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PubMed1972

Myocardial fibrosis and smooth muscle cell hyperplasia in coronary arteries of allylamine-fed rats.

Immature female Long-Evans rats were fed 2 g of allylamine-HCl kg of commercial diet for periods of 84-281 days. Coronary arteries and myocardium were examined in 16 control and 23 test rats. Cellular alterations in the arterial tributaries were found principally proximal to or within the areas of myocardial fibrosis. Whereas intimal smooth muscle cell (SMC) hyperplasia was prominent in vessels of smaller caliber, medial hyalinosis was seen frequently in arteries with diameters greater than 200 mu. Intimal hyperplasia developed in the peripheral coronary branches without any evidence of leukocytic infiltration or thrombus formation. It appeared that SMC hyperplasia in the intima contributed more often to a reduction of luminal patency than medial hyalinosis in allylamine-fed rats. On the basis of alterations in the coronary arteries and the localization of fibrosis, we believe that hypoxia is the cause of myocardial necrosis.

Alkenes↗

PubMed1986

Myocardial hypertrophy, fibrosis and infarction following exposure of the heart to radiation for Hodgkin's disease.

A 35 year old man was treated for stage IIA Hodgkin's disease by radiation to the upper thorax, axillae and neck. Three years later he presented with intractable and ultimately fatal congestive heart failure. Autopsy revealed massive biventricular hypertrophy with widespread subendocardial fibrosis and myocardial infarction, but with little coronary artery disease. Such a complex of features has not previously been described after radiation therapy and cannot be adequately explained by other known causes of heart muscle disease. Ventricular hypertrophy with extensive subendocardial fibrosis may be part of the spectrum of radiation heart disease.

Adult↗

PubMed2003

[Peculiarities of myocardial remodelling in rabbits' experimental hypercholesterolemia].

The aim of the investigation was to estimate the peculiarities of myocardial remodelling on the conditions of experimental hypercholesterolemia. Experiments were carried out on chinchilla breed male rabbits weighing from 2.3 to 3.0 kilos and being of three-four months of age (15 rabbits). Rabbits were fed daily with 0.2 g/kilo of cholesterol during twelve months. We defined the percentage volume, perimeter and the number of separate fibers per field of collagenous matrix and the volume of cardiomyocytes by computerized image analysis system connected with the microscope by CCD camera. We defined that various degree of stenosis of epicardial coronary arteries and their intramural branches leading to absolute lumen narrowing due to long duration of hypercholesterolemia (12 months) is the cause of chronic ischemia and remodelling of the myocardial structures of left and right ventricles. In case of chronic ischemia, cardiomyocytes in the left ventricle are replaced by multifocal reparative fibrosis, in the right ventricle such changes were not observed. Percentage volume of interstitial collagenous fibres increases about 1.2 (p<0.05) in the left ventricle and 1.26 times (p<0.05) in the right ventricle, i. e. interstitial fibrosis is being formed.

Analysis of Variance↗

PubMed1990

Interstitial cell infiltrate and myocardial fibrosis in dilated cardiomyopathy: a special type of cardiomegaly corresponding to sequelae of myocarditis.

We examined the relationship between interstitial cell infiltration and myocardial fibrosis in patients with clinically diagnosed dilated cardiomyopathy (DCM). Forty-two cases of DCM were divided into two groups, according to the mean number of the interstitial round cells per 10.2 x 10(4) square microns (Nic): the inflammatory group (Nic greater than or equal to 5) and noninflammatory group (Nic less than 5). The 12 cases in the inflammatory group were clinically similar to the 30 cases in the non-inflammatory group, but the inflammatory group exhibited a significantly (P less than 0.001) larger area of myocardial fibrosis (34.8% +/- 12.8% vs 17.5% +/- 8.2%), a significantly (P less than 0.01) higher frequency of diffuse perimyocytic-type fibrosis (83% vs 23%), fewer myocardial cells in the left ventricular wall (170 +/- 70 fibers vs 216 +/- 81 fibers), and significantly (P less than 0.01) greater hypertrophy of the myocytes (18.3 +/- 3.4 vs 15.3 +/- 2.7 microns). In addition, cases exhibiting marked fibrosis (fibrosis area greater than or equal to 25% of the myocardium) had a significantly higher Nic score (8.3 +/- 6.8) compared to cases with the less fibrotic type of DCM (4.0 +/- 5.7). We speculate that persistent or preceding inflammatory cell infiltration induces the myocardial fibrosis, especially the diffuse perimyocytic type, in the fibrosis-predominant type of DCM. Therefore, most of these cases may be a sequela of myocarditis, and more correctly termed post-myocarditic cardiomegaly.

Cardiomyopathy, Dilated↗

PubMed2002

Progressive cardiac hypertrophy and dysfunction in atrial natriuretic peptide receptor (GC-A) deficient mice.

OBJECTIVE: To investigate how permanent inhibition of guanylyl cyclase A receptor (GC-A) affects cardiac function. METHODS: Hearts of GC-A-/- and corresponding wild type mice (GC-A+/+) were characterised by histological, western blotting, and northern blotting analyses. Cardiac function was evaluated in isolated, working heart preparations. RESULTS: At 4 months of age, GC-A-/- mice had global cardiac hypertrophy (about a 40% increase in cardiac weight) without interstitial fibrosis. Examination of heart function found a significant delay in the time of relaxation; all other parameters of cardiac contractility were similar to those in wild type mice. At 12 months, the hypertrophic changes were much more severe (about a 61% increase in cardiac weight), together with a shift in cardiac gene expression (enhanced concentrations of atrial natriuretic peptide (3.8-fold), B type natriuretic peptide (2-fold), beta myosin heavy chain (1.6-fold) and alpha skeletal actin (1.7-fold) mRNA), increased expression of cytoskeletal tubulin and desmin (by 29.6% and 25.6%, respectively), and pronounced interstitial fibrosis. These changes were associated with significantly impaired cardiac contractility (+dP/dt decreased by about 10%) and relaxation (-dP/dt decreased by 21%), as well as depressed contractile responses to pressure load (all p < 0.05). CONCLUSIONS: Chronic hypertension in GC-A-/- mice is associated with progressive cardiac changes--namely, initially compensated cardiomyocyte hypertrophy, which is complicated by interstitial fibrosis and impaired cardiac contractility at later stages.

Animals↗

PubMed1994

Mineralocorticoids, hypertension, and cardiac fibrosis.

Uninephrectomized rats drinking 1% sodium chloride were given aldosterone (Aldo, 0.75 microgram/h, subcutaneous [s.c.] infusion), deoxycorticosterone (DOC, 20 mg/wk, s.c.), corticosterone (B, 2 mg/d, s.c.), or the antiglucocorticoid-antiprogestin RU486 (2 mg/d, s.c.) for 8 wk, and hemodynamic and tissue responses were compared with a non-steroid-treated control group. Aldo and DOC markedly increased systolic BP and caused considerable (40-50%) cardiac hypertrophy; B and RU486 caused neither hypertension nor cardiac hypertrophy. Measurements of ventricular cross-sectional areas showed hypertrophy due to an increase in mass of the left ventricle only. Cardiac hydroxyproline concentration was increased considerably by Aldo and DOC, to a lesser degree by RU486, and not by B. Aldo markedly elevated left ventricular interstitial collagen (2.5-fold vs control, P < 0.01 vs all groups); other steroid treatments also increased interstitial collagen over control (DOC x 1.8-, RU486 x 1.6-, B x 1.3-fold), with identical responses for right and left ventricles (r = 0.94). A different pattern of perivascular fibrosis was noted; DOC elevated perivascular collagen (2.1-fold vs control, P < 0.01 vs all other groups); RU486 raised levels 1.4-fold vs control, but neither Aldo nor B significantly affected perivascular collagen. These data are consistent with interstitial cardiac fibrosis reflecting type I (mineralocorticoid) receptor occupancy by administered Aldo or DOC, or by elevated endogenous B after type II (glucocorticoid) receptor blockade after RU486 administration; perivascular fibrosis may reflect a composite response after type I receptor agonist/type II glucocorticoid receptor antagonist occupancy.

Aldosterone↗

PubMed1992

Fibrosis of the human heart and systemic organs in adrenal adenoma.

In experimental animals, chronic mineralocorticoid (MC) excess is associated with fibrosis of the myocardium and systemic organs, where both a reactive, i.e. interstitial and perivascular, and reparative, i.e. microscopic scarring following cardiac myocyte necrosis, fibrosis are found. We sought to determine if a similar fibrous tissue response was present in human myocardium and systemic organs in association with adrenal adenoma. Postmortem specimens of heart, adrenals, pancreas, lungs, kidney and liver were obtained from 5 patients (age 67 +/- 5 years) with autopsy-proven adrenal adenoma. Documented histologically normal tissue from age-matched patients was used for comparison. Tissue sections were stained with the collagen specific stain Sirius Red F3BA and analyzed using normal and polarized light. Reactive and/or reparative fibrosis was found in the heart, pancreas, adrenal glands and lungs, but not in the kidney or liver. These observations support a link between chronic MC excess and fibrosis of the heart and systemic organs in humans with adrenal adenoma.

Adenoma↗

PubMed2000

Effects of myocardial edema on the development of myocardial interstitial fibrosis.

OBJECTIVE: The mechanism by which chronic myocardial edema causes cardiac dysfunction is poorly understood. We hypothesized that myocardial edema triggers cardiac fibrosis development resulting in cardiac dysfunction. Since collagen is the most abundant constituent of the interstitial matrix, we examined the effects of edema development on cardiac collagen metabolism. METHODS: We utilized a chronic pulmonary artery banded rat model that produces right ventricular hypertrophy with myocardial edema and left ventricular edema without hypertrophy or hyperplasia. Wet to dry ratios (index of edema), collagen type I and III concentrations, prolyl 4-hydroxylase (P4-H) and collagen type I and III mRNA levels, collagenase activity and transforming growth factor-beta were measured in both ventricles. RESULTS: Right and left ventricular wet to dry ratios were significantly elevated from 1 to 28 days after pulmonary artery banding compared to sham rats. Right and left ventricular collagen types I and III and P4-H mRNA levels increased significantly at 3 days followed by significant increases in right and left ventricular collagen concentration 7 days after pulmonary artery banding. Right ventricular collagenase activity increased at 3 days while left ventricular collagenase activity decreased 7 days after PA banding. CONCLUSIONS: We conclude that myocardial edema preceded the observed increase in collagen deposition and that edema may have triggered increased collagen synthesis by fibroblasts. leading to fibrosis development.

Animals↗

PubMed1979

Histopathological types of cardiac fibrosis in myocardial disease.

Myocardial fibrosis is a frequently observed pathologic finding. It is a common practice to differentiate macroscopic scarring and microscopic scarring, but there has been little attempt to distinguish the various types of interstitial fibrosis, and to determine their prevalence in different cardiac disorders. In this study, we have semiquantitatively assessed microscopic scarring, interfibre and perivascular fibrosis and a distinctive type of plexiform fibrosis. We examined ten hearts with congestive cardiomyopathy, ten with hypertrophic cardiomyopathy, ten with severe valvular aortic stenosis and ten normal hearts. Perivascular and interfibre fibrosis were quantitatively closely linked and most marked in the congestive cardiomyopathy and the valvular aortic stenosis groups. Plexiform fibrosis occurred maximally in the hypertrophic obstructive cardiomyopathy group, closely associated with myocardium exhibiting muscle fibre disarray. Our study demonstrates that although different types of interstitial fibrosis have particular associations with certain disease entities, the associations are not specific. The recognition of the prevalence of one or more types of interstitial fibrosis may, however, assist in the histopathologic diagnosis of certain myocardial disorders.

Adult↗

PubMed2001

Spironolactone and captopril attenuates isoproterenol-induced cardiac remodelling in rats.

The role of renin-angiotensin-aldosterone system in cardiac remodelling was studied in isoproterenol-induced cardiac hypertrophy in rats. The effects of captopril and spironolactone were compared. Isoproterenol treatment increased ventricular to body weight ratio (4.6 vs 3.7) and collagen area (22.6 vs 8.2%), and reduced systolic (89.93 vs 107.5 mm Hg) and diastolic (59.6 vs 70.8 mm Hg) pressure. In these animals, captopril decreased systolic (67.4 mm Hg) and diastolic pressure (31.9 mm Hg), whereas spironolactone regressed systolic pressure to control values (101.2 mm Hg). Captopril and spironolactone prevented cardiac hypertrophy (4.01 and 3.95). However, only spironolactone prevented myocardial fibrosis (11.3%).

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1985

Three autopsy cases of progression to left ventricular dilatation in patients with hypertrophic cardiomyopathy.

The hearts of three cases of congestive heart failure with dilated left ventricles developing in patients with symptomatic hypertrophic cardiomyopathy (HCM) were morphologically investigated. The results showed that disproportionate hypertrophy and dilatation of the left ventricles, accompanied by massive fibrosis and myocardial disarray, were present in the three patients. The mean percent area of fibrosis of the left ventricle was 34.7% and 47.4% at the upper third and lower third levels, respectively, and was much more frequently associated with disarray (84.4 +/- 12.3%). Moreover, the fibrosis was most extensive in the lateral wall of the left ventricle, followed by the posterior, anterior, and interventricular walls. The fibrosis was also diffuse regardless of the subendocardial or subepicardial region of the heart. The findings in the present study suggest that the disarray in this particular series of HCM might be responsible for the mechanism of the fibrosis leading to dilatation of the left ventricle.

Adolescent↗

PubMed2001

Prevention of aortic and cardiac fibrosis by spironolactone in old normotensive rats.

OBJECTIVES: Because the synthesis of aldosterone is mainly modulated by angiotensin II through type I receptor stimulation and because converting enzyme inhibition (CEI) does not modify aortic extracellular matrix in old normotensive rats, the aim of the present study was to determine whether inhibition of aldosterone formation was able to prevent aortic fibrosis in old Sprague-Dawley normotensive rats. BACKGROUND: We have previously shown that long-term aldosterone antagonism prevents the age-related increase in aortic collagen accumulation in young spontaneously hypertensive rats, independent of blood pressure changes. In contrast, we reported that the positive effects of CEI in the prevention of aortic collagen accumulation were related to the inhibition of angiotensin II actions on angiotensin II type I receptors. METHODS: For this purpose, we studied the histomorphometric and stiffness (echo-tracking technique) changes of an eight-week treatment with the aldosterone antagonist spironolactone by comparison with placebo. RESULTS: At the end of treatment, spironolactone in conscious animals did not change intra-arterial blood pressure, aortic and carotid wall thickness, and cardiac weight. Cardiac collagen density and, to a lesser extent, carotid collagen and elastin densities and contents were significantly decreased in association with an increase of carotid distensibility. CONCLUSIONS: These results show that in old normotensive rats, spironolactone can markedly prevent cardiac and, to a lesser extent, arterial fibrosis and improve arterial stiffness, despite a lack of hypotensive effect.

Age Factors↗

PubMed1983

[Roentgenmorphologic findings in scleroderma].

In 28 patients with progressive systemic sclerosis clinical symptoms are correlated with roentgen findings. The systemic disease of connective tissue shows typical roentgenological signs, such as soft tissue calcifications, generalized or localized osteoporosis, arthritis, dysfunction of oesophagus, small and large bowel, pulmonary fibrosis and cardiomegaly. A limited prognostic statement according to a clinical and radiological classification seems possible.

Adolescent↗

PubMed2004

Hypertensive myocardial fibrosis and diastolic dysfunction: another model of inflammation?

Excessive myocardial fibrosis deteriorates diastolic function in hypertensive hearts. Involvement of macrophages is suggested in fibrotic process in various diseased situations. We sought to examine the role of macrophages in myocardial remodeling and cardiac dysfunction in pressure-overloaded hearts. In Wistar rats with suprarenal aortic constriction, pressure overload induced perivascular macrophage accumulation and fibroblast proliferation with a peak at day 3, decreasing to lower levels by day 28. Myocyte chemoattractant protein (MCP)-1 mRNA was upregulated after day 1, peaking at day 3 and returning to insignificant levels by day 28, whereas transforming growth factor (TGF)-beta induction was observed after day 3, with a peak at day 7, and remained relatively elevated at day 28. After day 7, concentric left ventricular (LV) hypertrophy developed, associated with reactive fibrosis and myocyte hypertrophy. At day 28, echocardiography showed normal LV fractional shortening but decreased ratio of early to late filling wave of transmitral Doppler velocity, and hemodynamic studies revealed elevated LV end-diastolic pressure, suggesting normal systolic but impaired diastolic function. Chronic treatment with an anti-MCP-1 monoclonal neutralizing antibody inhibited not only macrophage accumulation but also fibroblast proliferation and TGF-beta induction. Furthermore, the neutralizing antibody attenuated myocardial fibrosis, but not myocyte hypertrophy, and ameliorated diastolic dysfunction without affecting blood pressure and systolic function. In conclusion, roles of MCP-1-mediated macrophage accumulation are suggested in myocardial fibrosis in pressure-overloaded hearts through TGF-beta-mediated process. Inhibition of inflammation may be a new strategy to prevent myocardial fibrosis and resultant diastolic dysfunction in hypertensive hearts.

Animals↗

PubMed1998

Early induction of transforming growth factor-beta via angiotensin II type 1 receptors contributes to cardiac fibrosis induced by long-term blockade of nitric oxide synthesis in rats.

We previously reported that the chronic inhibition of nitric oxide (NO) synthesis increases cardiac tissue angiotensin-converting enzyme expression and causes cardiac fibrosis in rats. However, the mechanisms are not known. Transforming growth factor-beta (TGF-beta) is a key molecule that is responsible for tissue fibrosis. The present study investigated the role of TGF-beta in the pathogenesis of cardiac fibrosis. The development of cardiac fibrosis by oral administration of the NO synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) to normal rats was preceded by increases in mRNA levels of cardiac TGF-beta1 and extracellular matrix (ECM) proteins. TGF-beta immunoreactivity was increased in the areas of fibrosis. Treatment with a specific angiotensin II type 1 receptor antagonist, but not with hydralazine, completely prevented the L-NAME-induced increases in the gene expression of TGF-beta1 and ECM proteins and also prevented cardiac fibrosis. Intraperitoneal injection of neutralizing antibody against TGF-beta did not affect the L-NAME-induced increase in TGF-beta1 mRNA levels but prevented an increase in the mRNA levels of ECM protein. These results suggest that the early induction of TGF-beta1 via the angiotensin II type 1 receptor plays a major role in the development of cardiac fibrosis in this model.

Administration, Oral↗

PubMed1999

Myocardial fibrosis in polymyositis.

Myocardial involvement in polymyositis is commonly suspected in noninvasive studies, but symptomatic cardiac disease is rare. We describe a 27-year-old woman with a 6 year history of severe polymyositis and persistent elevation of creatine phosphokinase-MB isoenzyme who suddenly developed congestive heart failure and bradycardia-tachycardia syndrome. Autopsy revealed severe myocardial fibrosis without inflammatory cell infiltrates concomitant to active polymyositis of the skeletal muscles despite intensive longterm immunosuppressive therapy.

Adult↗

PubMed1993

Myocardial fibrosis: role of angiotensin II and aldosterone.

In this report we review the replacement (i.e., scarring) and reactive (i.e., perivascular and interstitial fibrosis) fibrous tissue responses found in the myocardium in response to effector hormones of the renin-angiotensin-aldosterone system. Experimental data are presented to indicate: a) endogenous or exogenous elevations in plasma angiotensin II are associated with acute cardiac myocyte necrosis and subsequent microscopic scarring; b) chronic elevations in plasma aldosterone (ALDO), relative to Na+ intake, are associated with a perivascular and interstitial fibrosis of the coronary and systemic circulations and are also seen in response to chronic administration of the mineralocorticoid hormone deoxycorticosterone (DOC); and c) chronic mineralocorticoid excess, due to ALDO or DOC, is associated with enhanced urinary K+ excretion, cardiac myocyte necrosis and scarring. Pharmacologic agents which interfere with these effector hormones (e.g., ACE inhibition and ALDO receptor antagonism) protect the myocardium against this pathologic structural remodeling created by the reactive and replacement (reparative) fibrosis. Evidence is also presented to indicate that chronic ACE inhibition is associated with a regression in reactive myocardial fibrosis. Based on these experimental findings we would suggest that clinical trials are indicated to address the prevention and regression of myocardial fibrosis--an important determinant of pathologic structural remodeling and abnormal myocardial stiffness.

Aldosterone↗

PubMed2005

[MRI in chronic myocarditis].

In most cases inflammatory changes of the myocardium are asymptomatic. If inflammatory changes of the myocardium manifest with clinical symptoms, the condition is termed myocarditis. Myocarditis is regarded as a major cause for sudden death of young adults and accounts for up to 20% of the cases. In Europe viral infections represent the most important cause of myocarditis. In chronic myocarditis, viremia is often absent and myocardial fibrosis and dilated cardiomyopathy (DCM) resulting in heart failure can occur. The role of cardiac MRI in chronic myocarditis is not yet well understood. MRI is a sensitive tool detecting myocardial fibrosis on late images after application of paramagnetic contrast agents. The region of contrast accumulation is defined as "late enhancement" (LE). Data are available now suggesting that differentiating fibrosis due to myocardial infarction from inflammatory causes is facilitated using MRI late images. Fibrosis after ischemic infarction includes the subendocardial layer of the myocardium. If the subendocardial layer of the myocardium is not involved in the fibrosis, infarction is unlikely and can be reliably excluded as an important differential diagnosis in the vast majority of affected patients.

Chronic Disease↗