Soluble factors in COVID mRNA Vaccine-Induced Myocarditis Causes Cardiomyoblast Hypertrophy and Cell injury: A Case Report

Abstract

Background: Inflammation affecting the heart and surrounding tissues is a clinical condition recently reported following COVID mRNA vaccination. Assessing trends of these events related to immunization will improve vaccine safety surveillance and best practices for forthcoming vaccine campaigns. However, the causality is unknown, and the mechanisms associated with cardiac myocarditis are not understood. Case presentation: After the first dose, we reported an mRNA vaccine-induced perimyocarditis in a young patient with a history of recurrent myocardial inflammation episodes and progressive loss of cardiac performance. We tested this possible inflammatory cytokine-mediated cardiotoxicity after vaccination in the acute phase, and we found a significant elevation of MCP-1, IL-18, and IL-8 inflammatory mediators. Still, at the recovery phase, these cytokines decreased considerably. We used cardiomyoblast in culture to test the effect of serum on cell viability, observing that serum from the acute phase reduced the cell viability to 75%. We did not detect this cellular injury in the sera from the patient in the recovery phase. We also tested serum-induced hypertrophy, a phenomenon presented in myocarditis, and heart failure. We found that acute phase-serum has hypertrophy effects, increasing 25% of the treated cardiac cells' surface and significantly increasing B-type natriuretic peptide. However, we did not observe the hypertrophic effect in the recovery phase or sera from healthy controls. Conclusion: Our results opened the possibility of the inflammatory cytokine or serum soluble mediators-mediated toxicity associated effects. In this regard, identifying anti-inflammatory compounds that reduce inflammatory cytokines could be helpful to avoid vaccine-induced myocardial inflammation.

mRNA-LNP COVID-19 vaccine lipids induce low level complement activation and production of proinflammatory cytokines: Mechanisms, effects of complement inhibitors, and relevance to adverse reactions

“…anaphylatoxin/cytokine double hit) and start of symptoms can be reconciled. Examples for acute, subacute and chronic SAEs include the HSRs or anaphylaxis within minutes to hours [16][17][18][19] , heart inflammation [8][9][10][11][12][13][14][15] , coagulation disorders [21][22][23][24] , or skin diseases [25][26][27][28] can occur within days to months, and autoimmune phenomena 20 may arise without currently foreseeable time limit. A hypothesis that may explain these different latency periods postulates that the actions of effector immune cells, including the mast cells, basophil and neutrophil granulocytes, lymphocytes, macrophages and platelets, are discontinuous, graded in the sense that they manifest only after the activation state of their intracellular inflammatory signaling network reaches the reaction threshold.…”

“…Table 1 lists the vaccine's reported AEs categorized according to the affected organ systems. Of note, myocarditis/pericarditis [8][9][10][11][12][13][14][15] , HSRs/anaphylaxis [16][17][18][19] , autoimmune diseases 20 , thrombosis, thrombocytopenia and other coagulation disorders [21][22][23][24] skin [25][26][27][28] and ocular inflammations [29][30][31] , Guillain-Barre syndrome [32][33][34][35][36][37][38] and other neurologic problems 39,40 can all be linked to acute or subacute inflammatory processes that are also characteristic of SARS-CoV-2 infections.…”