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PubMed1986

Value of endomyocardial biopsy.

The role of endomyocardial biopsy may be restricted to the diagnosis of myocarditis. On the other hand, a broad utilization of the biopsy technique may be championed by those who believe that the light and electron microscopic characteristics of the tissue are important and that the biochemical features of the tissue may hold important clues to the diagnosis and therapy of dilated cardiomyopathy. The popularity of endomyocardial biopsy arises from the ease and safety of the procedure. Light microscopy of the tissue is useful not only to diagnose myocarditis but also to discover infiltrative cardiomyopathies and to characterize the dilated cardiomyopathies by the amount of fibrosis and cellular hypertrophy. Electron microscopy supplies more detailed information on the myofibrils, nuclei, tubular structures, mitochondria, glycogen, and lipofuscin. At present, these data are clinically applicable only to the anthracycline cardiomyopathies. On an investigational basis, subcellular characteristics may help us better understand the etiology and pathogenesis of dilated cardiomyopathy. The greatest promise lies in the biochemical assessment of tissue, which may uncover single or multiple biochemical abnormalities in heart failure. Although the clinical usefulness of endomyocardial biopsy is quite restricted at present, its future looks quite promising.

Amyloid↗
PubMed1985

[Acute idiopathic myocarditis having myocardial inflammatory swelling demonstrated by echocardiography: a case report].

A case of acute idiopathic myopericarditis with transient severe swelling and akinesis of the interventricular septum on echocardiograms was reported. A 35-year-old man was admitted to our CCU because of cardiogenic shock five days after the onset of "common cold". Electrocardiograms revealed low voltage and ST-segment elevation in all leads except for a VR and a VL. Serum CPK, GOT and LDH were slightly elevated. Echocardiograms showed severe asymmetrical septal hypertrophy (ASH, 20 mm), akinesis of the interventricular septum and moderate pericardial effusion. With improvement of the clinical course and of the hemodynamic data, the thickness and wall motion of the interventricular septum became normal. Serum antiviral antibodies were not elevated throughout the course. Transvenous percutaneous right ventricular endomyocardial biopsy revealed degeneration and fragmentation of the myofibrils with interstitial cellular infiltration and edema in the subacute phase (8th hospital day), but showed only focal fibrosis in the chronic phase. Coronary arteriograms and left ventriculograms in the chronic phase (50th hospital day) were normal. From these findings we can conclude that the severe transient ASH is due to myocardial inflammatory swelling.

Adult↗
PubMed2005

Noninvasive detection of myocardial fibrosis in arrhythmogenic right ventricular cardiomyopathy using delayed-enhancement magnetic resonance imaging.

OBJECTIVES: We evaluated the role of myocardial delayed-enhancement (MDE) magnetic resonance imaging (MRI) for noninvasive detection of fibrosis in Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). BACKGROUND: Arrhythmogenic right ventricular dysplasia/cardiomyopathy is characterized by fibro-fatty replacement of the right ventricle (RV) leading to arrhythmias and RV failure. Endomyocardial biopsy can demonstrate fibro-fatty replacement of the RV myocardium; however, the test is invasive and carries a risk of perforation. METHODS: Thirty consecutive patients were prospectively evaluated for ARVD/C. Magnetic resonance imaging was performed on a 1.5-T scanner. Ten minutes after intravenous administration of 0.2 mmol/kg of gadodiamide, MDE-MRI was obtained. Diagnosis of ARVD/C was based upon the Task Force criteria and did not include MRI findings. RESULTS: Twelve (40%) of 30 patients met the Task Force criteria for ARVD/C. Eight (67%) of the 12 ARVD/C patients demonstrated increased signal on MDE-MRI in the RV compared with none (0%) of the 18 patients without ARVD/C (p <0.001). Endomyocardial biopsy was performed in 9 of the 12 ARVD/C patients. Of the nine patients, four had fibro-fatty changes consistent with the diagnosis of ARVD/C. Each of these patients had increased RV signal on MDE-MRI. None of the patients without ARVD/C had any abnormalities either on histopathology or on MDE-MRI. Electrophysiologic testing revealed inducible sustained ventricular tachycardia (VT) in six of the eight ARVD/C patients with delayed enhancement, compared with none of the ARVD/C patients without delayed enhancement (p=0.01). CONCLUSIONS: Noninvasive detection of RV myocardial fibro-fatty changes in ARVD/C is possible by MDE-MRI. Magnetic resonance imaging findings had an excellent correlation with histopathology and predicted inducible VT on programmed electrical stimulation, suggesting a possible role in evaluation and diagnosis of patients with suspected ARVD/C.

Adolescent↗
PubMed1993

[Mechanisms of cardiac involvement in systemic scleroderma, apropos of 3 cases].

We studied myocardial manifestations of systemic sclerosis in three patients. Two patients were symptomatic. A transthoracic echocardiography, a coronary angiography, a cardiac catheterization, thallium scans with dipyridamol completed by thoracic cold exposure and endomyocardial biopsy with immunohistological study were performed. None of them have coronary stenosis. In the three cases abnormalities of myocardial perfusion were detected, two of them have fibrosis. The immunohistological study always showed an anusual expression of HLA DR on cardiac fibroblasts.

Aged↗
PubMed1983

[Endomyocardial biopsy as a method of surveilling adriamycin cardiac toxicity. 28 biopsies in 26 patients].

The aim of this study was to evaluate the role of endomyocardial biopsy in the surveillance of toxic, latent cardiomyopathy secondary to adriamycin (ADM) therapy, and to assess its value by comparison with non-invasive investigations such as echocardiography. Twenty six patients underwent endomyocardial biopsy and echocardiographic measurement of the fractional shortening of the left ventricular internal diameter after a total dose of 150 to 520 mg/m2 of ADM. Interstitial fibrosis was observed in 8 of the 20 interpretable cases on light microscopy (6 moderate, 2 severe). There were no cellular changes. Slight focal myofibril degeneration was observed in 8 cases, and vacuolisation corresponding to mild dilatation of the sarcoplasmic reticulum was observed in 9 cases out of the 22 technically interpretable cases on electron microscopy. In contrast to the findings of interstitial fibrosis, cellular degeneration correlated significantly with the total dose of ADM (p less than 0,01). We conclude that this histological study confirms the fact that myocardial changes are rare and slight with doses of less than 520 mg/m2 of ADM and that non-invasive techniques are adequate for follow-up until this dose is reached.

Adult↗
PubMed2006

Morphometric changes of the right ventricle in the first two weeks after clinical heart transplantation: analysis of myocardial biopsies from patients with complicated versus uncomplicated course.

OBJECTIVE: The early phase following heart transplantation (HTx) is characterized by the development of right ventricular myocardial fibrosis (MF) and cardiomyocyte hypertrophy (CH). The question is if there are differences in development of MF and CH between patients with complicated versus patients with uncomplicated postoperative course. METHODS: Endomyocardial biopsies were taken from 58 donor hearts before implantation and one and two weeks after HTx. According to the clinical course in the first year after HTx and the rejection grading (ISHLT), four groups were classified: (a) uneventful course, (b) transplant failure, (c) infections, and (d) rejection episodes > or = 1R. The volume densities of various tissue components and cardiomyocyte diameters were measured by stereological and morphometrical methods. RESULTS: From implantation to the first two weeks, most groups showed a significant increase of endomysial and perimysial connective tissues. There was a significant CH recognizable, especially in the rejection group. However, nucleus surface, a hypertrophy parameter, showed no significant change during follow-up. There were no statistically significant differences in volume densities of interstitial space, capillaries, nuclei and cardiomyocytes between the collectives and points in time. Sarcomere length as marker of contraction status of cardiomyocytes remained at the same level and showed no significant differences. Demographic data showed no significant differences and will be presented. CONCLUSIONS: Patients with complicated and uncomplicated courses show different degrees of histopathological changes after HTx. The extent of hypertrophy differs especially between the collectives. Measurement of endomysial connective tissue points to later postoperative course in the recipient. These findings may reflect a pattern of remodeling specific to the transplanted heart.

Adult↗
PubMed1980

Histopathological study on right endomyocardial biopsy of Kawasaki disease.

Fifty right ventricular endomyocardial biopsy specimens taken from patients with Kawasaki disease were studied. These were taken from 33 male and 17 female patients. Biopsies were examined for inflammatory cell infiltration, fibrosis, myocardial fibre disarrangement, and the cellular and nuclear changes of hypertrophy. A score of severity was prepared. The degree of abnormality was found to correlate with the duration of the disease, as did fibrosis found in 18 cases (36%), but inflammatory cell infiltration did not (13 cases, 26%). Coronary involvement was restricted to the male patients but the myocardial changes occurred in both sexes.

Cardiomegaly↗
PubMed1990

Chronic supraventricular tachycardia causes ventricular dysfunction and subendocardial injury in swine.

Chronic supraventricular tachycardia has been associated with ventricular dysfunction in humans and animals. However, this ventricular failure is poorly characterized, and the ultrastructural consequences of supraventricular tachycardia are unknown. We serially examined right and left ventricular function, endomyocardial ultrastructure, and creatine kinase activity in eight pigs at base line and again at 1, 2, and 3 wk following rapid atrial pacing. Left and right ventricular ejection fractions fell significantly from base line after 1 wk of chronic tachycardia. Three weeks of chronic pacing resulted in further deterioration in ejection fractions. Significant biventricular chamber dilatation developed and was associated with a reduction in end-diastolic wall thickness after 2 wk of tachycardia. Mitochondrial injury and diminished mitochondrial cytochrome oxidase staining of subendocardial myocytes were observed after 2 wk of tachycardia. Endomyocardial creatine kinase activity fell from control levels following 2 wk of pacing. Postmortem examination revealed a reduction in left ventricular wall thickness compared with 14 control animals. Fibrosis occurred along the subendocardial layer in paced animals, and glycogen content was also reduced. In summary, chronic supraventricular tachycardia resulted in severe biventricular pump dysfunction and chamber dilatation that were associated with ultrastructural alterations and reduced enzyme activity of the subendocardial myocytes. These ultrastructural and metabolic changes may be potential mechanisms responsible for the ventricular dysfunction and dilatation observed in this model.

Animals↗
PubMed1982

NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations.

The idiopathic hypereosinophilic syndrome (HES) represents a heterogeneous group of disorders with the common features of prolonged eosinophilia of an undetectable cause and organ system dysfunction. Fifty patients with the idiopathic HES were studied over 11 years of the National Institutes of Health. Multiple organ systems were involved; bone marrow hypereosinophilia was common to all patients, but the most severe clinicopathologic involvement was of the heart and nervous system. Postmortem gross pathologic examination of the hearts of patients with idiopathic and nonidiopathic HES suggested that the common mechanism of cardiac disease is the eosinophilia. Endomyocardial biopsy findings showed that the endothelial cells in the endocardium and of the microvasculature were the primary targets of the tissue damage. This damage initiates thrombosis; endocardial fibrosis and restrictive endomyocardopathy may follow. In-vitro culture of circulating eosinophil colony-forming units showed some normal studies, some studies showing increased progenitor cells committed to eosinophil development, and others showing an excess production of eosinophil colony-stimulating factor. Chemotherapy to lower the eosinophil counts has resulted in marked improvement of HES prognosis, as have agressive medical and surgical approaches to cardiovascular complications.

Cardiomyopathies↗
PubMed2005

[Serious clinical course of myocarditis with "apical ballooning": first presentation of pathogenicity of HHV6 subtype A in myocarditis].

We report of a 67 year-old female who has suffered a flu-like infection three days ago and presented with symptoms of acute coronary syndrome. Coronary heart disease could be excluded. The ventriculography showed a moderate reduced left ventricular function characterized by "apical ballooning". Endomyocardial biopsies and EDTA blood gave a direct proof of human herpes virus 6 subtype A. Histological and immunohistochemical analysis revealed a myocarditis with areas of interstitial macrophages and fibrosis. This case presents for the first time the cross-link of myocarditis with HHV6A infection and the appearance of "apical ballooning".

Aged↗
PubMedDate not supplied

Clinicopathologic characteristics of hypertrophic cardiomyopathy detected during mass screening for heart disease.

Between 1981 and 1992 a total of 10 patients with hypertrophic cardiomyopathy (HCM) were detected by mass screening for heart disease in Tokyo's Adachi Ward. Four were first grade elementary school children and six were first grade junior high school adolescents. Two-dimensional echocardiography at the initial evaluation revealed asymmetric septal hypertrophy in four patients, diffuse hypertrophy of the left ventricle in five, and poor left ventricular contractility with wall thinning in one (dilated phase). Three of the five patients with diffuse hypertrophy progressed to asymmetric septal hypertrophy during the average 4-year follow-up period. The degree of septal thickness and the left ventricular wall thickness index were significantly less than in those of young adult controls (12 +/- 3 versus 21 +/- 9 mm, p < 0.05; and 22 +/- 4 versus 28 +/- 16 mm, p < 0.05, respectively). Right ventricular endomyocardial biopsy specimens obtained from 9 of the 10 patients showed features typical of HCM (e.g., myocyte hypertrophy with myofibril disarray) in five patients and atypical features (mainly interstitial fibrosis with perivascular cell infiltration) in another four. One patient with dilated phase disease died of congestive heart failure 6 months after the initial evaluation. These results indicate that HCM detected during mass screening is a mild form of the disease and may have atypical pathologic features, such as interstitial fibrosis and perivascular cell infiltration, mimicking the sequela of chronic myocarditis.

Adolescent↗
PubMed2002

Myocardial ischemic injury after heart transplantation is associated with upregulation of vitronectin receptor (alpha(v)beta3), activation of the matrix metalloproteinase induction system, and subsequent development of coronary vasculopathy.

BACKGROUND: Myocardial ischemic injury after heart transplantation is associated with subsequent development of graft vasculopathy. Both vitronectin receptor (integrin alpha(v)beta3) and tissue factor play key roles in vascular endothelial cell injury. Matrix metalloproteinases (MMPs) are activated in ischemic injury models. METHODS AND RESULTS: Thirteen patients developed myocardial ischemic injury within 2 weeks of cardiac transplantation (ischemia group). These were compared with 10 transplantation patients who had no evidence of ischemia (control group). Endomyocardial biopsies were evaluated within 2 weeks of transplantation for alpha(v)beta3, tissue factor, and extracellular MMP inducer (EMMPRIN). At 1 year, MMPs were evaluated, and interstitial myocardial fibrosis was quantified. All patients underwent intravascular ultrasound at 1 month and 1 year after transplantation. Compared with control, the ischemia group demonstrated evidence of significant increased expression of alpha(v)beta3 (3.2-fold, P<0.001), tissue factor (2.5-fold, P<0.001), and EMMPRIN (1.9-fold, P=0.01). At 1 year, the ischemia group had a significant increase in myocardial fibrosis (24+/-1.8% versus 14+/-1.1%, P<0.001) and zymographic activity of MMP-2 (1.4-fold, P<0.001), MMP-3 (1.2-fold, P<0.001), and MMP-9 (1.3-fold, P=0.01). Coronary vasculopathy progression was also more advanced in the ischemia group (change in coronary maximal intimal thickness over 1 year 0.54+/-0.1 versus 0.26+/-0.06 mm; P=0.031). CONCLUSIONS: Myocardial ischemic injury after cardiac transplantation is associated with upregulation of alpha(v)beta3, tissue factor, and activation of the MMP induction system, which may contribute to the subsequent development of allograft remodeling and vasculopathy.

Adult↗
PubMed1985

On the interstitial fibrotic changes in acute and convalescent myocarditis obtained by serial endomyocardial biopsy.

In order to determine the characteristics of the interstitial fibrotic change of the myocardium in cases with viral or idiopathic myocarditis, right ventricular endomyocardial biopsy findings in 9 cases where serial endomyocardial biopsy had been performed at the acute (5-10 days after the onset of the disease), subacute (11-21 days) and convalescent stages (22-167 days) and in 1 case at the acute stage were analyzed. They were then compared with right ventricular endomyocardial biopsy findings from 58 cases with chronic right ventricular overloading and which were of various kinds of congenital and valvular heart diseases. The following results were obtained: Interstitial fibrosis was seen at the acute stage along with an increase in fibroblasts, macrophages and lymphocytes. An analysis of the interstitial changes revealed that, at the acute stage, thin collagenous fibers were prominent as well as interstitial edema and at the convalescent stage, the edema became less prominent and instead, thick collagenous fibers increased. Comparison with the 58 cases with chronic right ventricular overloading revealed that diffuse and/or subendocardial fibrosis and endocardial thickening were more frequent and statistically more significant in cases with myocarditis.

Acute Disease↗
PubMed1999

Histopathologic aspects of endomyocardial biopsy in pediatric patients with idiopathic ventricular tachycardia.

PURPOSE: The present study aimed to investigate the clinicopathologic findings and histopathologic characteristics of endomyocardial biopsy in pediatric patients with idiopathic ventricular tachycardia. METHODS: Histopathological findings of endomyocardial biopsy from 17 patients aged 7-15 years with idiopathic ventricular tachycardia (VT) but no organic heart disease were examined. Patients considered to have cardiomyopathy of the dilated, hypertrophic or specific form or arrhythmogenic right ventricular cardiomyopathy were excluded from this study. RESULTS: Advanced histopathologic findings, including myocyte hypertrophy, degeneration, interstitial fibrosis and disarrangement of muscle bundles, were disclosed in three cases (17.6%). One of these cases exhibited sustained VT with left bundle branch block configuration and showed increased frequency of VT during exercise testing. The remaining two cases had non-sustained VT with multifocal origin and had syncope episodes. Another 14 cases showed mild or no significant findings in the biopsy. CONCLUSIONS: These results indicate that advanced histopathology in endomyocardial biopsy is occasionally disclosed in cases of idiopathic VT, especially those of exercise-related VT or multifocal VT, and that these patients may be considered as having heart muscle disease.

Adolescent↗
PubMedDate not supplied

Right ventricular late filling termination time and its relation to interstitial collagen content in early transplanted heart: a color M-mode Doppler digital analysis.

BACKGROUND: Histologic changes in cardiac allografts resulting from fibrosis or acute rejection can modify ventricular diastolic function and ventricular inflow characteristics. These abnormalities may be detected by color M-mode Doppler echocardiography which has been shown to be sensitive in assessing ventricular diastolic function. METHODS: Twelve cardiac allograft recipients were prospectively studied with serial color M-mode and single-gated Doppler echocardiography, as well as with endomyocardial biopsy, with a follow-up of approximately 10 weeks. The myocardial interstitial collagen content as evaluated by videodensitometry was compared with right and left ventricular late filling termination times measured in the absence of a severe episode of rejection. RESULTS: A positive and significant correlation was found between the collagen content and the corresponding right ventricular late filling termination time (r = 0.89, p < 0.0001), but no correlation was found with the left ventricular late filling termination time. Moreover, variations in collagen content and variations in right ventricular late filling termination time were also highly correlated (r = 0.91, p < 0.0001). In allograft recipients who had episodes of rejection of grade 3A or greater, both right and left ventricular late filling termination times were significantly increased during rejection. CONCLUSIONS: Measurements of right ventricular late filling termination time by color M-mode Doppler echocardiography performed in the absence of acute rejection can be use to monitor the evolution of interstitial collagen content in cardiac allografts. The early detection of abnormally prolonged late filling termination time could be followed by endomyocardial biopsy to confirm the histologic changes.

Adult↗
PubMed2005

The impact of donor gender on cardiac peri-transplantation ischemia injury.

BACKGROUND: Cardiac allografts from female donors have been shown to be associated with increased risk of transplant vasculopathy. However, the influence of donor gender on peri-transplantation ischemic injury has not been evaluated. METHODS: A total of 361 patients (mean age, 52 +/- 10 years) underwent cardiac transplantation between January 1998 and December 2002. Patients were divided into 4 groups according to their donor-recipient gender status: Group A, male-male, 156; Group B, male-female, 37; Group C, female-male, 114; and Group D, female-female, 54. Serial right ventricular endomyocardial biopsy specimens were evaluated for ischemic injury during the first 4 weeks after transplantation. RESULTS: Patients were similar in baseline characteristics. An increased incidence of ischemic injury complicated by fibrosis (12.9%, p = 0.03) and subsequent development of transplant vasculopathy (Kaplan-Meier 6-year freedom from vasculopathy, 53.4%; p = 0.012) was noted in Group D. No survival difference was observed among the 4 groups, however. In Group D (F-F), 2 patients underwent retransplantation and 2 patients underwent revascularization. CONCLUSIONS: The transplantation of a female cardiac allograft into a female recipient is associated with increased risk of ischemic injury complicated by fibrosis and subsequent transplant vasculopathy.

Adult↗
PubMedDate not supplied

Programmed cell death in the myocardium of arrhythmogenic right ventricular cardiomyopathy in children and adults.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by fibrofatty replacement of the right ventricular myocardium. Recently, the myocardial loss in ARVC has been suggested to be related to apoptosis. However, it is still unknown whether this phenomenon is already established in the myocardium of pediatric cases with this disease. We examined the histopathologic characteristics of the ventricular myocardium in specimens obtained from 10 patients, including 3 children with ARVC, and investigated the occurrence of apoptosis in the myocardium by terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) assay and agarose-gel electrophoresis of DNA. Endomyocardial biopsy specimens from the 10 cases and a necropsy sample from one adult case with ARVC were examined. Histopathologic examination of biopsy specimens from the pediatric cases revealed extensive fibrosis. Typical fatty infiltration was demonstrated in one of the 3 pediatric cases. These findings were similar to those in adult cases; the histopathologic index based on the severity of myocardial damage, including myocyte degeneration and fibrosis, was not significantly different from that in adult cases. TUNEL assay revealed positive reactivity of the myocardial cells. The apoptotic index was 1.4 +/- 0.4% in children and 1.6 +/- 0.5% in adults (difference not statistically significant). Agarose-gel electrophoresis of a DNA extract of the myocardial tissue of the autopsy case revealed DNA fragmentation. Cases with idiopathic ventricular tachycardia and control cases with a cardiac transplant (with no rejection) had minimal histopathologic findings and negative reactivity in the TUNEL assay. These results indicate that myocardial damage is already established in cases diagnosed as ARVC in childhood, and suggest that the myocardial damage is closely related to apoptosis in children, as well as in adults, in this disease.

Adolescent↗