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PubMed1991

Persistent atrial standstill--clinical, electrophysiological, and morphological study.

Persistent atrial standstill (PAS) is a rare disorder characterized by absence of atrial activity on the surface and intracavity electrograms, absence of atrial mechanical activity, and inability to electrically stimulate the atria. Four patients (ages 18-60 years) with PAS were evaluated. One of these (no. 3) only had right atrial (RA) standstill, whereas left atrium (LA) showed spontaneous activity and could be stimulated electrically. As RA biopsy is not possible, right ventricular (RV) endomyocardial biopsy (EMB) was obtained to identify possible atrial pathology that revealed inflammatory myocarditis, 2; amyloidosis, 1; and myocardial hypertrophy with fibrosis, 1. Three patients were given permanent pacemakers. One of these with amyloidosis died suddenly. One is lost to follow-up. The others cases are persisting with PAS.

Adolescent↗

PubMed2000

Lisinopril-mediated regression of myocardial fibrosis in patients with hypertensive heart disease.

BACKGROUND: In arterial hypertension, left ventricular hypertrophy (LVH) includes myocyte hypertrophy and fibrosis, which leads to LV diastolic dysfunction and, finally, heart failure. In spontaneously hypertensive rats, myocardial fibrosis was regressed and LV diastolic function was improved by treatment with the angiotensin-converting enzyme inhibitor lisinopril. Whether this holds true for patients with hypertensive heart disease was addressed in this prospective, randomized, double-blind trial. METHODS AND RESULTS: A total of 35 patients with primary hypertension, LVH, and LV diastolic dysfunction were treated with either lisinopril (n=18) or hydrochlorothiazide (HCTZ; n=17). At baseline and after 6 months, LV catheterization with endomyocardial biopsy, Doppler echocardiography with measurements of LV peak flow velocities during early filling and atrial contraction and isovolumic relaxation time, and 24-hour blood pressure monitoring were performed. Myocardial fibrosis was measured by LV collagen volume fraction and myocardial hydroxyproline concentration. With lisinopril, collagen volume fraction decreased from 6.9+/-0.6% to 6. 3+/-0.6% (P:<0.05 versus HCTZ) and myocardial hydroxyproline concentration from 9.9+/-0.3 to 8.3+/-0.4 microg/mg of LV dry weight (P:<0.00001 versus HCTZ); this was associated with an increase in the early filling and atrial contraction LV peak flow velocity ratio from 0.72+/-0.04 to 0.91+/-0.06 (P:<0.05 versus HCTZ) and a decrease in isovolumic relaxation time from 123+/-9 to 81+/-5 ms (P:<0.00002 versus HCTZ). Normalized blood pressure did not significantly change in either group. No LVH regression occurred in lisinopril-treated patients, whereas with HCTZ, myocyte diameter was reduced from 22. 1+/-0.6 to 20.7+/-0.7 microm (P:<0.01 versus lisinopril). CONCLUSIONS: In patients with hypertensive heart disease, angiotensin-converting enzyme inhibition with lisinopril can regress myocardial fibrosis, irrespective of LVH regression, and it is accompanied by improved LV diastolic function.

Adolescent↗

PubMed2003

Utility of cardiac magnetic resonance imaging for the diagnosis of heart transplant rejection.

OBJECTIVES: To assess the value of the use of cardiac MRI to detect rejection (necrosis) and its ability to discriminate it from other pathologic alterations (edema and fibrosis). MATERIALS AND METHODS: A prospective and consecutive study was designed in which cardiac MRI was performed at the same time as the scheduled endomyocardial biopsy. The study period was from 31-10-01 to 01-05-02. Ten patients with claustrophobia were excluded. Sixty-four examinations were performed in the remaining 40 patients. MRI assessment was blinded to the biopsy result. The 17 biopsies performed were insufficient (too small sample). Rejection was defined as the presence of at least 1 focus of myocyte necrosis. Technique. A high-field (1.5 T) GE CV/i magnetic resonance imaging system was used to obtain pre- and postcontrast white and black blood anatomic sequences (breathhold fast spin-echo T1-weighted images), as well as myocardial cine, perfusion and viability sequences. Variables analyzed. Ejection fraction, ventricular volumes, pericardial effusion, hypertrophy, absolute and relative myocardial intensity and uptake. Statistics. Variables were normally distributed. Student's t test was used for quantitative variables and the chi2 test for proportions. RESULTS: Mean age, 51+/-13 years. Women 5, men 35. Time since HT, 13 to 3725 days. No significant differences were found between rejection and ventricular volumes or the presence of effusion and hypertrophy. Visual estimation of myocardial perfusion and viability sequences did not detect any significant changes. Uptake showed a clear trend to increase in patients with necrosis: 34+/-21 versus 23+/-17 for relative uptake, P<.05. There were also differences in uptake when fibrosis was present: 68+/-47 versus 102+/-48 in the group without fibrosis, P <.05; but not in the presence of edema: 93+/-55 versus 94 +/- 45 for absolute uptake. CONCLUSIONS: (1) Cardiac MRI is a promising technique for diagnosis of rejection. (2) Patients with myocyte necrosis show a clear trend toward increased myocardial uptake. (3) Interstitial fibrosis is associated with decreased levels of uptake.

Biopsy↗

PubMed1985

Pharmacotoxic myocardial disease: an endomyocardial study.

Drug-induced toxic changes in the myocardium have become an increasing problem. The effect of drugs on heart morphology may be acute or cumulative. In general, adverse drug reactions manifest themselves as myocarditis (toxic or hypersensitivity), cardiomyopathy with chamber dilatation, or restrictive disease. Drugs affecting embryologic development of the heart will not be discussed. Drugs causing myocarditis can be divided into: toxic myocarditis, e.g., cyclophosphamide. The morphologic changes are dose-related and have lesions of different ages, which include myocyte necrosis with hemorrhage and vasculitis. Fibrous endocarditis, e.g., methysergide. These reactions include thickening of the endocardium and sometimes the cardiac valves with fibrosis. Drugs causing hypersensitivity myocarditis, e.g., thiazide diuretics. In this case, the lesions are not dose-related, are the same age, and there is an eosinophilic infiltrate. Drugs causing cardiomyopathic-like changes of ventricular dilatation and failure, e.g., anthracyclines, particularly adriamycin. This group of drugs cause a gradual myofibrillar loss within cardiac myocytes and a sarcotubular dilatation which is characteristic. The damaged cells are replaced by fibrosis and ventricular failure ensues. With the rapid synthesis of new drugs, the problem of drug cardiotoxicity may be an ever-increasing problem. With the more widespread use of the endomyocardial biopsy, drug-induced heart disease can be documented and the effects of different methods of drug delivery and pharmacologic antagonists studied.

Antibiotics, Antineoplastic↗

PubMed1985

Current problems in establishing quantitative histopathologic criteria for the diagnosis of lymphocytic myocarditis by endomyocardial biopsy.

Both the clinical and the biopsy diagnoses of myocarditis are prone to false-positive and false-negative interpretations. False-positive clinical diagnoses probably most commonly result from a failure to recognize other disorders, such as cardiomyopathy and myocardial infarction, that may mimic myocarditis. False-negative clinical diagnoses may occur in patients with myocarditis in whom the signs and symptoms are atypical, absent, or misinterpreted. The two most common errors made by pathologists that produce false-positive tissue diagnoses appear to be a failure to recognize the number of lymphocytes that occupy the normal myocardial interstitium and a misinterpretation of noninflammatory interstitial cells as lymphocytes. Sampling error may be the most usual cause of false-negative tissue diagnoses. Since myocarditis is characterized by leukocytic and reparative responses, the most important features to evaluate in endomyocardial biopsy tissues are the type, distribution, and extent of the inflammatory infiltrate and the presence and extent of interstitial and endocardial fibrosis. Although no single histopathologic criterion is both sensitive and specific for myocarditis, it appears that quantitative evidence of an interstitial leukocytic infiltrate is currently the best available hallmark for myocarditis in biopsy specimens. It is suggested that a mean lymphocyte count greater than 5.0/high-power (X 400) microscopic field be considered indicative of lymphocytic myocarditis and that a mean count less than this be interpreted as myocarditis only if discrete clusters of lymphocytes are identified, since differentiation of low-grade diffuse infiltrates from expected normal lymphocytic populations is problematic at levels less than 5.0.

Biopsy↗

PubMed1994

[Heart function in chronic pressure overload caused by aortic stenosis: the role of collagen tissue].

The purpose of this study was to evaluate left ventricular (LV) structure-function interplay in aortic stenosis. LV structure was assessed from endomyocardial biopsies obtained in 27 patients with aortic stenosis. Total collagen volume fraction, orthogonal collagen fiber meshwork (cross-hatching) and endocardial fibrosis were determined by morphologic-morphometric evaluation. Control biopsy data were obtained from 6 pre-transplantation donor hearts whereas other 11 patients with normal cardiac function served as hemodynamic controls. LV biplane cineangiography and high-fidelity LV pressure measurement were carried out in all patients. Systolic function was assessed by LV biplane ejection fraction, diastolic function by time constant of relaxation, peak filling rates and passive elastic properties. Total collagen volume fraction (7.3 versus 1.6%, p < 0.01) as well as the degree of cross-hatching (1.7 versus 0.8 grade, p < 0.01) were significantly increased in patients with aortic stenosis with respect to controls. Endocardial fibrosis was present in 11/27 patients with aortic stenosis and in no patients of control group. In aortic stenosis in presence of increased total collagen volume fraction there were no changes in systolic and diastolic function, whereas in presence of changes in collagen architecture ejection fraction was depressed and passive elastic properties increased. In conclusion, in aortic stenosis, changes in collagen architecture are associated with altered systolic function and passive diastolic properties. The sole increase in total collagen volume fraction without a change in architecture leaves systolic and passive diastolic function unaltered. A prolongation of relaxation was present in aortic stenosis and appears to be mediated by muscle hypertrophy per se.

Aged↗

PubMed2000

Serum carboxy-terminal propeptide of procollagen type I is a marker of myocardial fibrosis in hypertensive heart disease.

BACKGROUND: This study was designed to investigate whether the serum concentration of the carboxy-terminal propeptide of procollagen type I (PIP), a marker of collagen type I synthesis, is related to myocardial fibrosis in hypertensive patients. METHODS AND RESULTS: The study was performed in 26 patients with essential hypertension in which ischemic cardiomyopathy was excluded after a complete medical workup. Right septal endomyocardial biopsies were performed in hypertensive patients to quantify collagen content. Collagen volume fraction (CVF) was determined on picrosirius red-stained sections with an automated image analysis system. The serum concentration of PIP was measured by specific radioimmunoassay. Compared with normotensives, both serum PIP and CVF were increased (P<0.001) in hypertensives. A direct correlation was found between CVF and serum PIP (r=0.471, P<0.02) in all hypertensives. Histological analysis revealed the presence of 2 subgroups of patients: 8 with severe fibrosis and 18 with nonsevere fibrosis. Serum PIP was higher (P<0.05) in patients with severe fibrosis than in patients with nonsevere fibrosis. Using receiver operating characteristic curves, we observed that a cutoff of 127 microg/L for PIP provided 78% specificity and 75% sensitivity for predicting severe fibrosis with a relative risk of 4.80 (95% CI, 1.19 to 19.30). CONCLUSIONS: These results show a strong correlation between myocardial collagen content and the serum concentration of PIP in essential hypertension. Although preliminary, these findings suggest that the determination of PIP may be an easy and reliable method for the screening and diagnosis of severe myocardial fibrosis associated with arterial hypertension.

Adult↗

PubMed2003

Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy.

The purpose of the study was to investigate interactions between myocardial nitric oxide synthase (NOS) and myocardial fibrosis, both of which determine left ventricular (LV) preload reserve in patients with nonischemic dilated cardiomyopathy (DCM). In previous animal experiments, chronic inhibition of NOS induced myocardial fibrosis and limited LV preload reserve. Twenty-eight DCM patients underwent LV catheterization, balloon caval occlusions (BCO; n = 8), intracoronary substance P infusion (n = 8), and procurement of LV endomyocardial biopsies for determinations of collagen volume fraction (CVF), of gene expression of NOS2, NOS3, heme oxygenase (HO)-1, and TNF-alpha, and of NOS2 protein. CVF was unrelated to the intensity of NOS2, NOS3, HO-1, or TNF-alpha gene expression or of NOS2 protein expression. Preload recruitable LV stroke work (PR-LVSW) correlated directly with NOS2 gene expression (P = 0.001) and inversely with CVF (P = 0.04). High CVF (>10%) reduced baseline LVSW and PR-LVSW at each level of NOS2 gene expression. In DCM, myocardial fibrosis is unrelated to the intensity of myocardial gene expression of NOS, antioxidative enzymes (HO-1), or cytokines (TNF-alpha) and blunts NOS2-related recruitment of LV preload reserve.

Adult↗

PubMed2005

Lymphocytic myocarditis after lung transplantation.

This study reports the development of lymphocytic myocarditis in a bilateral lung allograft recipient. A 23-year-old woman developed congestive heart failure and severe left ventricular dysfunction 32 months after a bilateral lung allograft for cystic fibrosis. She had taken oral acyclovir for infectious mononucleosis that was diagnosed 11 months previously. Her viral load for Epstein-Barr virus (EBV) increased, and an echocardiogram revealed a left ventricular ejection fraction of 25% and endomyocardial biopsy revealed lymphocytic myocarditis. She received valacyclovir (1 g x 3 times daily) and made a full recovery 6 months later.

Acyclovir↗

PubMed1990

In vivo quantitative ultrasonic evaluation of myocardial fibrosis in humans.

The aim of this study was to assess in vivo whether the regional ultrasonic reflectivity, evaluated by a real-time integrated backscatter analysis, was related to the local content of connective tissue in human myocardium as estimated by quantitative histology of endomyocardial biopsies. Sixteen patients with presumptive diagnosis of cardiomyopathy were ultrasonically studied by means of an M-mode-based echocardiographic system with quantitative integrated backscatter analysis capabilities. A 2.25-MHz transducer was used. The integrated value of the rectified radiofrequency signal of the interventricular septum was taken as integrated backscatter index and expressed in percent normalized for the pericardial interface (assumed to be 100%). All patients also underwent multiple left ventricular endomyocardial biopsies, which were stained with Masson's trichrome and studied with the use of a computer-assisted image analysis system. The percent integrated backscatter index was significantly higher in the presence of connective tissue area greater than 20% (eight patients) versus less than 20% (eight patients): 51 +/- 25% versus 26 +/- 11%, p less than 0.05. A significant correlation (p less than 0.05, R = 0.55) was found between percent integrated backscatter index and percent connective tissue area. In vivo on-line quantitative ultrasound analysis is feasible in man and reliably identifies variations in the regional extent of fibrosis in human myocardium.

Adolescent↗

PubMed2006

Frontiers in viral diagnostics.

Dilated cardiomyopathy (DCM) is a fatal myocardial disease with an incidence of 40:100,000. In recent years, viral infection as a causative agent for myocarditis followed by DCM has become a main topic of research. On the one hand, the virus violates the myocardial integrity itself; on the other hand, the virus induces inadequate local humoral and cellular defense reaction resulting in cardiomyocyte death, fibrosis, and overall cardiac dysfunction. Classical virological approaches are no longer sufficient to detect and identify the virus in the heart. The possibility of endomyocardial biopsies, as well as the further development of new high-specific and sensitive molecular approaches including real-time PCR or sequencing, allows us to detect and to identify the patient- specific causal virus and to predict the progression of disease and hopefully, in the future, to develop virus-specific treatment strategies.

Cardiomyopathy, Dilated↗

PubMed1987

The surgical pathology of hypertrophic cardiomyopathy.

The pathologic diagnosis of hypertrophic cardiomyopathy (HCM) rests on the gross cardiac morphology and the presence and extent of myofiber disarray in the interventricular septum. Little attention, however, has been focused on the features of HCM in endomyocardial biopsy or septal myomectomy specimens. We therefore examined nine right ventricular biopsy specimens and 89 myomectomy specimens from 98 patients with clinically diagnosed HCM. Myofiber disarray was present in three (33%) of the biopsy specimens and 52 (58%) of the septectomy specimens. Associated findings in both specimen types included myocyte hypertrophy and interstitial fibrosis. The myomectomy specimens also frequently contained areas of patchy fibrosis, abnormally thick coronary arteries, and a fibrous endocardial plaque. When myofiber disarray was present in myomectomy specimens, it was confined to the deepest portion in 79% of the specimens, confirming that the disarray is frequently confined to the middle transverse third of the septum. Endomyocardial biopsy specimens may be used to suggest the diagnosis of HCM; however, because of their small size and their relatively nonspecific pathologic changes, they are of limited value in making the diagnosis of HCM. Septal myomectomy specimens usually contain pathologic findings consistent with HCM. The role of the surgical pathologist in the myomectomy cases is to confirm that these changes are present and are characteristic of the disorder.

Adult↗

PubMed2006

Management strategies in pericardial emergencies.

BACKGROUND: The most frequent pericardial emergency is cardiac tamponade, but complications of an acute coronary syndrome and aortic dissection may also involve the pericardium. Acute pericarditis can also represent a medical emergency due to chest pain of upsetting intensity. Decompensations in chronic advanced constriction and in the clinical course of purulent pericarditis necessitate critical care as well. DIAGNOSIS AND MANAGEMENT: The diagnosis of cardiac tamponade is based on clinical presentation and physical findings, confirmed by echocardiography and cardiac catheterization. Tamponade is an absolute indication for urgent drainage, either by pericardiocentesis or surgical pericardiotomy. The approach for pericardiocentesis can be subxiphoid or intercostal using echocardiographic or fluoroscopic guidance. Urgent drainage, combined with intravenous antibiotics, is also mandatory in suspected purulent pericarditis. If confirmed, it should be combined with intrapericardial rinsing (best by a surgical drainage). Pericardiocentesis is contraindicated in cardiac tamponade complicating aortic dissection. This condition should immediately lead to cardiac surgery. Although pericardiectomy is the only treatment for permanent constriction, this procedure is contraindicated when extensive myocardial fibrosis and/or atrophy are demonstrated. CASE STUDY: Iatrogenic tamponade may occur during percutaneous mitral valvuloplasty, implantation of pacemakers, electrophysiology and radiofrequency ablation procedures, right ventricular endomyocardial biopsy, percutaneous coronary interventions, and rarely during Swan-Ganz catheterization. The authors report on a 79-year-old who suffered coronary perforation and cardiac tamponade during elective stent implantation. Tamponade was successfully treated with pericardiocentesis and implantation of a membrane-covered graft stent. Subsequent recurrent pericarditis/postpericardial injury syndrome with moderate pericardial effusion was initially treated with aspirin and then with aspirin and colchicine. At 6 months, the patient is in stable remission even after withdrawal of colchicine. CONCLUSION: Natural history of pericardial diseases can be complicated with pericardial emergencies requiring prompt diagnosis, intensive care with hemodynamic monitoring, and early aggressive management. Medical supportive measures, drainage of pericardial effusion, surgical pericardiotomy, and pericardiectomy should be applied when needed with no delay. This procedural approach also applies to iatrogenic interventions leading to tamponade.

Aged↗

PubMed1995

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

To investigate myocardial manifestations in progressive systemic sclerosis, we studied three patients with transthoracic echocardiography, cardiac catheterization with coronary angiography, thallium scans with dipyridamol completed by thoracic cold exposure and endomyocardial biopsy with immunohistology. Two patients were symptomatic. In the three cases, abnormalities of myocardial perfusion were detected without coronary stenosis. Two patients had myocardial fibrosis with a coronary spasm in one case. The immunohistological study always showed an unusual expression of HLA class II antigen on cardiac fibroblasts.

Aged↗

PubMed1993

Case report: left ventricular apical hypertrophy in progressive limb-girdle muscular dystrophy.

Cardiac involvement is uncommon in patients with limb-girdle muscular dystrophy. This report describes a patient in whom concentric hypertrophy localized to the apical left ventricle was revealed during a long clinical course of skeletal muscular dystrophy, with evolving electrocardiographic changes also compatible with apical hypertrophic cardiomyopathy. Endomyocardial biopsy revealed similar histologic changes in the skeletal muscle biopsy specimen, characterized by muscle fiber atrophy and hypertrophy with a mild degree of interstitial fibrosis. The pathogenesis of cardiac hypertrophy in this case is unclear. However, the pathologic findings suggest that the myocardium may be involved in the same dystrophic process as the skeletal muscles.

Cardiomyopathy, Hypertrophic↗

PubMed1989

Endomyocardial biopsy pathology in insulin-dependent diabetic patients with abnormal ventricular function.

We have previously shown impaired ventricular function in asymptomatic middle-aged type 1 (insulin-dependent) diabetic patients who had no evidence of coronary artery disease. The diabetic patients had normal coronary angiograms but reduced ventricular ejection fraction on exercise. To examine the possible contribution of small vessel disease to this functional abnormality, we compared endomyocardial biopsies from seven symptom-free type 1 diabetic patients with biopsies from seven age- and sex-matched non-diabetic subjects. Interstitial fibrosis was present in three diabetic patients, arteriolar hyalinization in three patients and arteriolar thickening was observed in five patients. Morphometry performed on electron micrographs showed no significant difference in the thickness of the capillary basal lamina between diabetics and controls. While the functional significance of the abnormalities on light microscopy is unclear, our findings indicate that the abnormality of cardiac function described in diabetes is not associated with thickening of the myocardial capillary basal lamina.

Adult↗

PubMed2001

Healing of acute myocarditis with left ventricular assist device: morphological recovery and evolution to the aspecific features of dilated cardiomyopathy.

Dilated cardiomyopathy may result from an acute myocarditis. Little is reported in vivo documenting the progression from the acute inflammatory disease to the healing phase. We describe the consecutive light and electron microscopy studies performed on five myocardial sample series in a 47-year-old female patient who was referred to our hospital with acute myocarditis. She was sustained with left ventricular assist device (LVAD) for 63 days, and then she died of cerebral hemorrhage. The first three consecutive endomyocardial biopsies (days 2, 4, 36 from onset) documented the acute and early healing phase of the inflammatory disease. In the last two biopsies (days 50 and 64 from onset) active inflammation and myocyte necrosis were absent. The histopathological features were those commonly observed in most patients diagnosed with dilated cardiomyopathy, namely myocyte hypertrophy, nuclear size and shape irregularities, and interstitial fibrosis. Overall, the myocyte morphology significantly improved and LVAD support likely contributed to the structural recovery. The major conclusions to be drawn from this case are: 1) the aspecific pathologic findings of dilated cardiomyopathy patients may result from an acute myocardial inflammation; 2) immediate endomyocardial biopsy in patients with clinically diagnosed myocarditis minimizes the risk of missing the diagnosis of inflammatory disease; to this aim a precise definition of "early onset" is especially needed; 3) LVAD support may contribute to the morphological recovery of severely damaged myocytes.

Biopsy↗

PubMed1985

[Right intraventricular biopsy. Indications and results. 116 cases].

The indications for endomyocardial biopsy were evaluated from 116 consecutive cases. The diagnostic value of this invasive but well tolerated procedure was in agreement with data from the literature. An accurate diagnosis, unforseeable in 8% of the patients, was established in 12%. The diagnosis of apparently primary myocardiopathy with ventricular dilatation was confirmed in 45 out of 59 cases; there were 3 cases of myocarditis, 3 cases of restrictive cardiopathy (haemochromatosis, fibroplastic endocarditis) and 1 case of hypertrophic cardiopathy. No tissue abnormality was noted in 6 cases. An accurate diagnosis was obtained by biopsy in 1 case of "eosinophilic lung" without overt cardiac involvement. In malignant diseases treated with anthracyclines in doses reaching maximal theoretical total dosage (30 patients), severe tissue lesions were present in 10% of the cases, incipient haemochromatosis in 16.6% and subendocardial fibrosis in 3.3%. However, total doses of up to 600 mg/m2 could be administered to 90% of the patients. Myocardial lesions could be demonstrated in 1 of 2 patients with collagen disease. Endomyocardial biopsy therefore seems to be justified in myocardiopathies with ventricular dilatation, in some collagen diseases with a tendency to cardiac involvement and to monitor treatment with anthracyclines in total doses higher than the theoretical maximum dosage.

Adolescent↗