SEARCH · PubMed Health

Results for “ENDOMYOCARDIAL FIBROSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources

PubMed1985

The reliability of the tracing-method of fine cardiac fibrosis at a magnification of x10--preliminary study for quantitative analysis of fibrosis in large tissue sections of hearts with cardiomyopathy.

to define the reliability of the tracing method of fine fibrosis at low magnification (x10), the percentage area of fine fibrosis was compared between the traced pictures at magnifications of x10 and x250, using an image analyzer (Olympus VIP-21). A total of 25 tissue areas, each approximately 4 x 7 mm, from the inner and middle thirds of the left ventricular free wall and ventricular septum were selected from ten hearts with hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) and were stained with Masson trichrome. The percentage areas of fine fibrosis traced at a magnification of x10 correlated well with those traced at a magnification of x250 (Y = 1.08X - 1.1, r = 0.95, P less than 0.01). It is concluded that the overall percentage area of fibrosis is the same at magnifications of x10 and x250, despite the fact that at x10 one is unable to detect individual fibers which can be detected at x250. The tracing method of fine cardiac fibrosis at a magnification of x10 is reliable. Therefore, fine fibrosis in large tissue sections of hearts with cardiomyopathy, such as entire transverse sections of the left ventricular wall, can be quantitatively analyzed by this method.

Cardiomyopathies↗

PubMed1982

The pattern of myocardial degeneration in nonischemic congestive cardiomyopathy.

The histopathologic features of nonischemic congestive cardiomyopathy (CCM) include diffuse and focal fibrosis, vacuolar degeneration, and myofiber hypertrophy. Eleven patients with CCM and five controls were studied. Fibrosis and degree of vacuolization were quantified by means of stereologic techniques; myocardial cell diameter was measured with an ocular micrometer. Five levels of the left ventricular free wall were examined. Area I was immediately subepicardial, and area 5 was immediately subendocardial. In all areas, fibrosis, vacuolization, and fiber diameter were significantly greater in the experimental group than in the control group (P less than 0.05). In addition, fibrosis and vacuolization had an umbrella distribution, which peaked in area 4, the area adjacent to the subendocardium (P less than 0.01). The distributions of fibrosis and vacuolar degeneration suggest compromised blood flow to the inner myocardial layers, with relative sparing of the immediate subendocardial region owing to its proximity to the left ventricular cavity.

Adult↗

PubMed2002

Efficacy of contrast-enhanced MR imaging in cardiomyopathy: an experimental study using Bio14.6 hamsters.

RATIONALE AND OBJECTIVES: Myocardial fibrosis was evaluated with magnetic resonance (MR) imaging in Bio14.6 hamsters. MATERIALS AND METHODS: Gated gradient-echo T1-weighted images and spin-echo images with gadopentetate dimeglumine enhancement (0.2 mmol/kg) were obtained. RESULTS: Myocardial enhancement persisted for 13 minutes after administration of gadopentetate dimeglumine, and myocardial signal intensity peaked at 13 minutes on gradient-echo T1-weighted images. The enhanced areas were greater in Bio14.6 hamsters at 25-42 weeks than at 10 weeks. Pathologic data revealed enhancement with inflammation at 10 weeks and fibrosis with vessel proliferation at 25-42 weeks. Pathologic fibrotic change was greater at 32-42 weeks than at 10 weeks. The myocardium of 42-week-old Bio14.6 hamsters showed remarkable contrast enhancement, which continued for 13 minutes. There was no correlation between gadolinium enhancement and pathologic findings in the evaluation of myocardial degeneration and fibrosis. CONCLUSION: Gadolinium-enhanced MR imaging was useful for estimating myocardial fibrotic changes with vessel proliferation and myocardial damage.

Age Factors↗

PubMed2005

Cardiomyopathy in Becker muscular dystrophy--does regional fibrosis mimic infarction?

We present a case of a 39-year-old man with Becker muscular dystrophy and severe congestive cardiac failure. Cardiac magnetic resonance imaging revealed subendocardial late gadolinium enhancement, similar to that seen in myocardial infarction. He had no risk factors for atherosclerotic coronary artery disease and coronary angiography was normal. We propose that regional subendocardial myocardial fibrosis which has been described histologically in the cardiomyopathy associated with Becker muscular dystrophy may resemble previous infarction at contrast enhanced cardiac magnetic resonance imaging.

Adult↗

PubMed2005

Protection from angiotensin II-induced cardiac hypertrophy and fibrosis by systemic lentiviral delivery of ACE2 in rats.

Angiotensin converting enzyme 2 (ACE2), a newly discovered member of the renin-angiotensin system (RAS), is a potential therapeutic target for the control of cardiovascular disease owing to its key role in the formation of vasoprotective peptides from angiotensin II. The aim of the present study was to evaluate whether overexpression of ACE2 could protect the heart from angiotensin II-induced hypertrophy and fibrosis. Lentiviral vector encoding mouse ACE2 (lenti-mACE2) or GFP was injected intracardially in 5-day-old Sprague-Dawley rats. This resulted in expression of mACE2 in cardiac tissue for the duration of the study. Infusion of 200 ng kg-1 min-1 angiotensin II for 4 weeks resulted in an 80 mmHg increase in systolic blood pressure, a significant increase in the heart weight to body weight ratio (HW:BW), and marked myocardial fibrosis in control rats. Transduction with lenti-mACE2 resulted in significant attenuation of the increased HW:BW and myocardial fibrosis induced by angiotensin II infusion. These observations demonstrate that ACE2 overexpression results in protective effects on angiotensin II-induced cardiac hypertrophy and fibrosis.

Angiotensin II↗

PubMed1995

Myocardial fibrosis and stiffness with hypertrophy and heart failure in the spontaneously hypertensive rat.

BACKGROUND: Fibrosis is commonly found in association with cardiac hypertrophy and failure, but the relation of the connective tissue response to the development of impaired cardiac function remains unclear. We examined passive myocardial stiffness, active contractile function, and fibrosis in the spontaneously hypertensive rat (SHR), a model of chronic pressure overload in which impaired cardiac function follows a long period of stable hypertrophy. METHODS AND RESULTS: We studied the passive and active mechanical properties of left ventricular (LV) papillary muscles isolated from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) at the ages of 12 months and 20 to 23 months. Seven of 15 SHR between 20 and 23 months of age had findings consistent with heart failure (SHR-F). In comparison to preparations from WKY rats and nonfailing SHR (SHR-NF), papillary muscles from the SHR-F group demonstrated increased passive stiffness (central segment exponential stiffness constant, kcs: SHR-F 95.6 +/- 19.8, SHR-NF 42.1 +/- 9.7, WKY rats 39.5 +/- 9.5 (mean +/- SD); SHR-F P < .01 versus SHR-NF, WKY rats). The increase in stiffness was associated with an increase in LV collagen concentration (SHR-F 8.71 +/- 3.14, SHR-NF 5.83 +/- 1.20, WKY rats 4.78 +/- 0.70 mg hydroxyproline/g dry LV wt; SHR-F P < .01 versus SHR-NF, WKY rats); an increase in interstitial fibrosis, as determined histologically (SHR-F 13.5 +/- 8.0%, SHR-NF 4.9 +/- 2.1%, WKY rats 3.6 +/- 0.8%; SHR-F P < .01 versus SHR-NF, WKY rats); and impaired tension development (SHR-F 3.18 +/- 1.27, SHR-NF 4.41 +/- 1.04, WKY rats 4.64 +/- 0.85 kdyne/mm2; SHR-F P < .05 versus SHR-NF; P < .01 versus WKY rats). CONCLUSIONS: The development of heart failure in the aging SHR is associated with marked myocardial fibrosis, increased passive stiffness, and impaired contractile function relative to age-matched nonfailing SHR and nonhypertensive control animals. These data suggest that fibrosis or events underlying the connective tissue response are important in the transition from compensated hypertrophy to failure in the SHR.

Aging↗

PubMed2006

Antifibrotic activity of an inhibitor of group IIA secretory phospholipase A2 in young spontaneously hypertensive rats.

The development of fibrosis in the chronically hypertensive heart is associated with infiltration of inflammatory cells and cardiac hypertrophy. In this study, an inhibitor of the proinflammatory enzyme, group IIA human secretory phospholipase A2 (sPLA2-IIA), has been found to prevent collagen deposition as an important component of cardiovascular remodeling in a rat model of developing chronic hypertension. Daily treatment of young male spontaneously hypertensive rats (SHR) with an sPLA2-IIA inhibitor (KH064, 5-(4-benzyloxyphenyl)-4S-(phenyl-heptanoylamino)-pentanoic acid, 5 mg/kg/day p.o.) prevented increases in the content of perivascular (SHR 20.6 +/- 0.9%, n = 5; SHR+KH064 14.0 +/- 1.2%, n = 5) and interstitial (SHR 7.9 +/- 0.3%, n = 6; SHR+KH064 5.4 +/- 0.7%, n = 6) collagen in the left ventricle of rat hearts, but did not affect numbers of infiltrating monocytes/macrophages, left ventricular hypertrophy (SHR 2.88 +/- 0.08, n = 12; SHR+KH064 3.09 +/- 0.08 mg/g body weight, n = 9), increased systolic blood pressure, or thoracic aortic responses. This selective antifibrotic activity suggests that sPLA2-IIA may have an important but specific role in cardiac fibrosis, and that its inhibitors could be useful in dissecting molecular pathways leading to fibrotic conditions.

Actins↗

PubMed1998

[Heart enlargement in an athlete--a diagnostic challenge].

Endurance training can result in an enlargement of the heart. These athlete's hearts are rarer than generally assumed. Pathological causes, resulting in an eccentric hypertrophy, have to be considered. We report on a 32 year old athlete performing approximately 10 hours of endurance training weekly. He consulted a physician because of a drop in performance. The eccentric left ventricular hypertrophy, diagnosed by means of echocardiography, was not interpreted as a solely physiological cardiac adaptation because the ejection fraction did not increase during exercise (stress-echocardiography), the left ventricular diastolic function (maximum E/A-ratio) was impaired at rest, and the ergometric performance was reduced in comparison to the heart size. The invasive diagnostics including myocardial biopsy demonstrate histologically a focal fibrosis as the result of former myocarditis. The fibrosis was possibly involved in the genesis of the eccentric hypertrophy based on structural dilatation through a preferably mesenchymal lesion. It remains open whether the long-term endurance training had forced the dilatation. This case demonstrates that pathological causes must be excluded if in athletes an enlarged heart does not concur together with a clearly increased ergometric performance. Stress-echocardiography and endomyocardial biopsy can considerably contribute to the differential diagnosis between physiological and pathological cardiac hypertrophy.

Adult↗

PubMed1998

Fibrosis, myocyte degeneration and heart failure in chronic experimental aortic regurgitation.

Myocardial fibrosis and myocyte degeneration have been reported in patients with chronic aortic regurgitation (AR), and may be related to the pathophysiology of congestive heart failure (CHF) in this disease. To define the relationship between myocardial histopathologic variations and CHF in chronic AR, we performed gross and microscopic evaluations of postmortem tissue from a rabbit model of chronic AR manifesting left ventricular (LV) responses to AR similar to those in humans. Moderate-to-severe chronic AR (echocardiographic regurgitant fraction = 52 +/- 13%) was induced by closed-chest aortic valve perforation in 11 New Zealand White rabbits; 5 control rabbits were sham operated. Six of the 11 AR rabbits died 1.5 +/- 0.8 years (range 0.6-2.8 years) after AR induction; all 6 had gross and histologic anatomic evidence of CHF at necropsy. The remaining 5 AR rabbits survived until sacrifice at 2.9 +/- 0.1 years of AR; none had pathologic evidence of CHF. Cardiac hypertrophy and the extent of LV fibrosis and myocyte necrosis all were greatest among the 6 AR CHF rabbits. No inflammatory response was apparent in any animal. Moderate-to-severe chronic experimental AR frequently results in CHF which is strongly associated with myocardial fibrosis and necrosis, without evidence of inflammation. These histopathologic variations may be pathophysiologically related to CHF development.

Animals↗

PubMed1989

Acute angular origin of left coronary artery from aorta: an unusual cause of left ventricular failure in infancy.

An unusual congenital anomaly of the left coronary artery, consisting of ostial stenosis caused by an acute angular origin of the vessel from the aorta in an infant, is presented. This anomaly resulted in progressive myocardial fibrosis and development of left ventricular congestive heart failure. The clinical state mimicked anomalous origin of the left coronary artery from the pulmonary artery.

Coronary Vessel Anomalies↗

PubMed1995

Molecular and cellular biology of the senescent hypertrophied and failing heart.

During aging, experimental studies have revealed various cellular changes, principal among which is myocyte hypertrophy, which compensates for the loss of myocytes and is associated with fibrosis. The expression of alpha-myosin heavy chain is replaced by that of the isogene beta-myosin, which leads to decreased myosin adenosine triphosphatase (ATPase) activity. In consequence, contraction is slower and more energetically economical. The Ca(2+)-ATPase of the sarcoplasmic reticulum and Na+/Ca2+ exchange activity are decreased, which probably explains the reduced velocity of relaxation. Membrane receptors are also modified, since the density of both the total beta-adrenergic and muscarinic receptors is decreased. The senescent heart is able to hypertrophy in response to overload and to adapt to the new requirements. Similar alterations are observed both in the senescent heart and in the overloaded heart, in clinical as well as in experimental studies; however, differences do exist, especially in terms of fibrosis and arrhythmias.

Adaptation, Physiological↗

PubMed2003

Elevated serum tryptase levels identify a subset of patients with a myeloproliferative variant of idiopathic hypereosinophilic syndrome associated with tissue fibrosis, poor prognosis, and imatinib responsiveness.

Since serum tryptase levels are elevated in some patients with myeloproliferative disorders, we examined their utility in identifying a subset of patients with hypereosinophilic syndrome (HES) and an underlying myeloproliferative disorder. Elevated serum tryptase levels (> 11.5 ng/mL) were present in 9 of 15 patients with HES and were associated with other markers of myeloproliferation, including elevated B12 levels and splenomegaly. Although bone marrow biopsies in these patients showed increased numbers of CD25+ mast cells and atypical spindle-shaped mast cells, patients with HES and elevated serum tryptase could be distinguished from patients with systemic mastocytosis and eosinophilia by their clinical manifestations, the absence of mast cell aggregates, the lack of a somatic KIT mutation, and the presence of the recently described fusion of the Fip1-like 1 (FIP1L1) gene to the platelet-derived growth factor receptor alpha gene (PDGFRA). Patients with HES and elevated serum tryptase were more likely to develop fibroproliferative end organ damage, and 3 of 9 died within 5 years of diagnosis in contrast to 0 of 6 patients with normal serum tryptase levels. All 6 patients with HES and elevated tryptase treated with imatinib demonstrated a clinical and hematologic response. In summary, elevated serum tryptase appears to be a sensitive marker of a myeloproliferative variant of HES that is characterized by tissue fibrosis, poor prognosis, and imatinib responsiveness.

Adolescent↗

PubMed1997

Chronic inhibition of NO synthesis produces myocardial fibrosis and arterial media hyperplasia.

Pathophysiological effects of nitric oxide (NO)-deficient hypertension are much better known than are the potential morphological changes. Hearts and main arteries were studied in 15 week old male Wistar rats administered NG-nitro-L-arginine methyl ester (L-NAME) for 4 weeks. A does of 40 mg/kg/day increased systolic arterial pressure by 30%, while heart rate decreased by 20%. Heart/body weight ratios were not significantly changed. Total cardiac RNA and DNA content and [14C]leucine incorporation into myocardial protein were, however, increased by 15%, 228% and 97%, respectively. Light microscopy of hearts showed subendocardial areas of necrosis along with different stages of healing. Morphometric evaluation demonstrated significant increase in myocardial fibrosis. Serum lactate dehydrogenase increased by 91%. Proliferation cell nuclear antigen (PCNA) immunohistochemistry indicated positive cells in areas of postischemic repair. Chronic inhibition of NO synthase (NOS) resulted in periarterial fibrosis and hyperplasia of the media in coronary arteries and aorta. RNA and DNA content, and [14C]leucine incorporation into protein of aorta increased by 255%, 95% and 49%, respectively. PCNA staining showed numerous positive nuclei in the media of coronary arteries and the aorta. It is concluded that inhibition of NOS leads to systemic hypertension with focal myocardial fibrosis reflecting reparative responses associated to ischemic injury. This sequence of alterations involves impaired arterial relaxation, and uncontrolled vascular medial proliferation attributed to the absence of smooth muscle cell proliferation inhibition by NO.

Animals↗

PubMed1997

Myocyte necrosis is the basis for fibrosis in renovascular hypertensive rats.

The pathogenesis of fibrosis and the functional features of pressure overload myocardial hypertrophy are still controversial. The objectives of the present study were to evaluate the function and morphology of the hypertrophied myocardium in renovascular hypertensive (RHT) rats. Male Wistar rats were sacrificed at week 4 (RHT4) and 8 (RHT8) after unilateral renal ischemia (Goldblatt II hypertension model). Normotensive rats were used as controls. Myocardial function was analyzed in isolated papillary muscle preparations, morphological features were defined by light microscopy, and myocardial hydroxyproline concentration (HOP) was determined by spectrophotometry. Renal artery clipping resulted in elevated systolic arterial pressure (RHT4: 178 +/- 19 mmHg and RHT8: 194 +/- 24 mmHg, P < 0.05 vs control: 123 +/- 7 mmHg). Myocardial hypertrophy was observed in both renovascular hypertensive groups. The myocardial HOP concentration was increased in the RHT8 group (control: 2.93 +/- 0.38 micrograms/mg; RHT4: 3.02 +/- 0.40 micrograms/mg; RHT8: 3.44 +/- 0.45 micrograms/mg of dry tissue, P < 0.05 vs control and RHT4 groups). The morphological study demonstrated myocyte necrosis, vascular damage and cellular inflammatory response throughout the experimental period. The increased cellularity was more intense in the adventitia of the arterioles. As a consequence of myocyte necrosis, there was an early, local, conjunctive stroma collapse with disarray and thickening of the argyrophilic interstitial fibers, followed by scarring. The functional data showed an increased passive myocardial stiffness in the RHT4 group. We conclude that renovascular hypertension induces myocyte and arteriole necrosis. Reparative fibrosis occurred as a consequence of the inflammatory response to necrosis. The mechanical behavior of the isolated papillary muscle was normal, except for an early increased myocardial passive stiffness.

Animals↗

PubMed2004

Increased deposition of von Willebrand factor in the rat heart after local ionizing irradiation.

BACKGROUND AND PURPOSE: Von Willebrand factor (vWf), a glycoprotein involved in blood coagulation, is synthesized by endothelial cells. Increased amounts of vWf in blood plasma or tissue samples are indicative of damaged endothelium. In the present study, mRNA expression and localization of vWf were determined in irradiated rat heart tissue. MATERIAL AND METHODS: Sprague-Dawley rats received local heart irradiation with a single dose of 0, 15, or 20 Gy. Hearts were dissected at different time points (up to 16 months) after irradiation. In a second experiment, rats were injected with the radioprotector amifostine (160 mg/kg, i. p.) 15-20 min before irradiation and sacrificed after 6 months. Immunohistochemistry was performed using a polyclonal anti-vWf antibody. Serial sections were subjected to a general rat endothelial cell immunostaining (RECA-1) or a collagen staining (picrosirius red). mRNA expression was determined by using PCR. RESULTS: In control tissue, all endothelial cells lining the lumen of the endocardium and coronary arteries, but not capillary endothelial cells, were stained for vWf. 1 month after irradiation with both 15 and 20 Gy, myocardial capillaries became immunoreactive. From 3 months onward, staining was observed also within the extracellular matrix (ECM) of fibrotic areas. At mRNA level, no changes in vWf could be observed at all time points after irradiation, suggesting that vWf deposition was not due to increased biosynthesis of the protein. In sections of amifostine-treated rat hearts, vWf staining was increased to a lesser extent. CONCLUSION: These dose- and time-dependent increases in deposition of vWf indicate the presence of damaged endothelium in the irradiated rat heart. These increases in vWf accumulation precede development of fibrosis in the subendocardial layer and myocardium of the left ventricles, right ventricles, and atria.

Amifostine↗

PubMed1975

[Coronaro-myocardial interplay determining the instantaneous mean ventricular shape (author's transl)].

A working hypothesis on the mechanism of diastolic chamber expansion based on functional anatomy and physiology is developed. It should be a major determinant of the momentary average chamber width. The sum of all intramyocardial fluid-filled spaces and the myocardium itself are considered in the working hypothesis as the hydraulic medium of a process which can be summarised under the term "cavernous body mechanism". The most important factor of this hydraulic system should represent the intramural fluid volume (hydraulic medium) and the contractile-elastic tension development in the transmural direction of the chamber wall. Morphological analysis of myocardial structure shows that an endoepicardial direction of force in the myocardial net can be recognised. The "motor" of circular fibres of the middle layer is surrounded by the spiral course of the fibres of the inner and outer layers of the chamber wall (uvula mechanism). It is interwoven by very dense bifurcating myocardial fibres (structural principle of the tongue). By these means, the width of the chamber cone is influenced decisively by an active decrease in wall thickness. The coronary perfusion pressure is thought to have a chamber dilating influence in the sense of a "cavernous body mechanism". The hypothesis presented helps us to understand pathological chamber dilation secondary to transmural myocardial fibrosis. Such a narrow functional coronary-myocardial interaction gives the myocardium two functions; besides haemodynamic pumping, the cardial muscle must function as an internal antagonist to favour diastolic chamber dilation.

Animals↗

PubMed2003

Sub-depressor dose of angiotensin type-1 receptor blocker inhibits transforming growth factor-beta-mediated perivascular fibrosis in hypertensive rat hearts.

Recently, we have shown that pressure overload transiently induces transforming growth factor-beta-mediated fibroblast proliferation and reactive myocardial fibrosis that extends from the perivascular space. However, the upper stream event of transforming growth factor-beta induction has remained unknown. Thus, we sought to determine whether angiotensin II mediates the fibrotic process in pressure-overloaded hearts. Male Wistar rats were administered orally everyday 0.1 mg/kg per day of candesartan, an angiotensin type-1 receptor blocker, or the vehicle from Day 7, and underwent a suprarenal aortic constriction (AC) at Day 0. This dose was the maximum dose of candesartan that does not induce the depressor effect in AC rats. In AC+ vehicle (control) rats, pressure overload induced myocardial transforming growth factor-beta expression and perivascular fibroblast proliferation at Day 3 and thereafter left ventricular hypertrophy associated with cardiomyocyte hypertrophy and perivascular fibrosis. AC+ candesartan rats showed suppressed transforming growth factor-beta expression and reduced number of proliferating fibroblasts, while not changing arterial pressure. Furthermore, perivascular fibrosis, but not myocyte hypertrophy, was significantly inhibited associated with reduced collagen mRNA expression. In conclusion, angiotensin II may play a role in reactive myocardial fibrosis in pressure-overloaded hearts, through the mechanism independent of hemodynamic change.

Administration, Oral↗

PubMed1998

The flat electrocardiogram--systole or asystole?

A case of stone heart syndrome is reported in a pregnant 27 year old West African patient, who suffered syncopal symptoms shortly before cardiac arrest. The electrocardiographic features were those of asystole, but direct examination of the heart at emergency thoracotomy in the A&E department revealed tetanic contracture of the organ. At necropsy, the heart was of normal weight but showed areas of fibrosis surrounding the bundle of His. The discrepancy between the ECG features and the physiological state of the heart raises the possibility that other cases of apparent asystole may not be what they seem.

Adult↗