COVID 19 has also been associated with myocardial inflammation and subsequent myocardial injury 2. The development and emergency approval of novel mRNA vaccines to combat this disease has also brought about its own set of challenges. As more and more people are vaccinated, cases of adverse events likewise continue to grow. One of the most worrisome COVID 19 vaccine related side effects involves the cardiovascular system, with myocarditis having been documented in adolescents and young adults after receiving mRNA vaccines4. For the purposes of this study, these findings will be collectively referred to as COVID 19-related myocarditis.
The COVID 19 virus has been shown to affect tissues through its action on the angiotensin-converting-enzyme 2 (ACE2)4. Although the pulmonary system is the main site of involvement, other organs, such as the heart, likewise contain ACE2 and as such, may be damaged through the same mechanism4. Other studies also postulate immune dysregulation as another pathophysiologic mechanism for COVID 19 related myocardial inflammation1. Evidence of cardiac involvement was first detected in patients hospitalized for COVID 19 infections. Cases of cardiac injury have also been reported in hospitalized patients following COVID 19 vaccination3. Similarly, mRNA vaccines have been linked to myocardial inflammation especially in young males ages 16-24 years old5.
Myocarditis pertains to non-ischemic inflammation of the myocardium resulting in myocardial damage 1. This may present as myocardial fibrosis, edema, and pericarditis4. Although this may be triggered by various causes, such as viral infections, toxins, and autoimmune diseases, its main pathophysiologic mechanism is an immune response targeting cardiomyocytes1. Patients may present with a wide clinical course ranging from subclinical myocarditis, to clinically evident myocarditis with preserved cardiac functions, to even arrhythmia and sudden cardiac death1.
Despite being a possible cause of morbidity and even mortality, the prevalence of COVID 19 related myocarditis is likely underreported due to the non-specificity of symptoms and difficulty in establishing the diagnosis 1,5. Though rarely performed, the gold standard for diagnosis is still myocardial biopsy wherein findings would show inflammation and myocyte damage1. However, acute myocarditis may be suspected in patients who fulfill at least one clinical and one diagnostic criteria1. Clinical criteria include acute chest pain, new onset dyspnea, palpitations, unexplained arrhythmia symptoms, syncope, aborted sudden cardiac death, and unexplained cardiogenic shock while diagnostic criteria would encompass electrocardiographic, Holter monitor, or stress test abnormalities, elevated troponin levels, functional and structural abnormalities seen in cardiac imaging, and typical tissue characterization features of edema and/or late gadolinium enhancement (LGE) seen in cardiac MRI1.
Cardiac MRI is the current gold standard when it comes to non-invasive assessment of cardiac structures 3,5. Its excellent depiction of cardiac function and anatomy is used to identify myocardial inflammation as well as to detect or exclude other related pathologies. As such, it plays an important role in the diagnosis of myocarditis. It not only depicts late gadolinium enhancement (LGE) and tissue edema, the two major criteria for myocardial inflammation based on the Revised Lake Louis criteria for myocarditis, but also shows systolic dysfunction and pericardial involvement, other supporting criteria for myocardial inflammation1. Based on the Revised Lake Louis criteria for myocarditis, the presence of either non-ischemic LGE or myocardial edema is possible evidence for myocardial inflammation while the presence of both indicates strong evidence of myocardial inflammation1. LGE is seen as hyperintense signals in T1-weighted images caused by retention of gadolinium-based contrast agents1. This signifies myocardial tissue injury and/or necrosis1. Myocardial edema, on the other hand, is seen in T2-weighted images as regional areas of hyperintensity, global T2 signal intensity ratio equal to or greater than 2, or regional or global increase of myocardial T2 relaxation time1. The presence of systolic dysfunction and pericardial involvement are supportive evidence but are not required for diagnosis1. Systolic dysfunction may be measured through functional parameters such as left ventricle (LV)/right ventricle (RV) end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), and ejection fraction (EF)4 while pericardial involvement may be evidenced by pericardial enhancement, pericardial edema, and/or pericardial effusion. All of these may be evaluated with cardiac MRI. This study aims to study COVID 19-related myocarditis based on these parameters.
Identification of COVID 19-related myocarditis is vital as this may have implications in patient management, particularly with regards to administration of subsequent doses of COVID 19 vaccines. Patients diagnosed with COVID 19-related myocarditis may benefit from deferring additional doses of mRNA vaccines, or changing regimens. Cardiac MRI findings may also be used in prognosis with studies suggesting that milder MRI abnormalities may indicate lower chances of future adverse events3.