[Endomyocardiopathy with eosinophilia].
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Adult↗
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Results for “ENDOMYOCARDIAL FIBROSIS”
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Heart transplant rejection with hemodynamic compromise: a multiinstitutional study of the role of endomyocardial cellular infiltrate. Cardiac Transplant Research Database.
BACKGROUND: The natural history of patients experiencing hemodynamic compromise with rejection has been incompletely characterized. This multiinstitutional study examined the outcome of such episodes, particularly with regard to the extent of cellular infiltrate on the index endomyocardial biopsy. METHODS: From January 1, 1990, through June 30, 1994, 3367 patients in the Cardiac Transplant Research Database experienced 4137 episodes of rejection. Severe hemodynamic compromise occurred in approximately 5% of the rejection episodes, and this proportion remained relatively constant over time. RESULTS: Recipient risk factors for rejection with severe hemodynamic compromise included black race, female recipient sex, and diabetes. The 3-month actuarial survival rate was 60% after rejection with severe hemodynamic compromise versus 95% after rejection with no or mild compromise. Low initial biopsy score conferred a higher early survival, but a lower survival at 2 years after rejection with severe hemodynamic compromise. Among patients who survive an initial rejection episode with severe hemodynamic compromise, survival at 2 years after an episode was 46% among those who had a low initial biopsy score versus 84% with a high biopsy score. CONCLUSIONS: Rejection with hemodynamic compromise, although rare, represents a major complication of heart transplantation with a poor long-term outcome. Survivors of hemodynamically compromising rejection episodes associated with low biopsy scores in the International Society for Heart and Lung Transplantation grading system have a significantly worse long-term outcome than survivors of episodes associated with high scores. These findings suggest that immunologic mechanisms other than lymphocytic infiltration of the cardiac allograft are important and distinct causes of allograft dysfunction.
Actuarial Analysis↗
[Unusual mitral valve insufficiency].
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Adolescent↗
[Mitral valve fibrous ring calcinosis in ischemic heart disease].
Calcinosis of the mitral fibrous ring (CMFR) was detected echocardiographically in 11.7% of the examinees with ischemic heart disease (IHD) at the age over 60 years. In CMFR the mitral opening significantly narrows, maximal transmitral diastolic gradient rises, mitral regurgitation becomes more pronounced. In one-third of the patients calcinosis involves the posterior wall disturbing its kinematics. Narrowing of the mitral opening in IHD patients accompanying CMFR is considered to be moderate nonvalvular mitral stenosis.
Aged↗
[Fibrinolytic therapy and anticoagulation. Pediatric experience].
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Adolescent↗
[Anatomo-clinical correlation (case 7/97--Hospital Santa Isabel--Cenprecor--Salvador, BA, Brazil)].
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Adolescent↗
Effectiveness of long-term beta-blocker therapy for dilated cardiomyopathy--echocardiographical follow-up.
To evaluate the effectiveness of long-term beta-blocker therapy for dilated cardiomyopathy (DCM), two groups (Group I: 18 patients, Group II: 17 patients) with DCM divided by the order at the entry were followed echocardiographically for 16.9 +/- 3.0 months in Group I and 21.4 +/- 3.9 months in Group II. Metoprolol (final dose: 60 mg/day) was administered in Group I, but not in Group II (the control), although the conventional treatment for heart failure was continued. The left ventricular end-systolic dimension and ejection fraction assessed by echocardiography improved significantly after 6 months in Group I, but not in Group II, even after 48 months, although there were no significant differences in baseline data between the two groups. The end-diastolic dimension decreased significantly after 12 months in Group I only. It was estimated, using the point count method on a left ventricular endomyocardial biopsy specimen taken at entry, that the improvement (delta EF) of the ejection fraction 12 months after metoprolol administration inversely correlated (r = -0.677, p less than 0.01) with percent fibrosis, indicating that the more myocardium remains, the more improvement is expected. These findings suggested a favorable effect of beta blockade in DCM, especially in cases with less fibrosis, showing that the endomyocardial biopsy could be of clinical use in selecting candidates for chronic beta-blocker therapy in DCM.
Adrenergic beta-Antagonists↗
Quantitative evaluation of the rate of myocardial interstitial fibrosis using a personal computer.
We investigated the reliability and reproducibility of an image-analyzing system run on a personal computer for measurement of myocardial interstitial fibrosis. Measurements of myocardial interstitial fibrosis in right ventricular endomyocardial biopsies obtained from patients with hypertrophic cardiomyopathy determined by this image-analyzing system were compared with measurements determined by the point-counting method. We also investigated the correlation between measurements of interstitial fibrosis obtained by image analysis and biochemical measurements of myocardial levels of hydroxyproline in normal and cardiomyopathic hamsters. The intra- and interobserver variability were significantly lower for measurements obtained by the image-analyzing system than for measurements obtained by the point-counting system. Reproducibility was superior with the image-analyzing method. The rate of myocardial interstitial fibrosis determined by the computer image-analyzing method was positively correlated with the hydroxyproline measurement (r = 0.89). Our results suggest that an image-analyzing system using a personal computer provides reproducible results with a high level of reliability.
Adult↗
Echocardiographic features of eosinophilic endomyocardial disease.
Nine patients with eosinophilic endomyocardial disease who had undergone angiocardiography with histological staging of their disease, were studied by M-mode and two dimensional echocardiography to determine the extent to which specific features of the disease could be evaluated by these non-invasive methods. In seven patients, amplitude processed two dimensional echocardiography showed regions where the relative intensity of endomyocardial echoes was greater than normal, and their distribution corresponded to known areas of fibrosis. Standard two dimensional echocardiography was normal in all but three patients. In eight patients M-mode echocardiography showed only non-specific abnormalities, but appeared to be useful in assessing the functional consequences of myocardial or mitral valve disease. After digitisation a reduction in the duration and an increase in the peak rate of dimension increase during filling was prolonged. It was concluded that amplitude processed two dimensional echocardiography might be useful in diagnosing the extent and severity of endomyocardial disease in patients with hyperosinophilia. These noninvasive techniques may thus provide a means for the early diagnosis of endomyocardial fibrosis and could be useful in assessing in progression or response to treatment.
Adult↗
Serious cardiovascular side effects of large doses of anabolic steroids in weight lifters.
Pathological cardiovascular manifestations are reported in four male patients, who had taken massive amounts of anabolic steroids while undergoing many years of strength training. One patient was referred because of ventricular fibrillation during exercise, one because of clinically manifest heart failure, and one because of arterial thrombus in his lower left leg. The fourth patient was persuaded to attend for a check-up because of a long history of massive use of anabolic steroids. All four patients had cardiac hypertrophy. Two of the patients had symptoms and signs of heart failure, and one of these two had a massive thrombosis in both right and left ventricles of his heart. After cessation of the use of anabolic steroids in the other patient with heart failure, left ventricular wall thickness reduced quickly from 12 to 10.5 mm, and fractional shortening increased from 14% to 27%. Endomyocardial biopsy revealed increased fibrosis in the myocardium in two of the three cases. HDL-cholesterol was 0.58 mmol.l-1 and 0.35 mmol.l-1 in the two patients still using multiple anabolic steroids at the time of investigation. The cardiovascular findings described in the present paper should warn all physicians and athletes about the possible serious acute and long-term side effects of the massive use of anabolic steroids.
Adult↗
Long-term hemodynamic follow-up of cardiac transplant patients treated with cyclosporine and prednisone.
To evaluate the long-term hemodynamic results in cardiac transplant patients treated with cyclosporine and prednisone, 19 patients were studied by cardiac catheterization and endomyocardial biopsy 13 +/- 3 months after transplantation. Immunosuppression consisted of 6 +/- 4 mg/kg/day cyclosporine and 20 +/- 8 mg/day prednisone. Eighteen patients were asymptomatic but had developed postoperative systemic hypertension (17 on antihypertensive therapy). These patients were compared with a normotensive control group of 18 patients without cardiovascular disease. Significant differences were found in heart rate; right atrial, pulmonary arterial, pulmonary arterial wedge, systemic arterial, and left ventricular end-diastolic pressures; cardiac index and stroke volume index; systemic and pulmonary vascular resistance; and end-diastolic volume index and left ventricular ejection fraction. The most frequent hemodynamic abnormalities included an elevated arterial pressure in 10 patients (56%), an elevated left ventricular end-diastolic pressure in six patients (33%), and a reduced ejection fraction in five patients (28%). Hemodynamic abnormalities tended to resolve or improve in the five patients restudied 2 years after transplantation. There was no significant relationship between fibrosis or inflammation on endomyocardial biopsy and hemodynamic abnormalities. We conclude that mild-to-moderate hemodynamic abnormalities are common in asymptomatic cardiac transplant patients receiving cyclosporine and prednisone.
Adult↗
[Is secondary myocardial hypertrophy a physiological or pathological adaptive mechanism?].
Physiological hypertrophy is present when the increase in myocardial mass resulting from chronic mechanical loading is associated with normal or enhanced myocardial function and myosin ATPase activity. Morphological alterations occurring during the formation of hypertrophy are fully reversible in physiological hypertrophy. In pathological hypertrophy myocardial function and myosin ATPase activity are depressed and morphological changes do not or only incompletely regress following the elimination of the stimulus of hypertrophy. In the experimental animal myocardial hypertrophy resulting from exercise conditioning or slight to moderate ventricular pressure overload fulfills the criteria of physiological hypertrophy. More severe sudden pressure overload is accompanied by depression of contractile function. These pressure overload models have however, little analogy to the more progressive development of pressure loading in humans. In young dogs and in cats with a gradually increasing pressure load, in vivo ventricular ejection fraction remained within normal limits 37 to 60 weeks after banding of the ventricular outflow vessel. In vitro myocardial function evaluated in the hypertrophied papillary muscle was, however, at least in part depressed, notably when hydroxyproline concentration was augmented. Following debanding in rats with aortic constriction hydroxyproline content did not regress suggesting that fibrosis once established is not reversible. In man myocardial hypertrophy from exercise conditioning is associated with normal ventricular function except in older athletes, who may show a subtle reduction in ventricular shortening. Patients with chronic pressure overload from aortic stenosis or volume overload from aortic insufficiency in whom the angiographic muscle mass is severely increased (greater than or equal to 180 g/m2) elicit a depressed left ventricular contractile function. Preserved left ventricular ejection performance in aortic valve disease is however not associated with normal myocardial structure because interstitial fibrosis evaluated from endomyocardial biopsies or biopsies obtained at surgery was found to be increased. Patients with depressed left ventricular contractility were characterized by having an abnormally high muscle fibre diameter. Normal function after surgery was not accompanied by normalization of myocardial structure: Interstitial fibrosis increased, fibrous content remained the same and cellular hypertrophy regressed incompletely regardless whether angiographic muscle mass had regressed to normal or remained still increased after surgery. In summary, the bulk of available functional and morphological data suggests that the occurrence of true physiological hypertrophy is probably limited to exercise conditioning and eventually to mild chronic mechanical overload. The more severe secondary hypertrophy such as in patients with aortic valve disease who undergo valve replacement, is not a physiological adaptation, but must be considered as a pathological process.
Adenosine Triphosphatases↗
[Giant left ventricular thrombi in the hypereosinophilic syndrome: report of two cases].
This is a report of two cases of the hypereosinophilic syndrome with an unusual apical filling defect suggestive of an intraventricular mass. Case 1 (45-year-old man): This patient had marked eosinophilia, congestive heart failure, and murmurs of aortic and mitral regurgitation. A subcutaneous cervical mass revealed histologic features of angiolymphoid hyperplasia with eosinophilia (so-called Kimura's disease). Left ventriculography confirmed mitral regurgitation with extensive obliteration of the left ventricular cavity. It was suspected that an extensive ventricular mural thrombus was superimposed on a thickened endocardium. Right ventricular endomyocardial biopsy showed focal regions of fibrosis in the myocardium, and infiltration of eosinophils were identified. Case 2 (70-year-old man): This patient had marked eosinophilia and congestive heart failure. Left and right angiography showed apical filling defects suggestive of intraventricular mass. Right ventricular endomyocardial biopsy showed focal areas of fibrosis, and infiltration of eosinophils were observed. Diagnosis of Löffler's endocarditis was made. It is suggested that the spectrum of ventricular abnormalities in these patients results from endomyocardial fibrosis of varying severity, and that eosinophilia may play a leading role or may associate with the genesis of the disease in these two cases.
Aged↗
Quantitative investigation of cardiomyocyte hypertrophy and myocardial fibrosis over 6 years after cardiac transplantation.
OBJECTIVES: This study was performed to determine the degree and time course over 6 years of cardiomyocyte hypertrophy and myocardial fibrosis of the cardiac allograft in transplanted patients. BACKGROUND: Diastolic dysfunction and to a certain extent systolic dysfunction are common cardiac findings after heart transplantation. The development of posttransplant cardiomyocyte hypertrophy and myocardial fibrosis likely contributes to these derangements. METHODS: Cardiomyocyte diameter and percent fibrosis were determined in serial endomyocardial biopsy specimens obtained from 1 month up to 6 years following heart transplantation in 50 patients. Endomyocardial biopsy specimens from 40 patients with primary dilated cardiomyopathy and 11 normal subjects were similarly analyzed for control data. Analyses were performed in a blinded format using a validated computerized image analysis system (Optimas 5.2). RESULTS: Early (1 month) cardiomyocyte enlargement decreased to the smallest diameter 6 months posttransplant, but thereafter progressively increased by 10% to 20% over the subsequent 5- to 6-year period. Although not statistically established, principal stimuli may include a discrepancy in body size (recipient > donor), coronary allograft vasculopathy and posttransplant systemic hypertension. Percent myocardial fibrosis rose early (1 to 2 months) posttransplant and thereafter remained at the same modest level of severity. CONCLUSIONS: Cardiomyocyte diameter of the transplanted heart gradually increases over time, while percent myocardial fibrosis rises early and remains in a modestly elevated plateau after 2 months posttransplant. These histostructural changes likely contribute to the hemodynamic and cardiac functional alterations commonly observed posttransplant.
Adolescent↗
Cyclosporine induced myocardial fibrosis: a unique controlled case report.
Many patients treated with cyclosporine in the Stanford Heart Transplant Program have exhibited perimyocytic fibrosis in the donor heart, seen on endomyocardial biopsy specimen. Although restrictive hemodynamic effects have not been observed up to three years after transplantation, there is a possibility that such changes could become a problem. With the increasing use of cyclosporine in non-cardiac organ transplantation, it is of interest to examine the effect of this drug upon the non transplanted heart. This was possible in a man who underwent a heterotopic heart transplantation 3 1/2 years ago, and who has been followed with serial endomyocardial biopsies from both hearts. Although there were no episodes of rejection the donor heart developed significant perimyocytic fibrosis which was not seen in the native heart. This study suggests that cyclosporine induced fibrosis only occurs in the transplanted heart.
Adult↗
Prognostic significance of conduction disturbance and reduction of left precordial voltage of electrocardiogram in hypertrophic cardiomyopathy.
To clarify the prognostic significance of electrocardiographic changes in hypertrophic cardiomyopathy, we retrospectively evaluated serial electrocardiograms in 77 patients with hypertrophic cardiomyopathy who were followed for more than 1 year. The electrocardiographic features analyzed were conduction disturbance and left precordial QRS voltage. There were 4 sudden deaths. Various conduction disturbances appeared in 32 (44%) of the remaining 73 patients. Intraventricular conduction delay was the most common (47%). The left precordial voltage decreased in 19 (26%), increased in 3, and did not change in 51. The left ventricular end-diastolic pressure at the initial investigation was significantly higher and clinical deterioration was more frequently seen in patients with a conduction disturbance or reduction of QRS voltage than in those without these electrocardiographic changes. Also, echocardiographic analysis showed that left ventricular dimensions increased significantly (from 4.4 +/- 0.6 to 4.8 +/- 0.7 cm in end-diastole and from 2.6 +/- 0.6 to 3.1 +/- 0.8 cm in end-systole; p less than 0.01, respectively) and left ventricular fractional shortening was reduced (from 41 +/- 8 to 36 +/- 11%; p less than 0.01) in the 32 patients with conduction disturbance during the follow-up period although absolute cavity size remained normal in 26 of these patients. These parameters did not change in those without conduction disturbance. Histopathological analysis of endomyocardial biopsies showed that myocardial fibrosis in the left ventricle was frequently associated with these electrocardiographic changes. However, such changes were not present in the sudden death patients. It is concluded that conduction disturbance and the reduction of QRS voltage are significant parameters which suggest a poor prognosis in patients with hypertrophic cardiomyopathy, but are not predictors of sudden death.
Adolescent↗
alpha-Interferon treatment for idiopathic hypereosinophilic syndrome.
Idiopathic hypereosinophilic syndrome (HES) is a poorly understood disorder characterized by a markedly elevated peripheral blood eosinophil count in the absence of known associated causes of hypereosinophilia. Idiopathic hypereosinophilic syndrome is associated with eosinophil-induced organ damage, including endomyocardial and pulmonary fibrosis, stroke, and gastrointestinal disease. Treatment of idiopathic HES is centered on the reduction of peripheral circulating eosinophils in an effort to diminish tissue infiltration and destruction. Multiple cytotoxic agents have been tried, with variable results. Prednisone and hydroxyurea have remained the therapies of choice in long term treatment of idiopathic HES. We report here the successful 2 year treatment of aggressive idiopathic HES, refractory to hydroxyurea and prednisone, with alpha-interferon.
Adult↗
[Cardiac manifestations of idiopathic hypereosinophilic syndrome].
BACKGROUND: The aim of our study is to describe the more common cardiac manifestations of idiopathic hypereosinophilic syndrome representing the major cause of mortality. MAIN POINTS: Current therapy consists of corticosteroid, hydroxyurea and interferon alpha. Recent publications confirm the activity of imatinib mesylate, a selective tyrosine kinase inhibitor, in patients with idiopathic hypereosinophilic syndrome. In cases with marked valvular compromise or with endomyocardial thrombosis or fibrosis, cardiac surgery can provide substantial benefits. PERSPECTIVES: A better understanding of the pathophysiology of this syndrome could lead to the development of new therapeutic agents.
Heart Diseases↗