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PubMed2001

Endomyocardial biopsy findings in 50 patients with idiopathic atrioventricular block: presence of myocarditis.

In patients with primary atrioventricular (AV) conduction disturbances, lesions are commonly believed to be limited to the conduction system. In the present study, myocardial lesions were analyzed histologically in patients with AV conduction disturbances to determine the presence of myocarditis. We studied 50 patients with second or third degree AV block in whom the cause was not clear (AVB group). Endomyocardial biopsy was performed from the right ventricle and examined by light microscopy. Tissue specimens also were obtained from 12 normal hearts at autopsy as a control group (N group). The diagnosis of myocarditis was based on the Dallas criteria. The myocyte transverse diameter was 15.4+/-4.1 microm in the AVB group and 11.7+/-3.1 microm in the N group (P<0.01). The fibrosis area ratio also was significantly higher in the AVB group than in the N group (10.1+/-6.7% vs 5.1+/-2.0%). The mean number of lymphocytes per 400-fold magnified field was significantly greater in the AVB group than in the N group (1.9+/-1.6 vs 1.3+/-0.4). In addition, disorganization of the cardiac myocytes was noted in 8 patients in the AVB group (16%), myocyte disarrangement in 39 patients (78%), myocytolysis in 23 patients (46%), and nuclear deformity in 21 patients (42%). Myocarditis was diagnosed in 3 of the 50 patients (6%). The present study demonstrates that myocardial lesions can be detected in a large proportion of patients with AV conduction disturbances. Furthermore, myocarditis is present in 6% of the cases.

Adolescent↗

PubMed1996

Cardiac sarcoidosis: diagnostic, prognostic, and therapeutic considerations.

Cardiac involvement in patients with sarcoidosis is an important consideration for those who are concerned with this strange disease. Sarcoidosis is not an acute malignant disease but may be noticed at the time of sudden, expected death as fatal myocardial sarcoidosis at autopsy. Even with modern advances in our ability to diagnose heart disease, cardiac sarcoidosis is still often overlooked because of its subclinical disease progression. In view of this, an extensive review of previously published literature and of our own case analyses has been carried out because of the authors' long-term experience with performing Konno's endomyocardial biopsy, which was originally developed in 1962 at the author's institution. However, the sensitivity of endomyocardial biopsy in detecting sarcoid granuloma is low (20-30%), and, instead, various kinds of nongranulomatous pathologies are often seen. During the course of our research it was found that there might exist a racial difference in cardiac sarcoidosis. Cardiac death was much more frequent in Japanese patients. The possibility that heart disease in sarcoidosis is caused by cor pulmonale due to advanced pulmonary fibrosis should be reevaluated because only a limited amount of background data is available. The author's review clarified the fact that cardiac sarcoidosis is caused by myocardial or pericardial involvement, resulting in various kinds of bradyarrhythmias or tachyarrhythmias and/or congestive heart failure. Electrocardiographic (ECG) and Holter monitor readings provide a simple and effective method for early detection of this disease. The incidence of ECG abnormalities in a total of 963 sarcoidosis patients was 22.1%, which was more frequent than that of the sex- and age-matched healthy control subjects (17.9%; p < 0.025). Echocardiography and radionuclide studies also provide useful clinical information. Careful follow-up and early corticosteroid administration followed by small maintenance doses may prevent the progression of the disease and improve prognosis. Owing to the progress in antiarrhythmic drugs and pacemaker implantation, the primary cause of death in cardiac sarcoidosis has changed from sudden death (1976 report) to congestive heart failure (1985 report).

Adrenal Cortex Hormones↗

PubMed1997

Increased accumulation of acidic fibroblast growth factor in left ventricular myocytes of patients with idiopathic cardiomyopathy.

To clarify the pathophysiologic role of fibroblast growth factors in idiopathic cardiomyopathy, we evaluated endomyocardial biopsy specimens obtained from 24 patients (nine with hypertrophic cardiomyopathy [HCM], 12 with dilated cardiomyopathy [DCM], and three with hypertensive hypertrophy) and six controls. All the specimens were stained for acidic fibroblast growth factor (aFGF) and basic FGF (bFGF) with immunohistochemistry. In situ hybridization was carried out for detection of aFGF mRNA. The average diameter of the myocytes, the percent area of interstitial fibrosis, and capillary vessel density were assessed in each biopsy specimen with morphometric methods. Positive staining of aFGF was observed in the myocytes of the biopsy specimens taken from 15 of 21 (71%) patients with cardiomyopathy (six of nine HCM, nine of 12 DCM) and all hypertensive hypertrophy patients but in none of the controls (p < 0.01). The average diameter of the myocytes was significantly larger in the patients with positive aFGF staining than in those with negative staining (23.1 +/- 1.5 versus 18.3 +/- 1.2 microm, p < 0.05). The percent area of fibrosis and the density of capillaries did not differ between the two groups. Intense expression of aFGF mRNA was observed in the myocytes from the patients with positive aFGF protein. In conclusion, the expression of FGF was significantly increased in myocytes obtained from the left ventricle of patients with cardiomyopathy. Acidic FGF may contribute to the hypertrophy of myocytes as the repair response to myocardial injury in patients with idiopathic cardiomyopathy.

Adult↗

PubMed1997

Myocardial osteopontin expression is associated with left ventricular hypertrophy.

BACKGROUND: Osteopontin (OP) has been identified in cultured rat cardiac fibroblasts, where it contributes to angiotensin II (AII)-induced remodeling processes; in cultured cardiomyocytes; and in macrophages in cardiac tissues with inflammation. However, the presence of OP has not been reported in histological sections of myocardial tissue. In the present study, we investigated (1) the regulation of OP mRNA expression in cultured rat cardiomyocytes; (2) the localization of OP mRNA in neonatal and adult normal and hypertrophied rat hearts; and (3) the histology of OP expression in myocardial specimens from humans either with myocyte hypertrophy or with no pathological changes. METHODS AND RESULTS: Cultured neonatal cardiomyocytes expressed OP mRNA and were immunoreactive for OP. Endothelin-1 (ET-1) and norepinephrine (NE) increased both OP and atrial natriuretic peptide (ANP) mRNA levels twofold to threefold (P<.01). OP mRNA was prominent in ventricular tissue from neonatal and adult rats with renovascular hypertension and aortic banding, whereas barely detectable levels were observed in normal adult cardiac tissue. ANP and OP mRNA levels in normal and hypertrophied ventricles correlated (r2=.87, P<.001). OP immunoreactivity and mRNA transcripts were predominantly found in cardiomyocytes not associated with inflammatory cells in sections from neonatal and adult hypertrophied hearts. No staining was detectable in normal adult hearts. Human myocardium with extensive fibrosis and cardiomyocyte hypertrophy obtained from explanted hearts with either idiopathic (n=5) or ischemic cardiomyopathy (n=7) demonstrated substantial myocyte immunoreactivity for both OP and ANP in right and left ventricles that was not associated with leukocyte infiltration. In situ hybridization identified cardiomyocytes as the major source of OP mRNA transcripts in these hearts. In contrast, OP immunoreactivity was not detectable in four of five endomyocardial biopsies with normal histology. CONCLUSIONS: The present study provides the first evidence that cardiomyocytes are a prominent source of OP in vivo and suggests that induction of OP expression is strongly associated with ventricular hypertrophy.

Animals↗

PubMed1999

Dilated cardiomyopathy is associated with significant changes in collagen type I/III ratio.

BACKGROUND: It is controversial whether myocardial fibrosis in end-stage dilated cardiomyopathy (DCM) is associated with altered collagen type I/type III (Col I/Col III) ratio. METHODS AND RESULTS: Patients with DCM (ejection fraction [EF] <50%, n=12) and with mild global left ventricular dysfunction (EF >50%, n=18) were examined. Col I, Col III, and transforming growth factors-beta1 (TGF-beta1) and -beta2 (TGF-beta2) gene expression in endomyocardial biopsies was evaluated by quantitative competitive reverse transcriptase-polymerase chain reaction (qRT-PCR). Collagen content was quantified after picrosirius red and immunohistological staining and by hydroxyproline assay. In patients with EF <50%, there was a pronounced 2- to 6-fold increase of myocardial Col I mRNA abundance (P<0.01), with a corresponding 1.6-fold increase at the protein level versus that found in patients with EF >50%. The Col III mRNA abundance showed a 2.0-fold increase (P<0.04). There was a relevant shift in the Col I/Col III mRNA ratio for DCM patients (Col I/Col III, 8.2) compared with patients with an EF >50% (Col I/Col III, 6. 4). In addition, total collagen content was increased in patients with EF <50% (n=3) (4.3+/-0.1%) compared with patients with EF >50% (n=8) (2.7+/-0.9%) (P<0.004). The biochemically determined ratio of hydroxyproline/total protein (n=12) was correlated to the Col I mRNA abundance (P<0.05, r=0.77). TGF-beta1 and TGF-beta2 showed elevated myocardial mRNA abundances (1- to 7-fold and 4- to 5-fold, respectively) in DCM patients. CONCLUSIONS: Differential increase of Col I and Col III leads to an increased Col I/Col III ratio in DCM myocardium. Because Col I provides substantial tensile strength and stiffness, this may contribute to systolic and in particular diastolic dysfunction in DCM.

Biopsy↗

PubMed1992

Morphometric investigation of intramyocardial arterioles in right septal endomyocardial biopsy of patients with arterial hypertension and left ventricular hypertrophy.

A reduced maximal coronary vasodilatator capacity is reported in patients with hypertensive heart disease, suggesting structural abnormalities of intramyocardial arterioles. Right septal endomyocardial catheter biopsies (EMCB) of 30 patients with arterial hypertension and of 10 heart donors were investigated morphometrically. In hypertension, the mean external diameter (21.9 +/- 3.0 vs. 17.4 +/- 2.9 microns, p less than or equal to 0.01) of arterioles and the mean arterial wall area (284 +/- 80 vs. 167 +/- 69 microns2, p less than or equal to 0.05) were increased as compared with heart donors. Perivascular fibrosis was markedly increased (260 +/- 183 vs. 41 +/- 30 microns2, p less than or equal to 0.05) as well as volume density of fibrosis (3.0 +/- 1.7 vs. 0.9 +/- 0.8 Vv%, p less than or equal to 0.01) in hypertensive heart disease. There was no significant correlation between echocardiographically determined left ventricular mass index (115 +/- 25 g/m2 for men and 104 +/- 12 g/m2 for women) and mean arteriolar wall area (r = +0.17) or volume density of fibrosis (r = +0.2) in hypertensive heart disease. Our investigations show that in patients with arterial hypertension there is a thickening of intramyocardial arteriolar walls and an increase in fibrosis. Intramyocardial vascular alterations seem to manifest in hypertension independent from left ventricular hypertrophy.

Aged↗

PubMed2006

Myocarditis and inflammatory cardiomyopathy: histomorphological diagnosis.

Myocarditis is a non-ischemic inflammatory disease of the myocardium associated with cardiac dysfunction. It most often results from infectious agents, hypersensitivity responses, or immune-related injury. In spite of the development of various diagnostic modalities, early and definite diagnosis of myocarditis still depends on the detection of inflammatory infiltrates in endomyocardial biopsy specimens according to Dallas criteria. Routine application of immunohistochemistry (for characterization of inflammatory cell infiltration) and Polymerase Chain Reaction PCR analysis (for identification of infective agents) has become an essential part of the diagnostic armamentarium for a more precise biopsy report. A new morphological classification is advanced to overcome the limits of Dallas criteria. A semiquantitative assessment of myocyte damage/inflammation (grading) as well as of fibrosis (staging) is indicated, thus providing histopathological diagnosis useful to the clinician for more appropriate patient risk stratification and for the application of new therapies. Consequently, the final diagnosis of myocarditis should be mainly based on three features: etiology, grade, and stage of the disease.

Cardiomyopathies↗

PubMed1999

Is apoptosis a mechanism of cell death of cardiomyocytes in chronic chagasic myocarditis?

The micropathology of chronic Chagas' myocarditis reveals foci of myocardial cell loss associated with an inflammatory infiltrate composed predominantly of lymphomononuclear cells and interstitial fibrosis. The loss of myocardial cells, a devastating phenomenon in this cardiopathy, has been classically attributed to necrosis. In the present study we examined whether the loss of myocardial cells in human chronic Chagas' heart disease could result from cell death by apoptosis. A total of 11 cases of chronic chagasic myocarditis were studied: four hearts were obtained at autopsy within 8 h after death and seven endomyocardial biopsies were taken from chagasic patients with an arrhythmogenic form of the disease. The coronary arteries of all chagasic cases showed no obstructive lesions. The diagnosis of Chagas' disease was based on previously established criteria. Five cases were selected as controls: three hearts were obtained at autopsy within 8 h after death and two endomyocardial biopsies were taken from nonchagasic patients with normal myocardium morphology. As positive controls we used cardiac muscles of myocardial infarction and rat mammary glands on the fourth day after weaning. The TUNEL method was used to identify apoptotic cells in the myocardium. The expression of p53 protein, which directly or indirectly triggers apoptosis, was evaluated using immunohistochemical technique. A few apoptotic cells were stained in chronic chagasic hearts, both biopsy and autopsy cases. However, the stained nuclei were restricted to the mononuclear infiltrate accounting for about 0.5% of the mononuclear cells in the infiltrate. In contrast, the nuclei of cardiomyocytes in both regions bordering on and distant from the microfoci of myocardial cell loss were not stained by the TUNEL method. Moreover, the expression of the protein p53 in cardiomyocytes in chagasic hearts was absent. The results of the present study demonstrating negative in situ labeling of fragmented DNA associated with absence of expression of p53 provide support to the hypothesis that apoptosis is not the mechanism of cell death in chronic chagasic myocarditis. This reinforces the general opinion that the loss of cardiac muscle fibers in chagasic cardiopathy is produced by necrosis. On the other hand, the present results give support to the concept that apoptosis probably play a role in the clearing of lymphomononuclear cells in the inflammatory infiltrate in chronic chagasic myocarditis.

Adult↗

PubMed1985

[Echocardiographic and endomyocardial biopsy findings of right-sided hypertrophic obstructive cardiomyopathy].

Echocardiographic and histological studies were performed for four patients with hypertrophic cardiomyopathy (HCM) with right-sided obstruction (group A) and for five HCM patients without right-sided obstruction (group B). The clinical diagnosis of HCM was established by cardiac catheterization and right and left ventriculography for all nine patients, and confirmed by necropsy in one patient in group A. M-mode and cross-sectional echocardiography were performed in all. Endomyocardial biopsy of the right ventricular septum was performed for all four patients in group A and for three patients in group B. M-mode echocardiography demonstrated no characteristic features suggesting right intraventricular obstruction, but cross-sectional echocardiograms, especially with short-axis views, reliably indicated conspicuous rightward septal protrusions in right-sided obstructive HCM. Histological changes in the right ventricular septum consisting of fibrosis of the interstitium and disarray of myocardial fibers were more striking in patients with HCM with right-sided obstruction than those without such obstruction.

Adult↗

PubMed1999

[Chagasic myocardiopathy: historical perspective].

Considerable advances in the clinical pathological and pathogenic aspects of Chagas disease have been made since the Brazilian physician Carlos Chagas described the disease in 1909. The disease caused by the flagellate protozoon parasite Trypanosoma cruzi is transmitted to humans by a blood sucking triatomine and much less frequently by blood transfusion. It is estimated that 18 million are infected and that about 100 million people from Latin America are at risk of contracting T. cruzi infection. One of the most important contributions to the knowledge of Chagas' disease has been the recognition of the natural history of the disease, which can be divided into three well defined periods: 1. The acute stage; 2. An undetermined or undifferentiated stage and 3. The chronic stage. The primary infection (first stage) occurs mostly unrecognized and clinically apparent acute chagasic myocarditis may appear in less than 5% of the infected individuals, usually children living in endemic areas. The majority of the cases of acute myocarditis are mild and reversible. Autopsied cases of acute chagasic myocarditis are uncommon and correspond to exceptionally severe or fulminant forms showing diffuse myocardial damage with myocytolisis, degenerative changes of myocardial fibers and marked intersticial cellular infiltration. The acute clinical manifestations of the infected individuals include fever, muscular pain, sweating, swollen lymph nodes, hepatospienomegaly. Following this initial stage, all patients enter the undifferentiated or undetermined stage of the chronic period (second stage), which lasts between 10 to 20 years. Of these, 20 to 30% (depending on marked geographical differences) develop symptoms or signs of visceral damage conforming the cohort that enter the third stage. Although megaesophagous and megacolon are not uncommon (mainly in Brazil), the most frequent and important clinical manifestation is a dilated cardiomyopathy. Thus, 70% or more of the infected individuals will never show any clinical manifestation of the disease. The ajmaline test and the endomyocardial biopsy are, probably, the most sensitive methods to unmask latent forms of chagasic myocarditis during the undifferentiated stage. In the most advanced stages of chronic chagasic myocarditis, pathological findings are those of a dilated cardiomyopathy. At autopsy, the apical aneurysm with thrombus in it is a frequent and distinctive finding. The histopathological picture is that of an active and chronic microfocal and disseminated myocarditis. In some cases fibrosis may be confluent, which accounts for the electrocardiographic patterns of myocardial necrosis. The widespread distribution of cardiac lesions also constitute the substrate for atrioventricular and intraventricular conduction disturbances and for atrial and ventricular arrhythmias. The clinical diagnosis of Chagas' heart disease is based on a triad of: positive epidemiology, positive serology and a combination of clinical findings (suggestive electrocardiograhic abnormalities, apical aneurysm, cardiac enlargement). The electrocardiogram in the most advanced forms, usually shows sinus bradycardia, right bundle branch block with or without left anterior hemiblock, primary T wave abnormalities, pathological Q waves and multiform ventricular premature beats. The pathogenesis of the myocardial lesions of acute and also chronic chagasic myocarditis appears to be related in large part to autoimmune mechanisms. The lack of correlation between the location and number of parasitized fibers and the severity, type, and extension of degenerative and inflammatory lesions supports this assumption. Experimental and clinical studies have demonstrated the presence of antibodies directed against different components of T. cruzi and crossreacting with human antigens in patients with chronic chagasic myocarditis. Microvascular dysfunction, myocardial ischemia and autonomic nervous system impairment have also been implica

Acute Disease↗

PubMed1995

Functional significance of myocellular hypertrophy in dilated cardiomyopathy: histomorphometric analysis on 40 endomyocardial biopsies.

Dilated cardiomyopathy is characterized by an increase in myocardial mass. In order to study the functional significance of myocellular hypertrophy in dilated cardiomyopathy, 40 left ventricular endomyocardial biopsies were investigated, by comparing morphometrical data with functional indexes. The extent of myofibril volume fraction was directly associated with a better functional condition, as measured by ejection fraction (p < 0.01) and cardiac index (p < 0.05). Patients with oversize nuclei (nuclear area being > or = 70 microns 2) had a worse functional status (p < 0.05), as determined by ejection fraction and cardiac index. Finally, the extent of interstitial fibrosis was directly correlated to mean right atrial pressure (p < 0.01), right ventricular end-diastolic pressure (p < 0.02) and mean pulmonary artery pressure (p < 0.02). In conclusion, a worse functional status correlates with a reduced myofibril volume fraction and an oversize nuclear area, as in hypertrophic cells undergoing regressive changes.

Adult↗

PubMed2003

Ventricular adrenomedullin is associated with myocyte hypertrophy in human transplanted heart.

Adrenomedullin (ADM) is a vasoactive and natriuretic peptide. While it is known that ADM is increased in failing human ventricles, the expression of ADM in human ventricular allografts remains unknown. The present study was designed to investigate tissue localization and intensity of ADM expression in ventricular biopsy specimens and to characterize ventricular ADM in human cardiac allografts. Thirty-three post-transplant endomyocardial biopsy specimens were examined immunohistochemically. The average score (range: 0-4) of ADM immunoreactivity (IR) was 2.4+/-0.9 (mean+/-standard deviation). Right ventricular (RV) systolic pressure was significantly increased with high ADM-IR (p=0.048) and the ADM-IR positively associated with myocyte size (r(2)=0.23, p=0.010). In contrast, ADM-IR was not associated with systemic blood pressure, serum creatinine, cyclosporine concentration, cardiac fibrosis, or allograft rejection. The present study shows that ADM-IR is present in human ventricular endomyocardium after transplantation, and ADM-IR is associated with the magnitude of RV pressure and myocyte size, suggesting an important role for ventricular ADM in the counteraction against overload as well as in the progress of myocyte hypertrophy after heart transplantation.

Adolescent↗

PubMed1989

Left ventricular myocardial structure in aortic valve disease before, intermediate, and late after aortic valve replacement.

Left ventricular biplane cineangiography, micromanometry, and endomyocardial biopsies were performed in 27 patients with aortic stenosis (AS) and in 17 patients with aortic insufficiency (AI). Twenty-three patients with AS and 15 with AI were restudied at an intermediate time (18 months after successful valve replacement), and nine patients with AS and six with AI were restudied late (70 and 62 months after surgery). Biopsy samples were evaluated for muscle fiber diameter, percent interstitial fibrosis, and volume fraction of myofibrils. In control biopsy samples obtained from five donor hearts at transplantation, these morphometric variables averaged 21.2 microns, 7.0%, and 57.2%, respectively. After surgery, mass determined by cineangiography decreased from 186 to 115 and 94 g/m2 in patients with AS and from 201 to 131 and 93 g/m2 in patients with AI. At the three studies, muscle fiber diameter was 30.9, 28.0, and 28.7 microns in patients with AS and was 31.4, 27.6, and 26.4 microns in patients with AI. Percent interstitial fibrosis was 18.2, 25.8, and 13.7% in patients with AS and was 20.4, 23.7, and 19.2% in patients with AI. Left ventricular fibrous content decreased from 34.2 to 29.8 and to 12.7 g/m2 in patients with AS and from 42.1 to 28.9 and to 18.9 g/m2 in patients with AI. Volume fraction of myofibrils was 57.7, 56.8, and 49.0% in patients with AS and was 56.8, 56.6 and 48.8% in patients with AI. Thus, the decrease of muscle mass determined by cineangiography at the intermediate time after valve replacement is mediated by regression of myocardial cellular hypertrophy in patients with AS and AI and in addition by a decrease of fibrous content in patients with AI. Late after surgery, left ventricular fibrous content also decreases in patients with AS. This late decrease associated with minor changes of end-diastolic volume may be important for improvement of increased diastolic myocardial stiffness. Even 6-7 years after valve replacement, incomplete regression of structural abnormalities of left ventricular hypertrophy still exists compared with the normal myocardium. The residually increased relative interstitial fibrosis and the small late postoperative decrease of volume fraction of myofibrils, associated with a prosthesis-related slight left ventricular pressure increase, are at the origin of a persistent systolic overload at the myofibrillar level.

Adult↗

PubMedDate not supplied

[Usefulness of endomyocardial biopsy in myocarditis and dilated cardiomyopathy].

Through an endomyocardial biopsy (EB) we studied 30 patients, 15 of them with suspicious clinical diagnosis of myocarditis (M) and 15 with dilated cardiomyopathy (DC). In only 4 (26%) out of the 15 patients with M we found inflammatory changes in the biopsy. By serendipity a metastatic malignant tumor was found in one patient. In 9 (60%) out of the 15 cases with DC the histological report was compatible with interstitial fibrosis, hypertrophic myofibrils, myositic degeneration and atrophy and in 2 of these patients inflammatory cell infiltration. In all patients in whom we found these inflammatory process the illness was present for less than 6 months. We concluded that in only a limited percentage of patients with the clinical diagnosis of M inflammatory changes are present (26% in our study). In patients with DC the information given in few cases (13%) an inflammatory cell infiltration could be seen. The probability of finding inflammatory changes is higher if the duration of the disease is less than 6 months. It is important to have in mind that through this method an occult pathology could be discovered.

Adolescent↗

PubMed1987

Myocarditis and cardiomyopathy: diagnosis by endomyocardial biopsy.

UNLABELLED: To investigate the incidence of myocarditis, 30 patients, with unexplained congestive heart failure, underwent endomyocardial biopsy. For each case three to five samples were examined on light and electron microscopy. Inflammatory infiltrates and injury to adjacent myocytes consistent with myocarditis were detected in 3 of the 30 cases (10%). Changes attributable to cardiomyopathy were found in the remaining 27 cases. Two of the three patients with biopsy-proven myocarditis were treated with prednisone and azathioprine. Their control biopsies six months later showed interstitial fibrosis and absence of inflammatory infiltrates. They clinically improved but hemodynamic and angiocardiographic patterns failed to show the expected improvement. The third patient affected by myocarditis died two weeks later. IN CONCLUSION: in our series of patients with unexplained congestive heart failure, the incidence of biopsy-proven myocarditis resulted low (10%). The results of the immunosuppressive treatment in two patients with myocarditis were unconclusive. Therefore the effectiveness of such therapy should be confirmed in a larger number of patients.

Biopsy↗

PubMed1990

[Cardiac sarcoidosis responsible for localized left ventricular ectasia and refractory ventricular tachycardia. Anatomoclinical study].

The authors report the case of a 63 year old woman admitted to hospital for recurrent refractory ventricular tachycardia. Echocardiography and cardiac scintigraphy showed global left ventricular function. Ventriculography confirmed the left ventricular dysfunction and also showed a localised aneurysm of the anterior left ventricular wall. Surgical resection of the aneurysm and an encircling endocardial ventriculotomy were performed but the patient died of a low output syndrome. Pathological examination of the excised tissue showed granulomatous lesions associated with fibrosis interrupting the striated myocardial bundles. The granulomata consisted in a large number of epithelioid histiocytes and very large giant cells with many nuclei. The diagnosis made retrospectively was that of cardiac sarcoidosis causing a ventricular aneurysm and global left ventricular dysfunction. The diagnosis of cardiac sarcoidosis is difficult in the absence of systemic extracardiac involvement because the clinical manifestations and complementary investigations are non specific. The diagnosis may be made by endomyocardial biopsy in 25 per cent of cases, thereby leading to specific treatment with steroids which is sometimes effective.

Cardiomyopathies↗

PubMed1981

The haemodynamic, histopathological and hormonal features of alcoholic cardiac beriberi.

Five cases of cardiac beriberi occurring in chronic alcoholics are described. The clinical diagnosis was based on the presence of biventricular failure, low dietary intake of thiamine and the therapeutic response to oral thiamine. Complicating cardiac disease was excluded by haemodynamic studies, left ventriculography; coronary angiography and endomyocardial biopsy. Haemodynamic measurements including quantitative left ventriculography are reported. They indicate that left ventricular function is depressed despite elevated cardiac output. Biopsy material was studied by light and electron microscopy. No lesion specific to beriberi was detected by either technique although the biopsies were quantitatively abnormal. The histological changes resemble those in early reports based on necropsy material, and consist of vacuolation and intercellular oedema in the early stages with myofibre hypertrophy, fibrosis and cellular infiltration in the chronic cases. The transketolase test and response to intravenous thiamine during catheter studies are valuable diagnostic tests. Plasma renin, angiotensin II and aldosterone levels were lower than in patients with low output heart failure. The incidence of cardiac beriberi appears to be greater than is generally realized.

Adult↗

PubMedDate not supplied

Cardiovascular manifestations of systemic lupus erythematosus: current perspective.

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Hormones↗