In a peer-reviewed case report published on April 25th, 2022, a young obese male who had diabetes mellitus and had allegedly contracted COVID-19 in January 2020 was referenced.
He had presented with abdominal pain and tests uncovered that he was suffering from myocarditis/cardiomyopathy likely due to mRNA-based COVID-19 vaccination.
A Left Ventricular Assist Device (LVAD) was implanted during his hospital stay.
The article states that “one should maintain a high index of suspicion that these vaccines may cause irreversible cardiomyopathy if the patient had prior COVID-19 infection.”
Six months after the young man’s COVID infection, he got the initial and booster shots of Moderna (May 19th, 2021, and October 7th, 2021).
One month after the second vaccine dose, the man presented to a community hospital complaining of left lower quadrant abdominal pain. His pulse rate was 116 beats per minute and his temperature was 36.5 degrees Celsius, with his respiratory rate at 18 breaths per minute and his blood pressure at 140/84 mmHg.
There was no history of cardiomyopathy or heart disease in the man’s family.
The man underwent a coronary angiogram, and the right side of his heart was catheterised. He was then transferred to the University Hospitals Cleveland Medical Centre for further examination and treatment.
An MRI was performed, and this showed the man’s left ventricle was severely dilated and had severely reduced function.
Despite his treatments, his cardiomyopathy showed no improvement which resulted in the placement of a durable mechanical support device.
The article alleges this case to be the first reported incidence of COVID-19 vaccination-induced cardiomyopathy that required durable mechanical support. It suggests “While prior literature noted a wide spectrum of presentations of myocarditis, most patients were asymptomatic and thus likely underrepresented the true incidence.”
The article concludes that patients who had a previous COVID infection but were later injected with mRNA vaccines may suffer permanent cardiomyopathy requiring mechanical cardiovascular support. It also says, “our case highlights an extreme consequence of dysregulated cytokine/inflammatory storm after the second dose of the COVID-19 vaccine.
Other peer-reviewed articles on this subject are surfacing.
One such article that was published on December 15th, 2021 talks about the recurrent waves of COVID-19 our world has allegedly been facing, claiming multiple studies have established that heart failure patients are at high risk of severe disease and poor outcomes with COVID-19. It suggests that over 250 million cases of COVID-19 have been reported worldwide, claiming the Delta variant, which was part of the fourth surge is highly infectious and transmissible.
Under the subheading “COVID-19 Mechanisms of Cardiac Injury”, this article stresses the importance of understanding how the virus acts and its mechanisms of injury to understand the impact of COVID-19 on heart failure.
It states: “SARS-CoV-2 infection is triggered by the binding of the S protein to its functional receptor angiotensin-converting enzyme 2 (ACE2) on the surface of host cells, typically via a type II pneumocyte. This viral complex is incorporated into the cytoplasm either by direct fusion with the cell membrane or via endocytosis. This leads to ACE1 downregulation, which activates the de novo renin-angiotensin-aldosterone system (RAAS) and causes an intense inflammatory response, increased pulmonary vascular permeability, and pulmonary edema.”