Myocarditis
Alisa McQueen, S. Margaret Paik in Pediatric Emergency Medicine: Illustrated Clinical Cases, 2018
Myocarditis is inflammation of the heart muscle with myocyte damage causing myocardial dysfunction and subsequent heart failure. Presentation varies from subclinical cases to sudden cardiac death. A mild prodrome (nonspecific upper respiratory infection or gastrointestinal symptoms) precedes cardiovascular symptoms by 7–14 days (congestive heart failure, palpitations, syncope). Tachypnea, grunting, increased work of breathing, and tachycardia are common. Variability in presentation and nonspecific labs make initial diagnosis difficult. Less invasive tests are preferred over biopsy due to procedural risks. Inflammatory markers are nonspecific. Cardiac enzymes (troponin T ≥ 0.01 ng/mL: Sn 100%, Sp 85%) are the most useful studies in the initial workup. Sinus tachycardia on ECG is common. Dysrhythmias (SVT and VT—as shown in this case), conduction abnormalities (heart block), and pseudo-infarct patterns have also been described. The chest radiograph is abnormal in 90% (cardiomegaly and pulmonary edema). Echocardiograph (ECHO) is abnormal in 98% (wall motion or valvular abnormalities). Neither ECHO, ECG, nor chest radiograph are specific for myocarditis but are helpful to rule out pneumonia, pulmonary embolism, structural abnormalities, and acute coronary syndrome. Cardiac MRI is more sensitive and specific than echocardiogram. Initial management is based on severity and includes supportive therapy and cardiovascular stabilization (monitoring, antiarrhythmics, vasodilators, inotropes, and diuretics). In fulminant disease, mechanical support (ECMO, VAD) acts as a bridge before transplant.
Molecular and Cellular Imaging of Myocardial Inflammation
Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer in Cardiovascular Molecular Imaging, 2007
Myocarditis is defined as inflammation and injury of the myocardium in the absence of ischemia (1). Myocarditis is most commonly caused by viruses but can also be caused by other infectious agents such as bacteria, fungi, and various parasites, as well as by numerous noninfectious agents such as certain drugs or chemical toxins. Spontaneous recovery usually occurs. However, sudden death or progression to dilated cardiomyopathy can occur in up to 10% of cases (9). The “gold standard” for diagnosis in patients with suspected myocarditis is percutaneous right ventricular endomyocardial biopsy (10). However, biopsy techniques are laborious and carry significant risk, particularly since the disease is often benign. Furthermore, sampling errors limit the sensitivity and specificity of biopsy techniques (10,11). It was estimated that it would require up to 17 biopsy specimens to achieve an 80% sensitivity for myocarditis (12). In addition, it is not possible to predict which of the acute cases will progress to chronic myocarditis and dilated cardiomyopathy based on the analysis of biopsy samples. For these reasons, the diagnosis of myocarditis is usually made through the exclusion of coronary artery disease on the basis of clinical and laboratory findings. A noninvasive imaging approach for accurately and specifically diagnosing and monitoring myocarditis is needed.
Innate Immune System in Cardiovascular Diseases
Shyam S. Bansal in Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Myocarditis originates from infectious (pathogens) or noninfectious (autoinflamma-tory) mechanisms. Infectious myocarditis may be caused by viruses, bacteria, parasites, or fungi [129]. In viral myocarditis, the hematological spread of viral particles results in direct infection of cardiomyocytes, cardiac fibroblasts, and/or endothelial cells, initiating cell damage and host immune responses. During the acute phase, tissue-resident innate immune cells are activated by various PAMPs and DAMPs, resulting in the production of interferons and pro-inflammatory cytokines (IL-12, IL-1β, TNF) with the resultant recruitment of neutrophils, monocytes, and dendritic cells. Not all PRRs are equivalent. TLR3-deficient mice have increased mortality, whereas TLR4-deficient mice have reduced inflammation [130]. In viral myocarditis models, there is a rapid loss of tissue-resident macrophages and a resulting influx of circulating monocytes [51, 131].
Myocarditis and autoimmunity
Published in Expert Review of Cardiovascular Therapy, 2023
Akira Matsumori
Myocarditis, inflammation of the myocardium, may be acute or chronic, and persistent inflammation may progress to cardiomyopathy [1–3]. Myocarditis is often difficult to diagnose clinically because it may present with various signs and symptoms and may mimic other common heart diseases. However, early diagnosis is important since the treatment is different depending on the etiology, and an appropriate therapy can improve clinical course and prevent sequelae to dilated cardiomyopathy. Myocarditis is often caused by viral infections, but it is also associated with systemic autoimmune diseases, bacteria and other microorganisms, and drugs and other substances [1–3]. Persistent inflammation following acute myocarditis may lead to the development of dilated cardiomyopathy or cardiac dysfunction. Cytokines and immune cells that contribute to the innate immunity are involved in the inflammation of the acute stage, and the acquired immunity plays a role in the chronic stage [1–3]. Autoantibodies against various epitopes present on the heart were considered to contribute to the development of the disease [3,4].
Severe multisystem inflammatory syndrome (MIS-C/A) after confirmed SARS-CoV-2 infection: a report of four adult cases
Published in Infectious Diseases, 2022
M. Sansone, M. Studahl, S. Berg, M. Gisslén, N. Sundell
A previously healthy 19-year-old male presented at the ear nose and throat (ENT) outpatient clinic with high fever and sore throat for three days, with onset five weeks after a nasopharyngeal PCR-confirmed mild SARS-CoV-2 infection. He was prescribed antibiotics for tonsillitis but presented two days later at the ED with hypotension, systemic inflammation (CRP 380 mg/L) andimpaired renal function (serum creatinine 185 μmol/L). Lymphocyte count was slightly low at 0.72 × 109/L (reference range 1.1–3.5) and PCR was negative for SARS-CoV-2 in a nasopharyngeal swab. CT scan showed general cervical and abdominal lymphadenopathy. Due to suspicion of urosepsis with shock, he was immediately transferred to the ICU for fluid resuscitation followed by endotracheal intubation the following day. Echocardiography showed normal EF, but NT-pro-BNP and troponin-I were high. Magnetic resonance imaging (MRI) of the heart showed typical signs of myocarditis. Bilateral non-purulent conjunctivitis was noted. Similar treatment as in case 1 was initiated on day two (IVIG for 2 days, anakinra i.v for 11 days, intravenous methylprednisolone for 6 days and tapering doses of oral prednisolone for 14 days). No infectious pathogens were isolated. On day three he was successfully extubated, rapidly improved and was discharged after 14 days.
A case of myocarditis following ChAdOx1 nCov-19 vaccination
Published in Acta Cardiologica, 2022
Olivier Van Kerkhove, Frank Renders, Mathias Leys
Myocarditis, an inflammatory disease of the myocardium, might lead to reduced cardiac function and in the most severe cases to mortality. Diagnoses of myocarditis are based on histological, immunological and immunohistochemical criteria, as defined by the WHO [1]. Typical causes are bacterial and viral infections, auto-immune diseases and severe toxins. Vaccination against coronavirus disease 2019 (COVID-19) has been suggested as a possible inducer of myocarditis. However, most cases were reported after vaccination with messenger RNA (mRNA) vaccines [2,3]. Myocarditis following viral vector vaccines seems to be a lot less common, and occurred only after administration of the Ad26COVS1 vaccine by Johnson & Johnson® (New Brunswick, NJ) [3,4]. Here, we report the first case of myocarditis following vaccination with ChAdOx1 nCov-19.
Related Knowledge Centers
- Arrhythmia
- Cardiac Arrest
- Chest Pain
- Dilated Cardiomyopathy
- Exercise Intolerance
- Inflammation
- Shortness of Breath
- Cardiac Muscle
- Heart Failure
- Shortness of Breath
- Viral Disease