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Results for “ENDOMYOCARDIAL FIBROSIS”

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PubMed1993

Structural causes of cardiac dysfunction in uremia.

While coronary heart disease is undoubtedly a major cause of cardiac morbidity and mortality in uremia, important noncoronary problems contribute to the common presence of cardiac problems. Based on clinical and experimental studies, we could show: (i) Left ventricular hypertrophy (LVH) can be dissociated, at least in part, from elevation of blood pressure. (ii) In uremia, PTH-dependent intermyocardiocytic fibrosis occurs; it may account, at least in part, for disturbed LV compliance and contribute to the arrhythmogenic potential. (iii) Blood pressure-independent abnormalities of intracardiac arterioles and reduced myocardial capillary supply are observed.

Animals↗

PubMed1989

[The influence of left ventricular function on surgical risk in mitral stenosis].

The influence of left ventricular (LV) function on surgical risk was assessed in 98 patients with mitral stenosis (MS) using echocardiographic studies including a dobutamine test in 42 cases. Intraoperative LV myocardial biopsy was also performed in 24 cases. Preoperatively, depressed LV function [% fractional shortening (%FS) less than or equal to 27%] was observed in 21 patients (21%). Seven patients had postoperative LV failure, five of whom had preoperative depression of LV function. Among these five patients, three had low cardiac output; and in the other two preoperative %FS was severely depressed. In cases of poor responses to preoperative dobutamine, postoperative improvement in %FS and the cardiac index were not as marked in the good-response group, and some of these patients had LV failure postoperatively. Percent fibrosis of the LV myocardium, which was demonstrated by intraoperative biopsy, correlated negatively with preoperative %FS, and %fibrosis was greater in the group responding poorly to dobutamine administration, especially in patients with postoperative LV failure. These results suggest that some patients with MS were developing LV failure postoperatively due to impaired myocardium. Myocardial fibrosis seemed to be an important causative factor in these patients. Preoperative evaluation utilizing dobutamine administration is useful in screening for high-risk patients.

Adult↗

PubMed2004

Amlodipine decreases fibrosis and cardiac hypertrophy in spontaneously hypertensive rats: persistent effects after withdrawal.

Our objective was to examine the effect of chronic treatment with amlodipine on blood pressure, left ventricular hypertrophy, and fibrosis in spontaneously hypertensive rats and the persistence of such an effect after drug withdrawal. We investigated the effects of treatment with 2, 8 and 20 mg/kg/day of amlodipine given orally for six months and at three months after drug withdrawal. Systolic blood pressure was measured using the tail-cuff method. At the end of the study period, the heart was excised, the left ventricle was isolated, and the left ventricle weight/body weight ratio was calculated as a left ventricular hypertrophy index. Fibrosis, expressed as collagen volume fraction, was evaluated using an automated image-analysis system on sections stained with Sirius red. Age-matched untreated Wistar-Kyoto and SHR were used as normotensive and hypertensive controls, respectively. Systolic blood pressure was reduced in the treated SHR in a dose-dependent way and after amlodipine withdrawal it increased progressively, without reaching the values of the hypertensive controls. Cardiac hypertrophy was reduced by 8 and 20 mg/kg/day amlodipine, but when treatment was withdrawn only the group treated with 8 mg/kg/day maintained significant differences versus the hypertensive controls. All three doses of amlodipine reduced cardiac fibrosis and this regression persisted with the two highest doses after three months without treatment. We concluded that antihypertensive treatment with amlodipine is accompanied by a reduction in left ventricular hypertrophy and regression in collagen deposition. Treatment was more effective in preventing fibrosis than in preventing ventricular hypertrophy after drug withdrawal.

Amlodipine↗

PubMed1991

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

To evaluate the effects of hypertension on cardiac hypertrophy, on myocardial structure, and on ventricular arrhythmias, 27 3-month-old spontaneously hypertensive rats were treated with enalapril (10 mg/kg) daily for 11 months and compared with 26 untreated control rats. Systolic arterial pressure was significantly decreased in treated rats, and at the end of the experiment, it was 199 +/- 3 mm Hg (treated) versus 237 +/- 3 mm Hg (controls) (p less than 0.001). At this time, spontaneous arrhythmias and induced arrhythmias either by programmed electrical stimulation (train of stimuli +1 or 2 extrastimuli) or by trains of eight stimuli at decreasing coupling intervals were observed in isolated heart preparations. Comparing enalapril-treated and control rats, spontaneous arrhythmias (9 of 27 versus 20 of 26, respectively; p less than 0.01), programmed stimulation-induced arrhythmias (3 of 26 versus 12 of 23, respectively; p less than 0.01), and trains of stimuli-induced arrhythmias (4 of 26 versus 14 of 19, respectively, p less than 0.001) were less frequent in the enalapril group. Left ventricular weight was decreased in treated rats by 18% (p less than 0.001). Enalapril administration diminished the fraction of myocardium occupied by foci of replacement fibrosis normally occurring in control rats by 59% (p less than 0.001). Finally, a significant correlation was found between left ventricular weight, the extent of myocardial fibrosis, and the occurrence of ventricular fibrillation. It was concluded that chronic treatment with enalapril, which resulted in attenuation of systemic arterial pressure by limiting cardiac hypertrophy and myocardial fibrosis, decreases the propensity of the heart of hypertensive rats to arrhythmogenesis.

Analysis of Variance↗

PubMed1995

Steroids, hypertension and cardiac fibrosis.

Though we normally think of mineralocorticoid receptors as mediating aldosterone action on the kidney and other epithelia, the same receptors are found at comparable levels in non-epithelial tissues such as hippocampus and heart. In all tissues mineralocorticoid receptors have identical, high affinity for aldosterone, corticosterone and cortisol. In tissues such as the heart and hippocampus they are unprotected by the enzyme 11 beta hydroxysteroid dehydrogenase, which converts glucocorticoids to inactive 11-keto congeners; in such tissues mineralocorticoid receptors are thus overwhelmingly occupied by glucocorticoids, reflecting their much higher circulating levels. The epithelial effects of mineralocorticoid receptors and glucocorticoid receptors appear relatively uncomplicated, paralleling findings in cotransfection systems (corticosterone and cortisol, as well as aldosterone, are agonist in mineralocorticoid receptors; activated mineralocorticoid receptors and activated glucocorticoid receptors equivalently transactivate gene expression). In non-epithelial tissues, most notably the brain, the actions (and possible interactions) of mineralocorticoid receptors and glucocorticoid receptors appear much more complex, and are yet to be established in detail. We have recently confirmed and extended the findings of Weber and his colleagues that administration of aldosterone or deoxycorticosterone to uninephrectomized rates drinking 1% NaCl solution for 8 weeks is followed by interstitial and perivascular cardiac fibrosis. Whether or not the effect of corticosteroids on cardiac fibrosis reflects direct actions on cardiac muscle, or other cellular constituents of the heart, there appears to be significant interplay between mineralocorticoid receptors and glucocorticoid receptors, and possible roles for agonist and antagonist occupancy of both receptor types.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Morphoregulatory interactions of endocardial endothelium and extracellular material in the heart.

The endocardium forms the inner lining of the cavities of the heart. The luminal surface of the cardiac wall is subjected to considerable cyclical physico-chemical forces. These forces can have structural and physiological consequences both for the endocardial endothelium and for the subjacent interstitial tissue. In the latter tissue space, the extracellular matrix (ECM) plays a dominant role during cardiogenesis. For example, this role becomes evident from the influence of fibronectin in the directional migration of proendocardial cells and in the formation of a trabeculated heart. In particular, the complex processes occurring in the valves of the developing heart illustrate a spatiotemporally regulated expression of ECM components and adhesion molecules. In the adult heart, the endocardial interstitial tissue consists of a thin basal lamina, a reticular lamina and a fibroelastic layer which contains some fibroblasts, smooth muscle cells and a heterogeneous population of nerve fibers. Unlike in arteries, elastic fiber in the fibroelastic layer of ventricular endocardium do not constitute an elastic lamina. Differences in thickness of the endocardium between atria and ventricles, as well as the diffuse and focal endocardial fibrosis during ageing have been related to mechanical stress and local turbulence of flow. Although endocardial fibrosis is a common pathological finding in various cardiomyopathies, our knowledge on the structural organization and on the pathogenetic role of ECM is very limited, mainly by the lack of suitable experimental models.

Age Factors↗

PubMed1999

Human chronic chagasic cardiopathy: participation of parasite antigens, subsets of lymphocytes, cytokines and microvascular abnormalities.

This article tries to demonstrate by new pathological findings (with the use of immunohistochemical technique and confocal laser microscopy) that chronic chagasic cardiomyopathy is a result of multiple factors involving myocarditis, immunodepression, severe fibrosis and microvessels dilatation and that all of these alterations are probably directly related with the presence of Trypanosoma cruzi parasites in the host associated with inadequate immunological response of the host.

Animals↗

PubMed1979

Congestive cardiomyopathy with segmental wall motion abnormalities and a non-uniform pattern of fibrosis.

A case of congestive cardiomyopathy in a 46-year-old smoker with single-vessel right coronary artery disease is presented. Segmental contraction abnormalities were present in the anterior wall. Pathologic analysis showed diffuse fibrosis consistent with a cardiomyopathy in areas of abnormal contraction and normal muscle in areas of normal contractility. Segmental wall motion abnormalities have been reported but none with microscopic studies of areas of both abnormal and normal contractility.

Cardiomyopathies↗

PubMed1985

Myocarditis and cardiomyopathy in the dog and cat.

Myocarditis and cardiomyopathy were diagnosed in 36 dogs from 11 litters, and myoendocarditis and restrictive cardiomyopathy were diagnosed in 51 cats. Most of the dogs and cats died unexpectedly. Spontaneous parvoviral infection in the dogs caused acute (myocytolysis with presence of intranuclear inclusion bodies in the myocytes), subacute (inflammatory reaction and myocytolysis), and chronic (fibrosis and myocytolysis) myocarditis, which led to extensive myocardial fibrosis and abnormality of the myocytes, similar to dilated cardiomyopathy in man. Spontaneous acute, subacute, and chronic myoendocarditis in the cats led to granulation, extensive fibrosis, and necrosis of the myoendocardium, i.e., like restrictive cardiomyopathy which occurs in man without eosinophilia. Thus, the dog and cat are important animal models of primary myocardial disease.

Acute Disease↗

PubMed1984

Computed tomography of mural thrombosis in the hypereosinophilic syndrome.

The hypereosinophilic syndrome characteristically involves multiple organs. Its most severe debilities are associated with cardiac and central nervous system complications. Endothelial damage can result in intracardiac thrombosis, endocardial fibrosis, and progressive congestive failure. Computerized tomography is of value in making the diagnosis of an intracardiac mass. Simultaneous evaluation of the pericardiac and extracardiac structures may aide in the distinction of a thrombus from a neoplasm.

Adult↗

PubMed1995

Left ventricular fibrosis in renovascular hypertensive rats. Effect of losartan and spironolactone.

Myocardial fibrosis resulting from arterial hypertension alters myocardial structure and function. Myocardial fibrosis is characterized by a pathological accumulation of types I and III collagens. We used an aldosterone antagonist (spironolactone) and an angiotensin II antagonist (losartan) to elucidate the respective role of these hormones and hypertension in the development of myocardial fibrosis in the Goldblatt model of two-kidney, one clip hypertension in the rat. Fibrosis was assessed by computer-assisted morphometry in the interstitial space, around coronary arteries, in microscar areas, and on left ventricular sections stained with Sirius red and by biochemical techniques. Morphometry was performed with both standard light and polarization microscopy; this latter method was used to quantify yellow-red and green collagen fibers. Concurrently, type I and type III collagen mRNAs were evaluated by a semiquantitative polymerase chain reaction method. The collagen content of the untreated two-kidney, one clip hypertensive rats increased mainly around the coronary arteries; the number and surface area of microscars also increased in chronic hypertension. Losartan treatment decreased systolic pressure and yellow-red collagen fiber content in all areas, whereas spironolactone treatment decreased green collagen fiber content without decreasing systolic pressure. mRNA levels for types I and III collagens showed profiles similar to those of yellow-red and green collagen fiber contents, respectively, suggesting that yellow-red collagen fibers are mainly type I collagen fibers and green collagen fibers are mainly type III collagen fibers. These results suggest that angiotensin II, possibly together with hypertension, and aldosterone, independently of hypertension, have a major influence on myocardial fibrosis, inducing type I and type III collagen deposits, respectively, mainly around coronary arteries.

Angiotensin II↗

PubMed1976

Functionally atrialized parchment-like right ventricle with extensive myocardial fibrosis of left ventricle.

A 18-year-old female with unusual type of parchment-like right ventricle died of intractable congestive heart failure was reported. A catheter study revealed the absence of systolic contraction of the right ventricle. The pressure tracing curve in the right ventricle was virtually the same as in the right atrium. At autopsy, there was an extensive myocardial fibrosis of the left ventricle in addition to the almost total absence of the myocardium of the right ventricle. The case was considered to be a unique type of idiopathic cardiomyopathy.

Adolescent↗

PubMed1988

Aortic and mitral valve replacement in idiopathic hypereosinophilic syndrome.

Idiopathic hypereosinophilic syndrome is a rare systemic manifestation of eosinophilia that may cause endocardial fibrosis. Endocardial fibrosis and overlying thrombus typically lead to a restrictive cardiomyopathy and heart failure. Occasionally mitral or tricuspid regurgitation (or both) occurs as a result of the fibrosis and thrombus formation. This report describes a patient with hypereosinophilic syndrome who was seen with an unusually localized form of cardiac involvement that resulted in predominantly aortic and mitral stenosis. This was treated with bivalvular replacement.

Adult↗

PubMed2002

Elevated mean arterial pressure in the ovariectomized rat was normalized by ET(A) receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis.

1. The influence of menopause on ventricular function and remodelling remains undefined. The following study examined the effect of ovariectomy on ventricular contractility, cardiac hypertrophy and extracellular matrix protein expression. 2. Elevated circulating levels of the vasoconstrictor endothelin-1 have been reported in post-menopausal women. Moreover, endothelin-1 has been shown to influence blood pressure, ventricular function and cardiac remodelling. In this regard, the potential pathophysiological role of endothelin-1 in the ovariectomized rat was assessed via the administration of the selective endothelin(A) receptor (ET(A)) antagonist BMS-182874. 3. In 3 and 6 week ovariectomized female Sprague - Dawley rats, uterus atrophy was associated with a significant increase in mean arterial pressure, and left ventricular systolic pressure, as compared to sham. By contrast, right ventricular contractile indices were normal in the ovariectomized rat. Despite increased systolic load, left ventricular hypertrophy was not evident, prepro-atrial natriuretic peptide (prepro-ANP) mRNA levels and collagen protein content were similar to sham. 4. The treatment of ovariectomized rats with BMS-182874 (60 mg kg(-1) per day) did not reverse uterus atrophy. However, BMS-182874 normalized mean arterial pressure, and left ventricular systolic pressure in the ovariectomized rat. 5. Thus, despite elevated blood pressure, ovariectomized rats were not associated with either cardiac hypertrophy or fibrosis. Lastly, endothelin-1, acting via the stimulation of the ET(A) receptor represents an integral mechanism implicated in the increase of mean arterial pressure following ovariectomy.

Animals↗

PubMed2002

Stimulation of peroxisome-proliferator-activated receptor alpha (PPAR alpha) attenuates cardiac fibrosis and endothelin-1 production in pressure-overloaded rat hearts.

Endothelin-1 (ET-1) production is increased in hypertrophied hearts accompanied with fibrosis. ET-1 is a potent mitogen of fibroblasts and ET receptor antagonists are reported to inhibit the proliferation of fibroblasts and cardiac fibrosis. Peroxisome-proliferator-activated receptor alpha (PPAR alpha), one of the nuclear hormone receptors, suppresses activator protein-1 (AP-1), one of the nuclear transcription factors. Activation of PPAR alpha is reported to inhibit thrombin-induced ET-1 production by repressing the AP-1 signalling pathway in vascular endothelial cells. We investigated effects of the PPAR alpha activator fenofibrate (80 mg/kg per day, per os) on mRNA levels of ET-1, collagen type I and type III and histological features of myocardial fibrosis in hypertrophied rat hearts due to pressure-overload by abdominal aortic banding (AB). The treatment with fenofibrate or vehicle was started 7 days before the AB operation. Four days after the AB operation, fenofibrate treatment significantly reduced ET-1 mRNA expression compared with vehicle treatment in AB rat hearts. Collagen type I and type III mRNA expression, and interstitial and perivascular fibrosis were attenuated in the fenofibrate-treated AB rat group. Since the ET-1 gene has AP-1 response elements in the 5'-flanking region, it is suggested that myocardial fibrosis is effectively inhibited by fenofibrate through suppression of AP-1-mediated ET-1 gene augmentation in the pressure-overloaded heart caused by aortic banding in rats.

Animals↗

PubMed1975

[On the mechanism of valve plane (author's transl)].

A detailed description of the functional sequence and mechanism of the valve plane movements is given as an extension of the studies on the functional morphology of cardiac movements. The valve plane mechanism is driven in the small, rapidly beating heart by the contraction of the external and internal spiral fibres of the myocardium which decreases the width of the chamber. The atrium is enlarged during systole by the descent of the valvular ring towards the apex. The auricular apendices must act as a compensation reservoir giving the atrial wall the necessary freedom of movement within the pericardial dome. Under these working conditions (hypovolaemia, decreased venous return pathophysiological consequences are discernible as subendocardial bleeding secondary to increased sliding movement of the inner layer of the myocardium against the middle layer. Chamber dilation as a consequence of endocardial fibrosis is explained as a result of progressive rigidity of endo-epicardial fixation. These structural changes progressively impair the systolic-diastolic changes in wall thickness.

Animals↗

PubMed2004

Combined transplantation of skeletal myoblasts and mesenchymal cells (cocultivation) in ventricular dysfunction after myocardial infarction.

OBJECTIVE: Cell therapy in the myocardium has been mainly performed with satisfactory results using 2 cell types: skeletal myoblasts (myogenic) and mesenchymal cells (angiogenic). This study assessed the combined transplantation of those 2 cell types (SMM) into infarcted rats. METHODS: Myocardial infarction was induced by ligature of the left coronary artery in 26 Wistar rats. After one week, the animals underwent echocardiography for assessing ejection fraction (EF%) and left ventricular end-diastolic and systolic volumes (EDV, ESV, mL). After 2 days, the animals were reoperated on and divided into 2 groups: 1) control (n = 10), which received 0.15 mL of culture medium; and 2) SMM (n = 16), which received 7.5x10(6) heterologous skeletal myoblasts and mesenchymal cells in the infarcted region. The cells were obtained from puncture of the iliac crest and biopsy of skeletal muscle, and were cultured in vitro. After one month, the animals underwent a new echocardiography. RESULTS: No significant difference in EF, EDV, and ESV was observed between the 2 groups on baseline echocardiographic values. One month after transplantation, the following was observed: a reduction in EF in the control group (29.31 +/- 5.6% to 23.54 +/- 6.51%; P = 0.048); and an increase in EF in the SMM group (24.03 +/- 8.68% to 31.77 +/- 9.06%; P = 0.011). The presence of neovascularization and muscle fibers was identified in the regions of myocardial fibrosis in the SMM group. CONCLUSION: Cocultivation of skeletal myoblasts and mesenchymal cells is functionally effective.

Animals↗

PubMed2003

Angiotensin II type 1 receptor blocker, valsartan, prevented cardiac fibrosis in rat cardiomyopathy after autoimmune myocarditis.

Favorable effects of angiotensin II type 1 receptor blockers on patients with ischemic or idiopathic dilated cardiomyopathy have already been suggested by several human trials but their effects on inflammatory cardiomyopathy remain unknown. We investigated the effects of the angiotensin II type 1 receptor blocker, valsartan, in chronic heart failure after inflammatory cardiomyopathy. Autoimmune myocarditis was induced in Lewis rats by injection with porcine cardiac myosin. In the phase of chronic heart failure, from day 28 until day 70, rats were treated by oral administration of valsartan. Three groups were designated: 1 ml saline, 10 mg/kg valsartan, and 30 mg/kg valsartan. On the 73rd day, hemodynamic parameters, pathological findings and the expression levels of r-ANP mRNA of the ventricle were examined, and were compared with the saline control. The ventricular weight/body weight ratio and area of fibrosis was decreased in the 30 mg/kg valsartan group. The left ventricular end-diastolic pressure and the central venous pressure were decreased in a dose-dependent manner in both valsartan groups, while the first pressure derivatives +dP/dt and -dP/dt did not differ among the three groups. A high dose of valsartan reduced the expression of tissue ANP mRNA compared with the saline group. In conclusion,valsartan suppressed myocardial hypertrophy and fibrosis, and it improved the hemodynamics and cardiac function in an animal model of post-myocarditis dilated cardiomyopathy.

Angiotensin Receptor Antagonists↗