Giant cell myocarditis triggered by a parvovirus B19 infection

Dennert, Robert; Schalla, Simon; Suylen, Robert Jan van; Eurlings, Luc W.; Heymans, Stéphane

doi:10.1016/j.ijcard.2007.12.020

Cited by 17 publications

(8 citation statements)

References 6 publications

(2 reference statements)

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“…16 Other conditions that have been more rarely reported in association with the development of GCM include drug hypersensitivity reaction and infection such as parvovirus B19 (diagnosed via cardiac DNA polymerase chain reaction [PCR]) or coxsackie B2 virus (diagnosed via serology and cardiac immunoblotting). [17][18][19] However, electron microscopic studies to date have not identified viral particles in GCM, and no microbiologic agent has been directly identified in cardiac tissue by microscopy, tissue culture, or inoculation in experimental animals. 4,20 GROSS AND HISTOLOGIC FINDINGS Giant cell myocarditis is most commonly diagnosed via endomyocardial biopsy (52%), evaluation of the heart at autopsy (23%) or explantation (21%), or via examination of apical wedge sections removed at the time of ventricular assist device placement (4%).…”

Section: Pathogenesismentioning

confidence: 99%

Giant Cell Myocarditis: A Brief Review

Brooks²

2016

Archives of Pathology &Amp; Laboratory Medicine

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Giant cell myocarditis (GCM) is a rapidly progressive and frequently fatal disease that mainly affects young to middle-aged previously healthy individuals. Early diagnosis is critical, as recent studies have shown that rapidly instituted cyclosporine-based immunosuppression can reduce inflammation and improve transplant-free survival. Before the 1980s, GCM was mainly a diagnosis made at autopsy. Owing to advancements in diagnostic and therapeutic options, it is now increasingly diagnosed on the basis of endomyocardial biopsies, explanted hearts, or apical wedge sections removed at the time of ventricular assist device placement. Histologic examination remains the gold standard for diagnosis; however, there are many possible etiologies for cardiac giant cells. Having a working knowledge of the clinicopathologic features that distinguish GCM from other giant cell–containing lesions is essential, since such lesions can have widely divergent management and outcome.

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Section: Pathogenesismentioning

confidence: 99%

Giant Cell Myocarditis: A Brief Review

Brooks²

2016

Archives of Pathology &Amp; Laboratory Medicine

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“…Patients usually die of heart failure and ventricular arrhythmia unless cardiac transplantation is performed 1 2. In addition to the idiopathic or primary form, GCM has been associated with other conditions including drug hypersensitivity,3 granulomatosis, neoplastic conditions, autoimmune and inflammatory diseases 4. However, the aetiology and pathogenesis of GCM is not well known.…”

Section: Discussionmentioning

confidence: 99%

Refractory cardiogenic shock following idiopathic giant cell myocarditis in a 19-year-old woman

et al. 2013

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Refractory cardiogenic shock following idiopathic giant cell myocarditis in a 19-year-old woman CLINICAL CASEA 19-year-old woman with no medical history except for facial acne treated with tetracyclines during the previous year presented to the emergency room referring 1-week history of worsening muscle weakness, palpitations and exertional dyspnoea. Physical examination revealed a tachycardic (130 bpm), tachypnoeic and hypotensive (blood pressure 90/50 mm Hg) thin woman with fever of 38.5°C, rash and jugular vein distention.An ECG showed sinus tachycardia with 0.5 mm elevation of the ST segment in the anterior and inferior leads. In laboratory studies, she had leukocytosis with neutrophilia and eosinophilia and mild rise of troponin I (4.8 mg/l), creatine kinase (524 U/l) and transaminases (aspartate aminotransferase of 765 U/l and alanine aminotransferase of 658 U/l). An echocardiogram revealed severe biventricular dysfunction with global hypokinesia and circumferential mild pericardial effusion. Signs of heart failure were found on her chest x-ray. In this clinical situation, we treated her with dobutamine, but she started to develop sustained ventricular tachycardia and refractory hypotension during the following hours. Coronary angiography showed no coronary lesions and an intra-aortic balloon pump was inserted for counterpulsation. The next morning, a new transthoracic echocardiogram revealed a left ventricular ejection fraction of 10% with a dilated left ventricle. She underwent a right heart catheterisation with endomyocardial biopsy and was diagnosed with giant cell myocarditis (GCM) (figure 1). We started treatment with intravenous, prednisolone (50 mg/day), intravenous immunoglobulin (30 g/day), ciclosporin and plasmaferesis with neither clinical nor haemodynamic improvement. Because of the patient's impaired clinical course, a biventricular assistance device (Abiomed BVS 5000) was inserted 5 days after her admission. As the prognosis of GCM is usually fatal, with no response to medical treatment, she was added to the emergency cardiac transplant waiting list, as her status was critical.

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“…Etiologic hypotheses include systemic autoimmune diseases [164][165][166][167][168], drug toxicity [169], infections [170][171][172], and complex combination of autoimmunity, infections and drug toxicity [173]. Infections reported in GCM include coxsackie B2 virus [170], parvovirus B19 [171], HCMV [172] and HIV1 infection [173][174][175][176][177][178][179][180][181][182][183][184]. In most cases, GCM is an isolated entity, while in about one-fifth of cases GCM occurs in association with autoimmune/immune-mediated diseases (Table 4.7), infections, drug toxicity, or syndromes such as immune reconstitution inflammatory syndrome (IRIS) in patients undergoing highly active antiretroviral therapy (HAART) against human immunodeficiency virus type 1 (HIV-1) [173,184,185] or even in patients taking common medications such as amoxicillin [183].…”

Section: Giant Cell Myocarditis and Geneticsmentioning

confidence: 99%