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PubMed1991

[A morphological analysis of the specimens obtained during endomyocardial biopsies in patients with a clinical diagnosis of dilated cardiomyopathy].

The authors summarize experience gained with a study of biopsy specimens obtained on endomyocardial biopsies from 88 patients with a clinical diagnosis of dilated cardiomyopathy. The diagnostic value of the study was equal to 70%. Dilated cardiomyopathy largely masked myocarditis and alcoholic cardiomyopathy which were diagnosed morphologically in 30 and 13% of the patients, respectively. No morphological alterations which would allow one to change the clinical diagnosis of dilated cardiomyopathy were discovered in 26% of cases. It has been shown that endomyocardial biopsy is an important tool of diagnosis. In order to introduce it on a broader scale, it is necessary that quantitative uniform criteria for the diagnosis of endomyocardial diseases, primarily myocarditis, be elaborated.

Adolescent↗
PubMed1990

Hemodynamic and scintigraphic improvement after steroid therapy in a case with acute eosinophilic heart disease.

A 70-year-old woman with active hypereosinophilic myocarditis presented with high fever and heart failure. Repeated right ventricular endomyocardial biopsies and 201-T1 myocardial scans before and after steroid therapy suggested that this treatment reversed the cardiac injury. Patients with hypereosinophilia may die from complications of eosinophilic infiltration and fibrosis in target organs, especially the heart. The findings in this patient suggest that steroids have benefit in this disease, at least in the short term.

Acute Disease↗
PubMed1981

[Relationships between hemodynamic values with prognostic significance and morphology of the left ventricle in patients with aortic insufficiency].

Hemodynamic parameters have recently been described which are of prognostic importance for the outcome of valve replacement in patients with aortic insufficiency. It was investigated whether pathological values for the left ventricular end-systolic volume index, the ejection fraction, the end-diastolic radius/wall thickness ratio, the end-systolic diameter (DS) and shortening of the diameter (Sh), and the end-diastolic volume index are accompanied by morphological alterations evaluated from left ventricular endomyocardial biopsies. Hypertrophy of the cardiac fibers was significantly increased in patients in whom preoperative Sh was less than 25% and DS greater than 55 mm. In contrast, left ventricular interstitial fibrosis did not differ between these patients and those with Sh greater than or equal to 25% and DS less than or equal to 55 mm.

Adolescent↗
PubMed1998

Myocardial DNA strand breaks are detected in biopsy tissues from patients with dilated cardiomyopathy.

BACKGROUND: Progressive damage of cardiomyocytes with interstitial and replacement fibrosis accompanied by less inflammatory cell infiltration is observed in patients with dilated cardiomyopathy (DCM), suggesting some other mechanisms rather than necrotic cell death. HYPOTHESIS: The aim of this study was to assess the possible involvement of apoptotic process in the pathogenesis of DCM and myocarditis. METHODS: Endomyocardial biopsy was performed in patients with DCM (n = 9), myocarditis (n = 4), or atypical chest pain syndrome (as controls; n = 5). The TUNEL method was used for in situ detection of oligonucleosomal DNA strand breaks. RESULTS: The TUNEL-positive cells were observed in three of nine patients with DCM and in all four with myocarditis, but in none of the controls. The TUNEL-positive nuclei were observed exclusively in cardiomyocytes in DCM, whereas in myocarditis they were detected mainly in interstitial cells and in a few myocytes. In DCM, interstitial fibrosis was greater in the TUNEL-positive than in TUNEL-negative patients (p < 0.05). In either DCM or myocarditis, electron microscopic examination could not reveal morphologic features of apoptosis of cardiomyocytes. CONCLUSION: The DNA strand breaks were detected in cardiomyocytes in patients with DCM and mainly in interstitial cells in myocarditis. It is possible that the DNA strand breaks can be involved in mechanisms of progressive loss of functional cardiac units in these myocardial diseases.

Adult↗
PubMed1984

Acute myocarditis. Role of histological and virological examination in the diagnosis and assessment of immunosuppressive treatment.

Twelve patients, who presented with congestive cardiac failure after a recent influenza like illness, had a clinical diagnosis of acute myocarditis confirmed histologically after endomyocardial biopsy. Eight were under 30 years of age. Serological testing suggested a viral aetiology in six patients. Nine patients were treated with immunosuppressive drugs (prednisolone and azathioprine in seven, prednisolone alone in two). At two months, seven patients showed clinical and haemodynamic improvement (ejection fraction rose from 26.8 to 49% and left ventricular end diastolic pressure fell from 26.4 to 16.2 mm Hg) with biopsy evidence of healed myocarditis. In two, activity persisted. At six months' follow up only four of these patients had maintained their improvement. One patient relapsed after stopping treatment, subsequently improving on its reinstatement. Two patients developed severe interstitial myocardial fibrosis with gradual deterioration. Virology and myocardial histology were complementary in the diagnosis of acute myocarditis in these young patients, whose response to immunosuppressive treatment was variable. An apparent early response could not be clearly separated from variables in the natural history of the condition. Serial endomyocardial biopsies showed a progression to congestive cardiomyopathy in two patients. Multicentre controlled trials will be necessary to assess fully the role of immunosuppressive treatment in this condition.

Acute Disease↗
PubMed1991

The Runme Shaw Memorial Lecture--transplantation of the heart and heart-lungs.

After ten years of experimental background, the first heart transplant at Stanford was performed on January 6, 1968. Six hundred and sixty-six patients have undergone 721 heart transplants since that date with an age range from five days to 64 years. The most common diagnosis has been cardiomyopathy with advanced coronary artery disease second. Current one and five year survival statistics are 81% and 60% respectively, with no difference in survival between the pediatric age group and adults. Percutaneous transvenous endomyocardial biopsy provides the gold standard for interpreting allograft rejection. At Stanford, 90 patients have undergone 91 heart-lung transplants since the first successful case in 1981. Twelve patients with cystic fibrosis have been transplanted and four of these recipients have been heart donors, the domino donor principle. Two double lung transplants have been performed utilising separate bronchial anastomoses. Fourteen patients have undergone 15 single lung transplants and three of these have been patients with the Eisenmenger syndrome where concomitant repair of the cardiac defect was carried out. One 12 year old patient received the right upper lobe of her mother as a total right lung transplant for bronchopulmonary dysplasia.

California↗
PubMed1985

Cardiac transplantation: indications, procurement, operation, and management.

Between July 1982 and April 1984, 22 patients underwent cardiac transplantations at the Texas Heart Institute with a cumulative follow-up of 188 patient-months (mean of 8.6 months and a range of 0.5 to 21). The actuarial survival rate at 20 months was 72%. Strict selection criteria for potential recipients and donors, optimal perioperative management, which includes endomyocardial biopsy, and most important the introduction of cyclosporine are the major factors that led to these increasing survival rates. The high incidence of cyclosporine-related complications, especially hypertension and myocardial fibrosis, will require long-term evaluation to adequately assess the therapeutic effectiveness of this new immunosuppressive agent.

Central Nervous System Diseases↗
PubMed2005

Simvastatin decreases myocardial tumor necrosis factor alpha content in heart transplant recipients.

BACKGROUND: Statins improve patient survival and decrease rejection episodes in heart transplant recipients. We studied the effects of simvastatin treatment on myocardial tumor necrosis factor alpha (TNF-alpha) expression; TNF-alpha is a potent pro-inflammatory cytokine associated with hypertrophy and fibrosis in heart transplant recipients. METHODS: We randomized 10 consecutive heart transplant recipients to receive either 20 mg/day simvastatin (n = 5) or placebo (n = 5) for 6 months after cardiac transplantation. Routine surveillance endomyocardial biopsy specimens were obtained from all patients. We analyzed tissues for myocardial TNF-alpha content, total collagen content, and myocyte size using semiquantitative immunohistochemistry. RESULTS: Myocyte size and total collagen content of placebo and simvastatin groups did not show a statistically significant difference at any biopsy time point. Myocardium TNF-alpha content (% tissue area stained) at 1 week after transplantation was similar in the simvastatin and placebo groups. At the 24(th) week after transplantation, when compared with Week 1 values, we found a significant decrease in myocardium TNF-alpha content in the simvastatin group (15.0% +/- 2.3% vs 5.8% +/- 2.4%, p = 0.02) that was not observed in the placebo group (15.0% +/- 1.5% vs 12.0% +/- 2.6%, p = not significant). CONCLUSION: Simvastatin treatment in heart transplant recipients decreased myocardium TNF-alpha expression. This decrease did not translate into a difference in the markers of hypertrophy. However, decreased myocardial TNF-alpha may be a marker of a general statin-mediated decrease in inflammation in the transplanted heart that leads to improved graft and patient survival.

Aged↗
PubMed2000

Graves' disease and low-output cardiac dysfunction: implications for autoimmune disease in endomyocardial biopsy tissue from eleven patients.

Classic high-output thyrotoxic heart disease is generally considered a direct effect of thyroid hormone. In contrast, the cause of the less common low-output heart failure is generally unknown. The aim of this study was to retrospectively evaluate available endomyocardial biopsy tissue from patients with coexistent Graves' disease and idiopathic low-output heart failure and determine whether the biopsy features were consistent with an autoimmune process. The study group consisted of 11 patients whose mean age was 47 years when they were diagnosed with hyperthyroidism and 52 years when diagnosed with cardiac dysfunction. Right ventricular endomyocardial biopsy tissue revealed severe lymphocytic myocarditis in a patient with severe ophthalmopathy and showed borderline myocarditis in a patient without ophthalmopathy. Biopsy tissues from 6 other patients showed appreciable myocyte hypertrophy and interstitial fibrosis, consistent with dilated cardiomyopathy. Two patients had nondiagnostic biopsy specimens, and 1 patient had features suggestive of arrhythmogenic right ventricular dysplasia. In conclusion, for the 11 patients with Graves' disease and unexplained systolic dysfunction, only 2 (18%) had lymphocytic infiltrates consistent with an autoimmune process. Thus, among patients with Graves' disease, most cases of low-output cardiac dysfunction appear to be due to causes other than an active autoimmune inflammatory process.

Autoimmune Diseases↗
PubMed1991

[Early myocardial involvement in collagen diseases. An endomyocardial biopsy study].

Endomyocardial biopsy was performed in three patients affected by systemic connectivitis (one case of systemic lupus erythematosus--SLE--, one of scleroderma and one of dermatomyositis). The analysis of the specimens revealed the presence of fibrosis and microvascular lesions (these latter only in SLE). Immunofluorescence showed in SLE and scleroderma perivascular IgG or perisarcolemmal IgM deposits respectively. Despite the scarcity of cardiac signs and symptoms, cardiac involvement can be early and frequent in connectivitis. The immune pathogenesis of the cardiac lesions seems to be possible because of the presence of immunocomplexes in the myocardium.

Adolescent↗
PubMedDate not supplied

Magnetic resonance imaging of human orthotopic heart transplantation: correlation with endomyocardial biopsy.

The ability of magnetic resonance imaging (MRI) to detect allograft rejection was studied concomitantly in two centers. In 29 patients MR images performed on a 0.5 T imager were compared with pathologic findings obtained by transvenous right ventricular endomyocardial biopsies. Eight patients had grade 1 or 2 acute rejection, and their myocardium thickness was increased significantly compared with values obtained in normal volunteers, in normal heart allograft patients, and in patients during the resolving phase of an acute rejection episode, whereas no abnormal signal intensity was found in the myocardium of heart allograft patients with acute rejection. This finding is quite in opposition to what was found in experimental models. This could be the result of the immunosuppressive regimen of those patients including cyclosporine, whereas few experimental studies included cyclosporine treatment. For chronic rejection or fibrosis, MRI did not allow the diagnosis because the MRI appearance was close to normal. Finally, MRI appears as a complementary technique to B-mode ultrasound in detecting nonimmunologic complications such as pericardial effusions and endocavitary processes. These data suggest that MRI could be used in the future to monitor rejection, to guide the timing of endomyocardial biopsy, and to assess the response after immunosuppressive treatment.

Adolescent↗
PubMed2002

A possible role for complement in the pathogenesis of chronic chagasic cardiomyopathy.

The membrane attack complex (MAC) of complement participates in several inflammatory and proliferative processes by releasing pro-inflammatory cytokines and growth factors from target cells. Chronic Chagasic cardiomyopathy (CCH) is a parasitic dilated cardiopathy, characterized by severe fibrosis and inflammation, which differs from idiopathic dilated cardiomyopathy (DCM). Trypanosoma cruzi, the pathogenic organism of CCH, is a strong complement activator and can also induce alternative pathway activation by mammalian cells. This study explored whether the myocardium in CCH patients has increased MAC deposition, an expression of complement activation, compared to DCM patients. MAC was semi-quantified in endomyocardial human samples (29 CCH subjects, 18 DCM subjects, and four controls) by immunohistochemistry. MAC was present in the sarcolemma of 38% of CCH, 5.5% of DCM (p<0.02), and 0% of controls, and in interstitial inflammatory cells of CCH. No difference was observed in the expression of the complement regulatory protein CD59, indicating that increased MAC deposition is likely to be the result of complement activation rather than decreased protection. It is proposed that the increased MAC deposition found in CCH, but not in DCM or controls, may help to explain the diffuse myocardial fibrosis and inflammation characteristic of the disease.

Adult↗
PubMed1993

Dilated cardiomyopathy and myocarditis in Kenya: an endomyocardial biopsy study.

We have studied, by light and electron microscopy, left ventricular endomyocardial biopsy specimens from 18 African patients (14 men) with idiopathic dilated cardiomyopathy in Nairobi. Nine patients (50%) had evidence of healing myocarditis, that is the presence of a mild inflammatory cell infiltration within the myocardium. Interstitial fibrosis was prominent in five patients (28%) and in all 18 specimens there were hypertrophied muscle fibres. Therefore, half of the patients with idiopathic dilated cardiomyopathy had histological signs of a previous myocarditis. There was no serological evidence of a previous or recent coxsackie infection or any other common viral infections. It seems probable that the myocarditis was due to an inappropriate immunological reaction to myocardial muscle.

Adult↗
PubMed1996

Clinical and histopathological studies in children with supraventricular tachycardia.

To determine whether myocardial changes in patients with supraventricular tachycardia (SVT) are primary or secondary to persistent tachycardia, 11 patients with SVT were studied. These patients were divided into 2 groups with respect to the type of SVT. Group I consisted of 5 patients with incessant SVT and one with multifocal atrial tachycardia, while group II consisted of 4 patients with paroxysmal supraventricular tachycardia and one with short-run supraventricular premature contraction. All of the patients underwent electrophysiological study and endomyocardial biopsy from the right ventricle following routine cardiac catheterization. In group II, there were no significant abnormalities in the clinical and hemodynamic parameters. In group I, 3 patients had clinical features of dilated cardiomyopathy including abnormal ECG, chest X-ray and hypokinesis on left ventriculography. Induction and termination of SVT were possible in 2 patients in group I and in 4 of the 5 patients in group II. The only significant histologic difference between group I and group II was fibrosis. A high incidence of histopathological abnormalities, such as hypertrophy, degeneration, interstitial fibrosis and disarray was observed in both groups. The incidence of significant pathology was higher in group I than in group II. Almost all of the patients were given antiarrhythmic drugs. One patient underwent a successful surgical procedure and normal cardiac function returned after resection of the foci of the right atrium. Our present results suggest that patients with SVT who have incessant or recurrent SVT should undergo not only intracardiac electrophysiologic study but also endomyocardial biopsy for the evaluation of myocardial damage, since SVT might be the initial sign of cardiomyopathy.

Adolescent↗
PubMed2005

Mineralocorticoid receptor antagonism ameliorates left ventricular diastolic dysfunction and myocardial fibrosis in mildly symptomatic patients with idiopathic dilated cardiomyopathy: a pilot study.

BACKGROUND: Mineralocorticoid receptor antagonism reduces mortality associated with heart failure by mechanisms that remain unclear. The effects of the mineralocorticoid receptor antagonist spironolactone on left ventricular (LV) function and chamber stiffness associated with myocardial fibrosis were investigated in mildly symptomatic patients with idiopathic dilated cardiomyopathy (DCM). METHODS AND RESULTS: Twenty-five DCM patients with a New York Heart Association functional class of I or II were examined before and after treatment with spironolactone for 12 months. LV pressures and volumes were measured simultaneously, and LV endomyocardial biopsy specimens were obtained. Serum concentrations of the carboxyl-terminal propeptide (PIP) and carboxyl-terminal telopeptide (CITP) of collagen type I were measured. The patients were divided into 2 groups on the basis of the serum PIP/CITP ratio (< or =35, group A, n=12; >35, group B, n=13), an index of myocardial collagen accumulation. LV diastolic chamber stiffness, the collagen volume fraction, and abundance of collagen type I and III mRNAs in biopsy tissue were greater and the LV early diastolic strain rate (tissue Doppler echocardiography) was smaller in group B than in group A at baseline. These differences and the difference in PIP/CITP were greatly reduced after treatment of patients in group B with spironolactone, with treatment having no effect on these parameters in group A. The collagen volume fraction was significantly correlated with PIP/CITP, LV early diastolic strain rate, and LV diastolic chamber stiffness for all patients before and after treatment with spironolactone. CONCLUSIONS: Spironolactone ameliorated LV diastolic dysfunction and reduced chamber stiffness in association with regression of myocardial fibrosis in mildly symptomatic patients with DCM. These effects appeared limited, however, to patients with increased myocardial collagen accumulation.

Adult↗
PubMed1986

Leukocytic infiltrates in idiopathic dilated cardiomyopathy. A source of confusion with active myocarditis.

The histologic criteria for the endomyocardial biopsy diagnosis of idiopathic dilated cardiomyopathy (IDCM) and active idiopathic/viral myocarditis are unclear. The present study was undertaken to characterize the nature of the inflammatory cell infiltrates in IDCM and thereby refine the differential diagnostic criteria for distinguishing IDCM from myocarditis using endomyocardial biopsy. We examined a mean of 6.2 large random sections from excised hearts of all cardiac transplant recipients at Stanford University with a diagnosis of IDCM, from June 1968 through June 1984. The 108 cases were evaluated for inflammatory cell type, extent, and location. Thirteen percent had no infiltrate, 32.5% had 1-5 foci of at least five inflammatory cells, 47% had 6-30 foci, and 7.5% had 30 or more foci. The infiltrates were primarily lymphocytic; while they were usually in the myocardial parenchyma, infiltrates were also located in zones of fibrosis, the endocardium, the epicardium, and surrounding vessels. Pretransplant biopsies in 56 of the 108 cases were available for review, and 55% of these contained inflammatory cell infiltrates. Agreement between the presence of infiltrates in the biopsy and the resected heart was obtained in 64%. This study highlights the high incidence of inflammatory cell infiltrates in the hearts of patients with IDCM. It reinforces the need for interpreting lymphocytic infiltrates in an endomyocardial biopsy with caution, as their mere presence does not necessarily imply a diagnosis of active myocarditis.

Adolescent↗
PubMed1993

Myocarditis associated with doxorubicin cardiotoxicity.

In contrast to previous reports, the authors were impressed by the frequency of myocarditis in the endomyocardial biopsy specimens of patients treated with anthracyclines. To examine this, they reviewed the histologic and electron microscopic results and immunoperoxidase stains of myocardial biopsy specimens from 11 patients with doxorubicin cardiotoxicity grades 1.0-3.0. Immunoperoxidase stains for lymphocytes, macrophages, and endothelial cells and induced expression of Class II antigen were performed using the avidin-biotin complex procedure. A full panel of monoclonal antibodies was employed on fresh-frozen tissue; a smaller panel was used with formaldehyde-fixed paraffin-embedded material. Four of the 11 endomyocardial biopsy specimens showed myocarditis, and 2 showed borderline myocarditis by the Dallas criteria. The infiltrating lymphocytes were generally characterized as T lymphocytes and were associated with induced Class II antigen expression by arterial endothelial cells. In addition, foci of replacement fibrosis, suggesting a chronic process, were identified. Although this association does not prove a causal relationship, these results suggest that myocarditis can be a component of doxorubicin-induced myocardial injury.

Adult↗