Dilated cardiomyopathy: Emerging role of endomyocardial biopsy

1986 ◽  
Vol 11 (8) ◽  
pp. 448-507 ◽  
Author(s):  
John B. O'Connell ◽  
Marie Rose Costanzo-Nordin ◽  
R. Subramanian ◽  
John Robinson
Keyword(s):  
Dilated Cardiomyopathy ◽  
Endomyocardial Biopsy

Current Role of Endomyocardial Biopsy in the Management of Dilated Cardiomyopathy and Myocarditis

2001 ◽  
Vol 76 (10) ◽  
pp. 1030-1038 ◽  
Author(s):  
Lambert A. Wu ◽  
Andre C. Lapeyre ◽  
Leslie T. Cooper
Keyword(s):  
Dilated Cardiomyopathy ◽  
Endomyocardial Biopsy ◽  
Current Role

Studies on Ultrastructure and Cytochemistry of Right Ventricular Endomyocardial Biopsy

1990 ◽  
Vol 48 (3) ◽  
pp. 256-257
Author(s):  
Xia Mingyu ◽  
Ma Wengshu ◽  
Wu Xiangh ◽  
Chen Dong
Keyword(s):  
Light Microscopy ◽  
Right Ventricular ◽  
Dilated Cardiomyopathy ◽  
Endomyocardial Biopsy ◽  
Heart Diseases ◽  
Ultrastructural Localization ◽  
Controlled Study ◽  
Myocardial Biopsy ◽  
Morphological Assessment ◽  
Rheumatic Heart

This paper describes morphological and cytochemistry changes of endomyocardial biopsy in 94 patients. The samples of myoicardium were taken from 32 patients with dilated cardiomyopathy, and sdudied with light and electron microscop. The cytochemical studies in some of these patients were performed at histological and ultrastructure level. This paper also reported the result of myocardial biopsy in 33 patients with serious dysrythmia.The result of this controlled study indicates that morphological assessment in both cardiomyopathy and congenital or rheumatic heart diseases showed no special changes. In patients of dilated cardiomyopathy, the decreased activity of myosin ATPase was secondary to cardial failure. The change of succinate dehydrogenase (SDHase) was not significant with light microscopy. But ultrastructural localization of SDHase activity is valuable. Its activity was found to be localized in endomembrane and ridge of the mitochondria, the activity of this enzyme was decrease, normal, or increase. SDHase activity was more intense in cardial myocytes well-functioning, or ultrastructurally well preserved hearts.

The role of dyslipidemia in idiopathic dilated cardiomyopathy

2008 ◽  
Vol 7 ◽  
pp. 29-29
Author(s):  
M SKWAREK ◽  
Z BILINSKA ◽  
L MAZURKIEWICZ ◽  
J GRZYBOWSKI ◽  
M KRUK ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Idiopathic Dilated Cardiomyopathy

The role of inflammation in recent-onset dilated cardiomyopathy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Chaloupka ◽  
J Krejci ◽  
H Poloczkova ◽  
P Hude ◽  
E Ozabalova ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Left Ventricular ◽  
Pcr Analysis ◽  
Myocardial Inflammation ◽  
Gene Variants ◽  
Absolute Increase ◽  
Recent Onset ◽  
Cardiotropic Viruses

Abstract Background The aetiology of recent-onset dilated cardiomyopathy (RODCM) includes inflammatory, genetic, toxic and metabolic causes. Delineating the role of inflammation on the genetic background could improve risk stratification. Purpose We aimed to ascertain the role of inflammation evaluated by serum CRP immunohistochemical and PCR analysis of endomyocardial biopsy (EMB) in conjunction with genetic testing in left ventricular reverse remodelling (LVRR) in 12-month follow-up. Methods 83 RODCM patients enrolled in this prospective observational study underwent 12-month echocardiographic follow up whole-exome sequencing, and EMB. Presence of cardiotropic viruses was determined by PCR analysis of the EMB samples. Inflammation was defined according to TIMIC immunohistochemical criteria as the presence of >7 CD3+ lymphocytes/mm2 and/or >14 infiltrating leukocytes (LCA+ cells/mm2). LVRR was defined as an absolute increase in LV ejection fraction > +10% and a relative decrease of LV end-diastolic diameter >−10% at 12 months. Results LVRR occurred in 28 (34%) of all cases. PCR analysis uncovered cardiotropic viruses in 55 (66%) patients, with highest prevalence of parvovirus B19 (47%). (Figure 1) EMB analysis detected inflammation in 28 (34%) cases and inflammation significantly positively predicted LVRR (P=0.019). Sequencing identified disease-related gene variants (ACMG class 3–5) in 45 (54%) patients. Carriers of non-titin gene variants showed a lowest probability of 12-month LVRR (19%) P=0.041. Combination of genetic findings and inflammation did not improve the prediction of LVRR in 12 months. (Table 1) Conclusion Both myocardial inflammation and disease-causing variants can be identified in a large proportion of RODCM cases. Prognostic value of CRP and virus detection is low. Non-titin disease-related variants carriers of are less likely to reach LVRR. In contrast, myocardial inflammation detected by EMB predicts favourable remodelling in 12 months. Figure 1 Funding Acknowledgement Type of funding source: None

scholarly journals Endomyocardial Biopsy in Pediatric Myocarditis and Dilated Cardiomyopathy: A Tool in Search for a Role

2022 ◽  
Vol 9 (1) ◽  
pp. 24
Author(s):  
Mara Pilati ◽  
Micol Rebonato ◽  
Roberto Formigari ◽  
Gianfranco Butera
Keyword(s):  
Endomyocardial Biopsy ◽  
Ventricular Dysfunction ◽  
Diagnostic Technique ◽  
Left Ventricular ◽  
Severe Left Ventricular Dysfunction ◽  
Myocardial Diseases ◽  
Pediatric Heart Failure ◽  
Diagnostic Work ◽  
Work Up

Endomyocardial biopsy (EMB) is a well-known diagnostic tool for the investigation and treatment of myocardial diseases and remains the gold standard for the diagnosis of myocarditis. Due to its invasiveness, with a complication rate ranging from 1 to 15%, its role in the diagnostic work-up of pediatric heart failure is not well established. The aim of this review is to define the role of EMB as diagnostic technique in the work up of children presenting with severe left ventricular dysfunction with the support of our center experience.

Massive parallel sequencing questions the pathogenic role of missense variants in dilated cardiomyopathy

2017 ◽  
Vol 228 ◽  
pp. 742-748 ◽  
Author(s):  
Martin G. Dalin ◽  
Pär G. Engström ◽  
Emil G. Ivarsson ◽  
Per Unneberg ◽  
Sara Light ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Massive Parallel Sequencing ◽  
Pathogenic Role ◽  
Parallel Sequencing ◽  
Missense Variants
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