Interobserver variability in the pathologic interpretation of endomyocardial biopsy results.

Shanes, Jeffrey G.; Ghali, Jalal K.; Billingham, M. E.; Ferrans, Víctor J.; Fenoglio, John J.; Edwards, William D.; Tsai, Chun-Chin; Saffitz, Jeffrey E.; Isner, Jeffrey M.; Furner, Sylvia

doi:10.1161/01.cir.75.2.401

Cited by 233 publications

(84 citation statements)

References 18 publications

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“…First, EMB remains the main tool to diagnose AM, although it presents well-recognized accuracy limits, related to the number and sites of bioptic samples, 23,24 proper timing of the procedure 25 and histopathological interpretation. 26 Consequently, the real incidence of suspected AM without criteria for EMB remains uncertain.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Evolution and Prognostic Stratification of Biopsy-Proven Active Myocarditis

et al. 2013

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Background-Active myocarditis is characterized by large heterogeneity of clinical presentation and evolution. This study describes the characteristics and the long-term evolution of a large sample of patients with biopsy-proven active myocarditis, looking for accessible and valid early predictors of long-term prognosis. Methods and Results-From 1981 to 2009, 82 patients with biopsy-proven active myocarditis were consecutively enrolled and followed-up for 147±107 months. All patients underwent clinical and echocardiographic evaluation at baseline and at 6 months. At this time, improvement/normality of left ventricular ejection fraction (LVEF), defined as a LVEF increase > 20 percentage points or presence of LVEF≥50%, was assessed. At baseline, left ventricular dysfunction (LVEF<50%) and left atrium enlargement were independently associated with long-term heart transplantation-free survival, regardless of the clinical pattern of disease onset. At 6 months, improvement/normality of LVEF was observed in 53% of patients. Persistence of New York Heart Association III to IV classes, left atrium enlargement, and improvement/normality of LVEF at 6 months emerged as independent predictors of long-term outcome. Notably, the short-term reevaluation showed a significant incremental prognostic value in comparison with the baseline evaluation (baseline model versus 6 months model: area under the curve 0.79 versus 0.90, P=0.03). Conclusions-Baseline left ventricular function is a marker for prognosis regardless of the clinical pattern of disease onset,and its reassessment at 6 months appears useful for assessing longer-term outcome.

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Section: Discussionmentioning

confidence: 99%

Long-Term Evolution and Prognostic Stratification of Biopsy-Proven Active Myocarditis

et al. 2013

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“…This is underlined by the fact that all tissue samples from the control group were completely virus negative. Previous studies with histologic investigation of myocardial lesions in cases of SIDS based on conventional stainings revealed only unspecific findings (6), and diagnosis often is not reliable because of considerable interobserver variability (22).…”

Section: Discussionmentioning

confidence: 99%

Role of Virus-Induced Myocardial Affections in Sudden Infant Death Syndrome: A Prospective Postmortem Study

et al. 2004

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The cause of sudden infant death syndrome (SIDS) is an unresolved problem of high relevance. Previous studies indicate a role of infections. In our prospective study, we investigated the frequency of virus-induced myocardial affections in SIDS. Postmortem samples from SIDS victims and control subjects were investigated prospectively. Pediatric cases of unnatural death served as controls. Samples were studied for enteroviruses, adenoviruses, parvovirus B19, and Epstein-Barr virus applying PCR. Immunohistochemical investigations for inflammatory cells, the necrosis marker C5b-9 (m) complement complex, and the enteroviral capsid protein VP1 were performed. Overall, 62 SIDS victims were studied. As controls, 11 infants were enrolled. Enteroviruses were detected in 14 (22.5%), adenoviruses in 2 (3.2%), Epstein-Barr viruses in 3 (4.8%), and parvovirus B19 in 7 (11.2%) cases of SIDS. Control group samples were completely virus negative. Compared with controls, immunohistochemical investigations partially revealed a significant increase in the number of T lymphocytes in SIDS myocardial samples (p Ͻ 0.05). Furthermore, cases with elevated numbers of leukocytes and macrophages, microfocal C5b-9 (m) ϩ necroses, and enteroviral VP1 capsid protein within the myocardium were detected. Applying a comprehensive combination of molecular and immunohistochemical techniques, our results demonstrate a clearly higher prevalence of viral myocardial affections in SIDS. Our results emphasize the importance of PCR-based diagnosis of viral myocardial affections. We suggest preliminary criteria for cellular immunohistochemical diagnosis of viral myocardial affections derived from our findings. The diagnosis of sudden infant death syndrome (SIDS) is established by comprehensive exclusion of all other possible causes of death in the age group. Myocarditis is a widely known explanation for sudden death in cases of suspected SIDS as well as in older children (1). Recent clinical studies and anecdotal communications reported on different viruses in such cases applying molecular techniques to detect the genome sequences of enteroviruses (EV) (2), adenoviruses (AV) (3), Epstein-Barr virus (EBV) (4), and parvovirus B19 (PVB19) (5) in clinical and autopsy samples, respectively. Until recently, a maximum percentage of up to 17% of cases of sudden unexpected death in infancy showing-if at all-histologic hints of viral myocardial affections was assumed (6). The aim of our study was to determine the incidence of virus-induced myocardial affections in cases of SIDS with modern immunohistochemical and molecular pathologic methods. METHODS

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“…Despite the availability of the Dallas criteria (21), pathologists have yet to agree on what constitutes myocarditis (40). Clearly, several variables are at play and potentially include the infant's age, general health, genetic background (13), underlying immune status, exposure to certain risk factors (41), safety of the sleep environment (Hauck FR 1997 Bedsharing: review of epidemiologic data examining links to SIDS.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Inflammation, Cellular Death, and Viral Detection in Sudden Infant Death Caused by SIDS, Suffocation, or Myocarditis

et al. 2009

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ABSTRACT:The significance of minor myocardial inflammatory infiltrates and viral detection in SIDS is controversial. We retrospectively compared the demographic profiles, myocardial inflammation, cardiomyocyte necrosis, and myocardial virus detection in infants who died of SIDS in a safe sleep environment, accidental suffocation, or myocarditis. Formalin-fixed, paraffin-embedded myocardial sections were semiquantitatively assessed for CD3 lymphocytes and CD68 macrophages using immunohistochemistry and for cardiomyocyte cell death in H&E-stained sections. Enteroviruses and adenoviruses were searched for using PCR technology. The means of lymphocytes, macrophages, and necrotic cardiomyocytes were not statistically different in SIDS and suffocation cases. Enterovirus, not otherwise specified, was detected in one suffocation case and was the only virus detected in the three groups. Very mild myocardial lymphocyte and macrophage infiltration and scattered necrotic cardiomyocytes in SIDS are not pathologic, but may occur after the developing heart is exposed to environmental pathogens, including viruses. (Pediatr Res 66: 17-21, 2009)

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Interobserver variability in the pathologic interpretation of endomyocardial biopsy results.

Cited by 233 publications

References 18 publications

Long-Term Evolution and Prognostic Stratification of Biopsy-Proven Active Myocarditis

Long-Term Evolution and Prognostic Stratification of Biopsy-Proven Active Myocarditis

Role of Virus-Induced Myocardial Affections in Sudden Infant Death Syndrome: A Prospective Postmortem Study

Myocardial Inflammation, Cellular Death, and Viral Detection in Sudden Infant Death Caused by SIDS, Suffocation, or Myocarditis

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