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Results for “ENDOMYOCARDIAL FIBROSIS”

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At least 757 records · Page 42Linked to original sources
PubMed1995

Collagen VI in the extracellular matrix of normal and failing human myocardium.

Our own previous studies of the composition of the extracellular matrix of human failing hearts showed that collagen VI seems to play a major role in the origin of cardiac fibrosis. Therefore, collagen VI was investigated in more detail in tissue samples taken from clinically normal left ventricle and from myocardium failing because of dilated cardiomyopathy. Tissue sections prepared with collagen VI antibodies were examined by fluorescence microscopy using conventional or confocal laser scanning microscopy. In normal myocardium, collagen VI was located in both, endomysium and perimysium, in blood vessels it surrounded closely individual myocytes. Failing myocardium showed enlargement of the extracellular space and collagen VI was abundant. The localisation was perivascular as well as interstitial in fine or thick bundles enclosing the myocytes completely. In hearts with far progressed failure areas of replacement fibrosis containing increased amounts of collagen VI were evident. Double-staining for vimentin and collagen VI revealed a close interaction with fibroblasts. Although the function of collagen VI is not yet entirely clear it seems obvious that collagen VI plays an important role in the development of fibrosis in the failing heart.

Actins↗
PubMed1989

Relation between coronary stenosis and myocardial lesions determined by a semiquantitative approach to myocardial fibrosis and hypertrophy due to ischemia.

To clarify the cause of myocardial hypertrophy in ischemic heart disease, the relation between the extent of fibrosis and myocyte diameter was examined in patients with cardiac hypertrophy of unknown etiology except for coronary sclerosis. In 79 unselected cases, the heart weight tended to be higher in patients with severe coronary stenosis and fibrosis. In a morphometric study of 33 additional hearts of patients without a clinical history of hypertension, valvular disease or diabetes mellitus, 15 of which had anterior infarction, a positive correlation (r = 0.63) was observed between myocyte diameter and the percent area of fibrosis in the anterior wall of the left ventricle. In the heart of patients with severe coronary stenosis (more than 75% luminal narrowing), the regression coefficient was 0.83. The hearts of 8 patients with nontransmural infarction showed a strong correlation between myocyte diameter and fibrosis, compared with the hearts of 7 patients with transmural infarction. In most cases, the main mechanism of hypertrophy in ischemic heart disease was considered to be compensatory hypertrophy for existence of myocardial fibrosis.

Adult↗
PubMed1997

Remodeling after myocardial infarction in humans is not associated with interstitial fibrosis of noninfarcted myocardium.

OBJECTIVES: This study was specifically designed to evaluate whether noninfarcted hypertrophic myocardium in patients with end-stage heart failure after myocardial infarction (MI) is associated with an increase in interstitial fibrous tissue. BACKGROUND: Postinfarction remodeling consists of complex alterations that involve both infarcted and noninfarcted myocardium. The question arises whether ventricular dysfunction is due to physical events, such as inadequate myocardial hypertrophy to compensate for increased tangential wall stress, or is caused by the development of progressive interstitial fibrosis in noninfarcted myocardium. METHODS: Fifteen hearts were obtained as cardiac explants (n = 13) or at autopsy (n = 2) from patients with end-stage coronary artery disease. Sixteen normal hearts served as reference hearts. Samples were taken from the left ventricular (LV) wall that contained the infarcted area, the border area and noninfarcted myocardium remote from scar areas. Collagen was quantified biochemically and microdensitophotometrically. Collagen type I and III ratios were analyzed by using the cyanogen bromide method and immunohistochemical staining, followed by microdensitophotometric quantification. RESULTS: In noninfarcted myocardium remote from the scar areas, total collagen levels and collagen type I/III ratios did not differ statistically from those in reference hearts. These observations contrasted with high total collagen content and high collagen type I/III ratios in scar and border areas. CONCLUSIONS: Remodeling of LV myocardium after MI in patients with end-stage heart failure is not necessarily associated with interstitial fibrosis in noninfarcted hypertrophic myocardium remote from scar areas. This finding raises questions regarding therapeutic interventions designed to prevent or retard the development of interstitial fibrosis.

Adult↗
PubMed2004

Hypertensive heart disease: effects of lifestyle modifications and antihypertensive drug treatment.

Target-organ protection in hypertensive patients has become increasingly important. This review will focus on hypertensive heart disease that is mainly characterized by myocardial hypertrophy and increased interstitial fibrosis. Cardiac remodeling develops as an adaptive response but actually represents a powerful independent risk factor for cardiovascular morbidity and mortality. The review will begin with a brief discussion on the complex pathophysiology of hypertensive cardiac remodeling and its clinical consequences. The effects of nonpharmacologic and pharmacologic antihypertensive treatments on the development and progression of hypertensive heart disease are presented. Finally, the impact of the regression of myocardial hypertrophy and fibrosis on cardiac function and cardiovascular risk are discussed.

Antihypertensive Agents↗
PubMed1995

Structural remodelling of the heart by fibrous tissue: role of circulating hormones and locally produced peptides.

Symptomatic heart failure is accompanied by diastolic ventricular dysfunction due largely to an extensive reactive and reparative fibrosis. Experimental evidence suggests a clear association between myocardial fibrosis and chronic inappropriate elevations in circulating angiotensin II (Ang II) and/or aldosterone. Although not entirely elucidated, injury follows Ang II-associated release of adrenal medullary catecholamines and aldosterone-induced myocardial potassium depletion. Increasing evidence indicates locally produced cardiac Ang II plays an important role in tissue repair that may underlie myocardial remodelling, the fibrous tissue accumulation both at and remote to the site of myocardial infarction (MI). Angiotensin converting enzyme (ACE) binding density markedly increases at these fibrous tissue sites after experimental MI, indicating an involvement in wound healing regardless of the cause and location of fibrosis; cells expressing Ang II receptors are primarily myofibroblasts. Therapy with ACE inhibitors and aldosterone receptor antagonist have each been shown to attenuate development of fibrosis.

Aldosterone↗
PubMed1995

Pathogenesis of myocardial fibrosis in spontaneously hypertensive rats (SHR).

The pathomechanisms of myocardial fibrosis are incompletely understood. Coronary microvessels (MV), interstitial reactions and focal myocardial lesions characterized by morphological signs of ischaemia were found in 39 spontaneous hypertensive rats (SHR) and 33 control rats aged 3, 13, 27, 52 and 78 weeks, using new morphological preparations and measuring methods. In the developing phase of spontaneous hypertension (SH) the numerical and area densities (developed for up to 13 weeks) of MV were lower than at 3 weeks and lower than control. The same was true for the fibrotic tissue density. However, all values were increased in the manifest phase of SH (27-78 weeks). The increase in interstitial tissue is topologically and causally related to pathological MV reactions that represent morphologically chronically increased contractions. Small MV that mostly elude detection with conventional staining methods are of particular importance. The first phase of manifest SH (27th-52nd week) is characterized by a generalized development of myocardial fibrosis; the late phase (52nd-78th week) by a reinforced localized fibrosis that is attributable to the enhanced progression of focal ischaemic myocardial lesions. The septal region is not included in this phase. Thus, in the two phases of manifest SH, the pathomechanisms responsible for the development of myocardial fibrosis must be different.

Animals↗
PubMed2007

Arachidonic acid metabolism as a potential mediator of cardiac fibrosis associated with inflammation.

An increase in left ventricular collagen (cardiac fibrosis) is a detrimental process that adversely affects heart function. Strong evidence implicates the infiltration of inflammatory cells as a critical part of the process resulting in cardiac fibrosis. Inflammatory cells are capable of releasing arachidonic acid, which may be further metabolized by cyclooxygenase, lipoxygenase, and cytochrome P450 monooxygenase enzymes to biologically active products, including PGs, leukotrienes, epoxyeicosatrienoic acids, and hydroxyeicosatetraenoic acids. Some of these products have profibrotic properties and may represent a pathway by which inflammatory cells initiate and mediate the development of cardiac fibrosis. In this study, we critically review the current literature on the potential link between this pathway and cardiac fibrosis.

Animals↗
PubMed1989

Myocardial stiffness and reparative fibrosis following coronary embolisation in the rat.

The structural nature of fibrillar collagen involved in the replacement fibrosis which accompanies discrete areas of cell necrosis remains uncertain, as does its influence on the diastolic and systolic stiffness of the intact myocardium. This study, using 15 micron diameter microsphere embolisation of the rat myocardium, was undertaken to address these issues. Collagen volume fraction (trichrome), fibrillar collagens (picrosirius-polarisation technique), and the stress-strain relations of the intact myocardium (isolated hearts) were determined 30 d after the infusion of microspheres into the left ventricle. Significant differences from controls included: (a) the presence of hypertension secondary to renovascular embolisation; (b) a greater volume fraction of collagen that included not only a meshwork of short, taut appearing, thick and thin collagen fibres, interposed between muscle in areas of cell loss, but also a perivascular fibrosis involving intramyocardial coronary arteries; (c) elevated active stiffness, and (d) a more exponential diastolic stress-strain relation with increased stiffness at strains of 5% or more. These findings suggest that the replacement fibrosis accompanying myocyte necrosis has distinguishing morphological features involving fibrillar collagen and which because of its structure, alignment, and location relative to muscle leads to enhanced myocardial stiffness, including a more exponential rise in the diastolic stress-strain relation. The perivascular accumulation of collagen suggests that additional factors other than microsphere induced necrosis were responsible for this reactive fibrosis.

Animals↗
PubMedDate not supplied

Are myocardial fibrosis and diastolic dysfunction reversible in hypertensive heart disease?

Diastolic dysfunction is an important factor contributing to the appearance of symptomatic heart failure, particularly among elderly women with arterial hypertension. In hypertensive heart disease, the presence of cardiac fibrosis is an important determinant of abnormal myocardial stiffness that contributes to diastolic dysfunction. Recent studies indicate the feasibility of a pharmacology-based regression of fibrosis and improvement in diastolic stiffness.

Aged↗