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Heart & vascular pathology

Inflammatory disease

Infective myocarditis

Author: R. Amita, M.D.

Last author update: 1 May 2014

Last staff update: 24 October 2024 (update in progress)

Copyright: 2014-2024, PathologyOutlines.com, Inc.

PubMed Search: Infective myocarditis [title]

Table of Contents

Cite this page: Amita R. Infective myocarditis. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/heartinfectiousmyocarditis.html. Accessed December 26th, 2024.

Definition / general

The term 'myocarditis' was first introduced by Corvisart
It is defined by WHO / International Society and Federation of Cardiology (ISFC) as an inflammatory disease of the heart muscle, diagnosed by established histological, immunological and immunohistochemical criteria

Epidemiology

Postmortem data identify myocarditis in 8.6% to 12% of cases of sudden death in young adults
The Myocarditis Treatment Trial reported the incidence of biopsy proven myocarditis in patients with unexplained heart failure to be 9.6%

Pathophysiology

Murine models of enteroviral myocarditis suggest viral myocarditis is characterized by 3 phases
Acute: entry of virus into myocytes, mediated through specific receptors such as the transmembrane coxsackievirus and adenovirus receptors (CAR)
Subacute: acute injury of the myocytes, induced by virus replication leading to myocyte necrosis
- This exposes the intracellular antigens (e.g. cardiac myosin) and activates the host immune system
- The first phase is virus induced myocyte injury; the second phase is autoimmune mediated injury due to activated virus specific T cells which may target host organs by molecular mimicry
- The immune response declines with virus elimination; ventricular function usually recovers without sequelae or it may persist leading to the
Chronic phase, characterized by myocardial remodeling and development of dilated cardiomyopathy (DCM)

Etiology

Parvovirus B19, Coxsackie B virus, human herpesvirus 6 (HHV6) type B, adenovirus (Arch Cardiovasc Dis 2009;102:559 - Table 1)

Clinical features

Highly nonspecific
Patient may be asymptomatic or present with signs / symptoms of myocardial infarction or cardiac failure, including chest pain and cardiac arrhythmias

Diagnosis

Endomyocardial biopsy is the gold standard to diagnose myocarditis
As myocarditis is a focal disease, four to five biopsy samples obtained in more than one area of the right ventricular (RV) septum should be analysed using light microscopic examination and immunohistochemical assays

Laboratory / cardiac testing

Leukocytosis and increased CRP levels but normal values do not exclude myocarditis
Cardiac biomarkers such as troponins and creatine kinase lack specificity but may help to confirm the diagnosis of myocarditis
Higher levels of troponin T may have prognostic value
Serology of infective organisms is helpful
Interpretation of antibody assays is complicated by other confounders such as reactivation or reinfection (e.g. HSV) or by cross reactions (e.g. EBV or enterovirus)
ECG: widely used as screening tool despite low sensitivity
- Findings vary from nonspecific T wave and ST segment changes to ST segment elevation mimicking an acute myocardial infarction
- Atrial or ventricular conduction delays, supraventricular and ventricular arrhythmias can occur in patients with myocarditis
- The presence of Q waves or a new left bundle branch block (LBBB) are associated with higher rates of cardiac death or heart transplantation

Radiology description

Chest Xray: cardiomegaly due to chamber dilation or pericardial effusion; may show pulmonary venous congestion, interstitial infiltrates, pleural effusions
Echocardiography:
- Evaluates cardiac chamber size and wall thickness
- Assess systolic and diastolic function
- Rule out other causes of cardiac failure such as valvular heart disease or other cardiomyopathies (hypertrophic or restrictive cardiomyopathy)
- Before an endomyocardial biopsy (EMB) procedure, echo is needed to exclude pericardial effusion and intracavitary thrombi
Cardiovascular MRI: edema in T2 weighted imaging indicates acute myocardial inflammation
- Myocardial early gadolinium enhancement: T1 weighted segmented inversion recovery gradient echo sequence shows a difference in signal intensity between diseased and healthy myocardial regions with Gd-DTPA accumulation in late gadolinium enhancement (LGE) imaging
- Combination of these findings is currently regarded as the most sensitive and specific noninvasive approach to diagnose myocarditis

Radiology images

Images hosted on other servers:

MRI: acute myocarditis

Increased T2-weighted signal intensity

Echocardiograms

Gadlinium-enhanced cardiac MRI

Prognostic factors

Depends on clinical presentation, clinical parameters and EMB findings
Patients with acute myocarditis and preserved left ventricular ejection fraction (LVEF) have a good prognosis with a high rate of spontaneous improvement without sequelae
Patients with fulminant viral myocarditis and hemodynamic compromise at presentation have an excellent long term prognosis and are more likely to experience complete recovery if aggressive treatment or mechanical circulatory support is initiated early during the fulminant phase

Case reports

14 year old boy with family history of dilated cardiomyopathy induced by viral myocarditis (Case Reports in Cardiology 2012;2012)
15 year old boy with myocarditis mimicking acute coronary syndrome following influenza B virus infection (Cases J 2009;2:6809)
19 year old woman with viral myocarditis (Mayo Clin Proc 2009;84:1001)
23 year old man with idiopathic acute myocarditis during treatment for controlled malaria infection (Malar J 2014;13:38)
27 year old man with parvovirus B19 associated fulminant myocarditis successfully treated with immunosuppressive and antiviral therapy (Antivir Ther 2010;15:681)
34 year old man with acute myocarditis from coxsackie infection, mimicking subendocardial ischemia (Hellenic J Cardiol 2009;50:147)
46 year old woman with fulminant myocarditis (Rev Port Cardiol 2012;31:503)
Two cases of dengue myocarditis (Infection 2013;41:709)

Treatment

As no pathogen specific therapy of viral myocarditis has been shown to improve survival, treatment is symptomatic and based on clinical presentation

Diagrams / tables

Images hosted on other servers:

Pathophysiological process of viral myocarditis

Algorithm for diagnosis in suspected myocarditis

Treatment algorithm based on EMB findings

Gross description

Findings are nonspecific and include normal or dilated chambers
May have softening and pallor of ventricles
May have pericardial effusion and pericarditis with viral or bacterial myocarditis
Late stages may show fibrosis that is focal or diffuse but the distribution is often random (see the image below), in contrast to the subendocardial fibrosis typically seen in ischemia

Microscopic (histologic) description

Dallas criteria:
- Acute myocarditis: lymphocytic infiltrates in association with myocyte necrosis
- Borderline myocarditis: inflammatory infiltrates without evidence of myocyte necrosis
Due to high interobserver variability, IHC is increasingly used for diagnosis

Microscopic (histologic) images

Images hosted on other servers:

Endomyocardial biopsy

Acute and chronic myocarditis

Immunohistochemistry & special stains

CD3 for T cells
CD68/PGM1 for activated macrophages
HLA-DR to assess HLA class II
EMB is considered to be inflamed by immunohistochemical detection of focal or diffuse mononuclear infiltrates (T lymphocytes and macrophages) with 14 cells / mm2, in addition to enhanced expression of HLA class II antigen

Molecular / cytogenetics description

Nested PCR / real time PCR in EMB
In situ hybridization techniques for identification of replicating viral genomes

Additional references

eMedicine: Myocarditis Pathology [Accessed 27 February 2018], Duke Medicine: Cardiovascular System [Accessed 27 February 2018]

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