individuals via similar mechanisms.5

To illustrate how distinct inflammatory mechanisms could co‐exist, interact, and why they can be difficult to separate out, it may help to consider what we know of myocardial inflammation caused by or following COVID‐19 infections. Data suggest that forms of myocarditis can result from the following: myocellular lysis from replicating virions; myocardial injury secondary to systemic hyperinflation; adaptive immune responses targeting infected cells (lymphocytic infiltrates are typical here); and postinfectious Multi‐System Inflammatory Syndrome.6, 7, 8

To belabor the point: in otherwise apparently similar clinical presentations of myocarditis, myocardial biopsy may detect evidence of viral infection, but frequently fails to do so. Histology commonly identifies CD3+ lymphocytes, but eosinophilic, granulomatous, giant‐cell, and mixed infiltrates are detected in others cases of ”myocarditis,” each of which is associated with different outcomes.2, 9 Humoral responses to virus and/or self may also be important, resulting in antibody‐mediated myocardial injury as well as effects resulting from agonist/antagonist activity if/when receptor epitopes are targeted.2

These diversions, which seek to emphasize heterogeneity in cause and effect, have meaningful clinical implications; in developing strategies to suppress persistent inflammation, a mechanistic “dichotomy” (between immunologically mediated myocardial injury that targets viral antigen on chronically infected heart cells, and immunologically mediated myocardial injury directed against self‐antigens) is of key importance. Notably, as suggested below, this dichotomy alongside the other limitations described above, are considerably less relevant when considering postvaccine myocarditis from a purely clinical perspective.
Detection, Defining, and Management of Postvaccine Myocarditis

Sandeep et al.1 adopt a pragmatic approach to the detection and management of postvaccine myocarditis in children and adolescents. Their approach can be considered a 3‐part pathway.

First, the approach to detection and diagnosis assesses the probability that a presentation with acute myocardial injury is causally related to recent vaccination. Diagnosis is considerably more straightforward than in other settings where myocarditis might be suspected, because most presentations currently confer a high pretest probability.

A unique combination of typical features currently characterizes the vast majority of cases of postvaccine myocarditis: near identical, easily ”detected” pathogenetic agents; typical temporal features; and similar clinical features typically including chest pain, ECG changes, and troponin elevation. Clinical presentations share yet other strikingly similar features, including sex (overwhelmingly male), young age (more clearly defined when adult cases are studied), when vaccine exposure occurred (within 5 days of a second mRNA vaccine is typical; intriguingly, some data infer that presentations after the first dose can develop if infection with COVID‐19 acts as the first ”vaccine”10), and medium‐term outcomes appear to be overwhelmingly benign.10, 11, 12, 13, 14, 15

Considering and eliminating alternative causes of acute myocardial injury also receive due attention in this part of the pathway; these alternative causes include other forms of myocarditis. In fact, postvaccine myocarditis strongly resembles a form of acute myocarditis that commonly presents on acute coronary syndrome pathways with cardiac symptoms (usually cardiac chest pain), ECG abnormalities, troponin elevation, and unobstructed arteries.16 Often referred to as “acute coronary syndrome– like” myocarditis, presentations often follow on the heels of symptoms of a mild resolving/resolved viral infection, and young male adults form the majority of patients; it must be asked whether both phenomena are similar forms of ”triggered, self‐limiting, acute autoimmune myocarditis.”  READ MORE HERE.

Copyright © 2022 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell
This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

https://doi.org/10.1161/JAHA.122.026873

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