COVID-19 postvaccination myocarditis: Diagnosis
COVID-19 postvaccination myocarditis: Diagnosis
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Prevalence of Post-COVID-19 Vaccination Myocarditis Click here.
Management of Post-COVID-19 Vaccination Myocarditis Click here.
COVID-19 postvaccination myocarditis: Diagnosis
Types of Vaccine Related Myocarditis
Vaccine-related Myocarditis is not limited to COVID-19 Vaccines. Following types of vaccination can be associated with myocarditis
COVID-19 Vaccines
Timing of PostVaccination Myocarditis
Post-vaccination myocarditis tend to occur within 30 days after vaccination.
Terminology
Myocarditis is an inflammatory disease of the myocardium.
Inflammatory cardiomyopathy is myocarditis accompanied by cardiac dysfunction.
Dilated cardiomyopathy can be caused by inflammatory cardiomyopathy and it is a dilation and impaired contraction of one or both ventricles.
Symptomatic myocarditis is a myocarditis associated with symptoms.
Asymptomatic myocarditis denotes symptoms free myocarditis.
Acute myocarditis is a type of myocarditis developing over time less than 3 (three) months.
Chronic myocarditis is a type of myocarditis developing over time greater than 3 (three) months.
Subacute myocarditis is defined as myocarditis developing over the time close to 3 (three) months, characterized by an increase in autoimmune-mediated injury with activated T cells and B cells and subsequent antibody production creating cardiac autoantibodies along with inflammatory proteins.
Myocarditis post COVID-19 Vaccination: Official Narrative
The mainstream medicine position on the of post-vaccination myocarditis is that:
Given the infrequency and the mild nature of the myocarditis and pericarditis cases, the benefits of vaccination greatly exceed the small increased risk.
The mainstream medicine is focused on selected studies which claim that majority of the cases of post-vaccination myocarditis are “mild”. Furthermore, according to those studies, most patients with post-vaccine myocarditis responds well to medical treatment and has rapid symptom improvement. Three of such studies are quoted most frequently:
Witberg G, Barda N, Hoss S, et al. Myocarditis after covid-19 vaccination in a large health care organization. N Engl J Med. 2021;385(23):2132-2139. doi:10.1056/NEJMoa2110737
Mevorach D, Anis E, Cedar N, et al. Myocarditis after BNT162b2 mRNA vaccine against Covid-19 in Israel. N Engl J Med. 2021;385(23):2140-2149. doi:10.1056/NEJMoa2109730
“Use of mRNA COVID-19 Vaccine After Reports of Myocarditis Among Vaccine Recipients: Update from the Advisory Committee on Immunization Practices; June 2021”
Myocarditis post COVID-19 Vaccination: Counter-Narrative
The design of the studies cited by the Officialdom is less than perfect. In addition to the reports of mild cases, there have been also reports of fulminant myocarditis occurring after mRNA vaccine.
Myocarditis is a dangerous condition affecting one of the most critical organs: heart. It is associated with substantial morbidity and mortality. Neglecting its significance is frivolous, unreasonable and not in the best interest of patients.
Diagnostic Clues
Post-viral myocarditis should be suspected in patients presenting within 1 month post vaccination who maybe asymptomatic or present with new and unexplained cardiac signs and symptoms such as:
Excessive fatigue or exercise intolerance.
Chest pain.
Unexplained heart palpitations (sinus tachycardia).
S3, S4, or summation gallop.
New-onset or worsening heart failure.
Cardiogenic shock.
Respiratory distress/tachypnea.
Hepatomegaly.
AND with following results of the ancillary studies:
Abnormal echocardiogram,
A rise in cardiac biomarker levels,
ECG changes of:
acute myocardial injury,
arrhythmia (atrial or ventricular arrhythmia, partial or complete heart block, new-onset bundle branch block).
Chest X-Ray with new cardiomegaly.
Asymptomatic post-vaccination Myocarditis
Myocarditis is a serious potentially life-threatening condition affecting one of the most vital organs: heart. It is associated with substantial morbidity and mortality. Therefore it is reasonable to perform the diligent diagnostic evaluation even of the asymptomatic patient who presents within 1 month after COVID-19 vaccination.
Sudden Cardiac Death due to Post-Vaccination Myocarditis
Cases of Sudden Cardiac Death in otherwise healthy person should also prompt suspicion of post-vaccination myocarditis. Myocarditis may present with unexpected sudden death.
In an autopsy series of patients under age 40 who presented with sudden death in the absence of known heart disease, myocarditis was responsible for 22 percent of cases under age 30 and 11 percent in older subjects.
In another autopsy study of sudden death occurring in competitive athletes, myocarditis was present in 6 percent of cardiovascular deaths.
In a series of autopsies in military recruits, myocarditis accounted for 20 percent of deaths due to identifiable structural cardiac abnormalities.
Diagnostic Evaluation
The diagnostic evaluation of patients with suspected myocarditis should include the following components:
History
History should focus on search for symptoms of myocarditis and heart failure (HF).
Nonspecific characteristics.
A number of clinical features of post-vaccination myocarditis are nonspecific, such as myalgias, fatigue, general malaise.
The post-vaccination myocarditis has been reported to occur especially in male adolescents and young adults after administration of the mRNA COVID-19 vaccines: Pfizer’s BNT162b2, Moderna’s mRNA-127 and Novavax NVX-CoV2373 vaccine but NOT after Janssen/Johnson & Johnson adenovector COVID-19 vaccine.
Specific Cardiac manifestations.
Heart failure. Some patients can present with a syndrome of HF and dilated cardiomyopathy. In many patients who develop HF, fatigue and decreased exercise capacity are the initial manifestations. However, rapidly evolving diffused severe myocarditis can result in acute myocardial failure and cardiogenic shock. Signs of RV failure include:
increased jugular venous pressure,
hepatomegaly, and
peripheral edema.
Patients with predominant LV involvement present with symptoms of pulmonary congestion including:
dyspnea,
orthopnea,
pulmonary rales, and,
in severe cases, acute pulmonary edema.
Chest pain. Chest pain in patients with myocarditis may reflect associated pericarditis. Myocarditis can mimic myocardial ischemia and/or infarction both symptomatically and on the ECG, particularly in younger patients. Elevated troponin in the setting of pericarditis is often due to epicardial inflammation and termed "myopericarditis."
Palpitations (Arrhythmias). A number of arrhythmias may be seen in patients with myocarditis. Sinus tachycardia is more frequent than serious atrial or ventricular arrhythmias, while palpitations secondary to premature atrial complex (PAC; also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) or, more often, ventricular extrasystoles are common. Bradyarrhythmia and syncope due to new-onset unexplained heart block may also occur.
Physical Examination
There are no specific physical examination findings for myocarditis, however following signs can be observed:
In patients with HF, the physical examination may reveal signs of fluid overload (including elevated jugular venous pressure and edema), as well as other evidence of cardiac dysfunction (eg, a third heart sound).
If LV or RV dilation is severe, auscultation may reveal murmurs of functional mitral or tricuspid regurgitation.
A pericardial friction rub and/or effusion may be detected in some patients with myocarditis and associated pericarditis (myopericarditis).
Initial laboratory testing
Initial laboratory testing, should include
ECG. Most patients with HF with reduced ejection fraction (HFrEF) have a significant abnormality on an electrocardiogram.
A normal ECG makes LV systolic dysfunction unlikely.
An ECG has relatively high sensitivity for identifying patients with HFrEF (eg, 89 percent) but more limited specificity (eg, 56 percent). In contrast, patients with HF with preserved ejection fraction (HFpEF) commonly display a normal 12-lead ECG, though the presence of atrial fibrillation (AF) or paced rhythm greatly increase the probability that HFpEF is present.
Although the ECG is less predictive of HF than the B-type natriuretic peptide (BNP; or N-terminal pro-BNP [NT-proBNP]) level, the ECG may show findings that favor the presence of a specific cause of HF (eg, low voltage in amyloid heart disease) and can also detect arrhythmias (eg, AF) that suggest heart disease and may cause or exacerbate HF.
The ECG is particularly important for identifying evidence of acute or prior myocardial infarction or acute ischemia. Ischemia may cause symptoms of dyspnea similar to HF and may also cause or exacerbate HF.
Initial blood tests. Recommended initial blood tests for patients with symptoms and signs of HF include:
Cardiac troponin T or I in patients with acute decompensated HF and/or suspected acute coronary syndrome. Cardiac troponin I and T are specific and sensitive biomarkers of myocardial injury. Their measurement can be performed using sensitive or high sensitivity tests. A high sensitivity troponin assay was first approved for use in the United States in 2017. There are at least five companies that make high-sensitivity assays.
Natriuretic peptide. B-type natriuretic peptide (BNP) is a natriuretic hormone initially identified in the brain but released primarily from the heart, particularly the ventricles. Cleavage of the prohormone proBNP produces biologically active 32 amino acid BNP as well as biologically inert 76 amino acid N-terminal pro-BNP (NT-proBNP). (NP [BNP or NT-proBNP]) levels provide evidence as to whether HF is present. In patients with dyspnea at rest, the negative predictive value of a normal plasma NP level is high. NP levels are often (but not exclusively) elevated in patients with HFrEF, but may be normal in a substantial number of patients with HFpEF. Thus, the presence of an elevated NP level increases the likelihood that HF is present, but a normal level does not exclude it, particularly in patients with a normal LVEF or obesity. Conversely, elevations can be caused by elevated right heart pressures, renal dysfunction, or many systemic diseases.
A complete blood count, which may suggest concurrent or alternate conditions. Anemia or infection can exacerbate preexisting HF.
Serum electrolytes, blood urea nitrogen, and creatinine may indicate associated conditions. Hyponatremia generally indicates severe HF, though other causes should be considered. Renal impairment may be caused by and/or contribute to HF exacerbation. Baseline evaluation of electrolytes and creatine is also necessary when initiating therapy with diuretics and/or angiotensin converting enzyme inhibitors.
Liver function tests, which may be affected by hepatic congestion. In one study, gamma-glutamyltransferase level >2 times the upper limit of normal was the only standard initial blood test that added diagnostic value to the history and physical examination.
Fasting blood glucose to detect underlying diabetes mellitus.
Erythrocyte sedimentation rate and c-reactive protein levels, are useful - although these have nonspecific markers of inflammation.
Chest radiograph. The heart size on chest radiograph varies from normal to enlarged with or without pulmonary vascular congestion and pleural effusions. In some cases, biventricular cardiomegaly is associated with the absence of pulmonary congestion such as in those with RV and/or moderate or severe tricuspid regurgitation. However, chest radiography has limited sensitivity for identification of cardiomegaly or for diagnosis of HF.
Cardiac imaging
Cardiac imaging for myocarditis includes:
Echocardiography – An echocardiogram is performed in all patients with suspected myocarditis to evaluate regional and global ventricular function, valvular function, and other potential causes of cardiac dysfunction.
Coronary angiography – Coronary angiography is indicated in selected patients with clinical presentation indistinguishable from an acute coronary syndrome, lifestyle-limiting coronary disease despite medical therapy, or high-risk features for ischemic heart disease on noninvasive testing.
Cardiovascular magnetic resonance imaging – Cardiovascular magnetic resonance (CMR) imaging is indicated in patients with suspected myocarditis with elevated troponin level and/or ventricular dysfunction, without a clear cause such as ischemic heart disease. CMR may provide supportive evidence of myocarditis.
Endomyocardial biopsy
Indications for endomyocardial biopsy (EMB) should be reviewed in patients with clinically suspected myocarditis. The decision on whether to proceed with EMB should be based upon the likelihood that EMB will significantly impact patient management.
Indications for EMB include unexplained new-onset HF of less than two weeks duration associated with hemodynamic compromise or unexplained new onset HF of two weeks to three months duration associated with a dilated left ventricle and new ventricular arrhythmias, Mobitz type II second-degree atrioventricular (AV) block, third-degree AV block, or refractory HF.
Diagnostic Criteria
A definitive diagnosis of myocarditis is based upon EMB, including:
Histology:
The Dallas Criteria were used for long time and can be summarized as follows:
Active myocarditis: the presence of an inflammatory infiltrate of the myocardium with necrosis and/or degeneration of adjacent myocytes not typical of the ischaemic damage associated with coronary artery disease (CAD).
Borderline myocarditis: the presence of an inflammatory infiltrate of the myocardium without necrosis or degeneration of adjacent myocytes.
Discussion of Dallas Criteria. The Dallas criteria were proposed in 1986 and provided a histopathological categorization by which the diagnosis of myocarditis could be established. Dallas criteria myocarditis requires an inflammatory infiltrate and associated myocyte necrosis or damage not characteristic of an ischemic event. Borderline myocarditis requires a less intense inflammatory infiltrate and no light microscopic evidence of myocyte destruction. These criteria have been used exclusively by American investigators over the last 2 decades. Sampling errors, variations in expert interpretations, variance with other markers of viral infection and immune activation in the heart, and variance with treatment outcomes - all suggest that the Dallas criteria are no longer adequate.
Chow et al demonstrated by biopsying postmortem hearts of patients who had died with myocarditis that from a single endomyocardial biopsy, histological myocarditis could be demonstrated in only 25% of samples. With >5 biopsies, Dallas criteria myocarditis could be diagnosed in approximately two thirds of subjects. A recent MRI study used focal imaging abnormalities to guide heart biopsy investigation of possible myocarditis. The authors showed that the earliest myocardial inflammatory abnormalities were evident in the lateral wall of the left ventricle, and only these sites revealed myocarditis by histological examination. Therefore, there is considerable sampling error associated with establishing the diagnosis of myocarditis.
Immunohistochemical stains and detection of viral genomes by molecular techniques, mainly polymerase chain reaction.
Differential diagnosis
When a patient presents with suspected myocarditis, the differential diagnosis includes other conditions with similar symptoms and signs, including:
other causes of myocardial injury (including ischemic heart disease and stress cardiomyopathy), and
other types of cardiomyopathy,
valvular heart disease,
congenital heart disease, and
pulmonary disease.
Echocardiography is helpful for distinguishing many of these disorders.
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