scholarly journals Atrial Giant Cell Myocarditis as a Cause of Heart Failure

2022 ◽  
Vol 4 (1) ◽  
pp. 66-71
Author(s):  
Christina Paitazoglou ◽  
Martin W. Bergmann ◽  
Katharina Tiemann ◽  
Andrea Wiese ◽  
Ulrich Schäfer ◽  
...  
2017 ◽  
pp. bcr-2017-219574 ◽  
Author(s):  
Ioannis Kasouridis ◽  
Joaquim Majo ◽  
Guy MacGowan ◽  
Andrew L. Clark

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Michael H. Chiu ◽  
Cvetan Trpkov ◽  
Saman Rezazedeh ◽  
Derek S. Chew

Background. Idiopathic giant cell myocarditis (GCM) has a fulminant course and typically presents in middle-aged adults with acute heart failure or ventricular arrhythmia. It is a rare disorder which involves T lymphocyte-mediated myocardial inflammation. Diagnosis is challenging and requires a high index of suspicion since therapy may improve an otherwise uniformly fatal prognosis. Case Summary. A previously healthy 54-year-old female presented with hemodynamically significant ventricular arrhythmia (VA) and was found to have severe left ventricular dysfunction. Cardiac MRI demonstrated acute myocarditis, and endomyocardial biopsy showed giant cell myocarditis. She was treated with combined immunosuppressive therapy as well as guideline-directed medical therapy. A secondary prevention implantable cardioverter defibrillator (ICD) was implanted. Discussion. GCM is a rare, lethal myocarditis subtype but is potentially treatable. Combined immunosuppression may achieve partial clinical remission in two-thirds of patients. VA is common, and patients should undergo ICD implantation. More research is needed to better understand this complex disease. Learning Objectives. Giant cell myocarditis is an incompletely understood, rare cause of myocarditis. Patients present predominately with heart failure and dysrhythmia. Diagnosis is confirmed by histopathology, and immunosuppression may improve outcomes. ICD implantation should be considered. In the absence of treatment, prognosis is poor with a median survival of three months.


2020 ◽  
Vol 7 (1) ◽  
pp. 7-10
Author(s):  
Althea C. G. Neblett ◽  

Giant cell myocarditis is a rare condition first described in 1905. It has a reported incidence range from 0.007% to 0.051%. It affects female and male individuals, equally, and usually occurs in young and middle-aged persons. The underlying aetiology of giant cell myocarditis is unknown but it is thought to be mediated by T-lymphocytes. Diagnosis is made via histological examination of myocardial tissue and is characterized by a mixed inflammatory cell infiltrate with multinucleated giant cells and cardiomyocyte necrosis, predominantly affecting the ventricles. The following report describes a rare case of giant cell myocarditis in a 71-yearold man with a history of hypertension and heart failure, who died while waiting to be seen in the emergency department. Autopsy findings revealed an enlarged, dilated heart with histologic features in keeping with giant cell myocarditis, along with features of heart failure. Diagnosis of giant cell myocarditis is less common in the elderly age group, possibly due to a less severe disease process in this age group and it may be misdiagnosed because older individuals may have other cardiovascular diseases (CVDs).


2021 ◽  
Author(s):  
Emanuele Bobbio ◽  
Kristjan Karason

Activation of the inflammatory system occurs in most patients with advanced heart failure, regardless of etiology, and contributes to the pathophysiological milieu and the progression of the disease. The term inflammatory cardiomyopathy (ICM) refers to a group of disorders for which an acute or chronic myocardial inflammation is the central cause of abnormal cardiac structure or impaired cardiac function. The most common cause of inflammatory cardiomyopathy is lymphocytic myocarditis, which is most usually triggered by a viral infection, and occasionally by other infectious agents. Rare causes of specific inflammatory cardiomyopathies include cardiac sarcoidosis, giant cell myocarditis and eosinophilic myocarditis. Inflammatory cardiomyopathy can also occur in connection with autoimmune inflammatory diseases. Typical manifestations of inflammatory cardiomyopathy include chest pain, heart failure, and arrhythmias, but these symptoms and signs are unspecific. Although non-invasive diagnostic methods are emerging, the gold standard of diagnosis is the histological examination of an endomyocardial biopsy. Owing to the invasive nature of this technique and a modest diagnostic sensitivity, its use is limited. Therefore, the identification of inflammatory cardiomyopathy is elusive and the true incidence of the condition remains unknown. In most cases of lymphocytic myocarditis, recovery occurs within a few weeks following supportive treatment. In patients with cardiac sarcoidosis, giant cell myocarditis or eosinophilic myocarditis the use of immunosuppressive treatment is recommended, as is the case in myocarditis associated with autoimmune disorders. Such interventions may also have beneficial effects in chronic viral myocarditis once the virus has been cleared. In severe cases, treatment with mechanical circulatory support and/or heart transplantation may be required. Randomized intervention trials including antiviral, immunomodulating, or immunosuppressive agents are lacking. Similarly, new molecular-based methods and therapies tailored to specific pathogeneses have a potential to improve diagnosis and outcomes in patients with inflammatory cardiomyopathy. Still, such techniques and interventions are to be evaluated in adequate randomized controlled studies.


2001 ◽  
Vol 71 (6) ◽  
pp. 2036-2038 ◽  
Author(s):  
Abraham Oomman ◽  
Panchapakesan Ramachandran ◽  
Parachuri V Rao ◽  
Maligail R Girinath

Author(s):  
Afsaneh Amiri ◽  
Golnaz Houshmand ◽  
Sepideh Taghavi ◽  
Monireh Kamali ◽  
Nasim Naderi

In this case report, we present a 46-year-old lady who has developed a rapidly progressive heart failure after an episode of COVID-19. The pathologic examination of her endomyocardial biopsy specimens was compatible with GCM and she was successfully treated with a combined immunosuppressive therapy regimen.


2006 ◽  
Vol 15 (4) ◽  
pp. 228-230 ◽  
Author(s):  
Paul L. van Haelst ◽  
Johan Brügemann ◽  
Gilles F. Diercks ◽  
Albert Suurmeijer ◽  
Dirk J. van Veldhuisen

Author(s):  
Emanuele Bobbio ◽  
Marie Björkenstam ◽  
Bright I. Nwaru ◽  
Francesco Giallauria ◽  
Eva Hessman ◽  
...  

AbstractHeart transplantation (HTx) is a valid therapeutic option for end-stage heart failure secondary to cardiac sarcoidosis (CS) or giant-cell myocarditis (GCM). However, post-HTx outcomes in patients with inflammatory cardiomyopathy (ICM) have been poorly investigated. We searched PubMed, Scopus, Science Citation Index, EMBASE, and Google Scholar, screened the gray literature, and contacted experts in the field. We included studies comparing post-HTx survival, acute cellular rejection, and disease recurrence in patients with and without ICM. Data were synthesized by a random‐effects meta‐analysis. We screened 11,933 articles, of which 14 were considered eligible. In a pooled analysis, post-HTx survival was higher in CS than non-CS patients after 1 year (risk ratio [RR] 0.88, 95% confidence interval [CI] 0.60–1.17; I2 = 0%) and 5 years (RR 0.72, 95% CI 0.52–0.91; I2 = 0%), but statistically significant only after 5 years. During the first-year post-HTx, the risk of acute cellular rejection was similar for patients with and without CS, but after 5 years, it was lower in those with CS (RR 0.38, 95% CI 0.03–0.72; I2 = 0%). No difference in post-HTx survival was observed between patients with and without GCM after 1 year (RR 1.16, 95% CI 0.05–2.28; I2 = 0%) or 5 years (RR 0.98, 95% CI 0.42–1.54; I2 = 0%). During post-HTx follow-up, recurrence of CS and GCM occurred in 5% and 8% of patients, respectively. Post-HTx outcomes in patients with CS and GCM are comparable with cardiac recipients with other heart failure etiologies. Patients with ICM should not be disqualified from HTx. Graphic abstract


2017 ◽  
Vol 26 ◽  
pp. S125-S126
Author(s):  
M. Lwin ◽  
R. Jayasinghe ◽  
A. Dashwood ◽  
S. Hunt ◽  
S. Manawaar

Sign in / Sign up

Export Citation Format

Share Document