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Results for “ENDOMYOCARDIAL FIBROSIS”

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At least 1,171 records · Page 65Linked to original sources
PubMed1985

Surgical experience with thrombotic and fibrotic forms of non-tropical eosinophilic endomyocardial disease.

Surgical treatment in 8 cases of non-tropical eosinophilic endomyocardial diseases with (4 patients) and without (4 patients) eosinophilia is reported. Follow-up results (1 to 4 years) in the 6 survivors, including hemodynamic re-study, were excellent even in patients operated on in the thrombotic stage (3) or with hypereosinophilia (2), or with dominant right ventricular involvement (3). Two-dimensional echocardiography gave the correct description of the pathologic stage and ventricular involvement in 6 of the 8 cases before catheterization.

Adult↗
PubMed1983

Morphology of the heart in hypertrophy.

Cardiac hypertrophy involves not only an increase in heart size but progressive, initially subtle, structural changes in muscle cells. The ability to describe these changes in detail has contributed greatly to our understanding of their possible functional significance. Structural and functional correlations in the evolving progression of cardiac hypertrophy are examined.

Cardiomegaly↗
PubMed1990

Relationship between decrease in afterload and beneficial effects of ACE inhibitors in experimental cardiac hypertrophy and congestive heart failure.

The beneficial effect of angiotensin-converting enzyme (ACE) inhibitors on myocardial mass and contractility in hypertension and, possibly, congestive heart failure (CHF) may be related to their ability to induce a decreased afterload. This has been assessed in four experimental models--renovascular hypertension, DOCA-salt hypertension, spontaneously hypertensive rats (SHR) and myocardial infarction (MI)--and in normotensive mature rats. In renovascular hypertension, ACE inhibitors normalized blood pressure as well as left ventricular hypertrophy and hypocontractility. In the DOCA-salt model, blockade of the renin-angiotensin system by ACE inhibitors did not decrease blood pressure and therefore had no effect on cardiac mass and contractility. In the SHR model, the arterial smooth muscle cell is functionally and structurally abnormal; as a result, cardiac overload led, over time, to a terminal, decompensated phase of CHF. ACE inhibitors, by decreasing blood pressure, reversed cardiac hypertrophy, hyperfibrosis and atrial natriuretic factor (ANF) oversecretion and prevented overload and time-induced CHF. In the MI model, ACE inhibitors decreased blood pressure and thereby decreased overload and reversed cardiac hypertrophy, hypocontractility, hyperfibrosis and ANF oversecretion. In normal ageing, heart function and structure are modified over time. ACE inhibitors, by blocking a 'normal' signal upstream, allowed a 'normal' effector system to decrease blood pressure and prevented the development of age-dependent cardiac hypertrophy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Gap junction alterations in the failing heart.

Electrical and mechanical integration between myocytes is mediated by three types of intercellular junction, the fascia adherens, desmosome and gap junction. Gap junctions are responsible for electrical coupling, and consist of clusters of plasma membrane channels that directly link the cytoplasmic compartments of neighbouring cells. Each channel consists of two hemichannels (connexons; one from each plasma membrane) aligned across the narrow extracellular gap, and each hemichannel is constructed from six connexin molecules. Using specific anticonnexin43 antibodies for immunofluorescence localization in combination with confocal laser scanning microscopy, alterations in the expression of connexin43 gap junctions have been investigated in chronic ischaemic heart disease and heart failure due to ischaemic cardiomyopathy. Two major alterations are apparent: (1) disturbance in the spatial distribution of gap junctions at the border zone of healed infarcts, and (2) reduction in the quantity of immunodetectable connexin43 in regions of normal gap junction distribution distant from infarct scars. These changes are likely to contribute to electromechanical dysfunction in ischaemic heart disease and heart failure, and appear to form part of a wider pattern of altered expression of different connexin types in the diseased heart.

Connexin 43↗
PubMed1995

The renin-angiotensin-aldosterone system and myocardial collagen matrix remodelling in congestive heart failure.

In chronic heart failure, various regulatory systems including the Frank-Starling mechanism, the neuro-hormonal response, cardiac growth and peripheral oxygen delivery may be operative. Recently, the inter-relationship of the renin-angiotensin-aldosterone system (RAAS) and cardiac growth has drawn clinical interest. In the pressure-or volume-overloaded heart, the development of myocyte growth is primarily dependent on ventricular loading. Non-myocyte cell growth involving cardiac fibroblasts may also occur but this is not primarily regulated by the haemodynamic load. Cardiac fibroblast activation is responsible for the accumulation of fibrillar type I and type III collagens within the interstitium and adventitia of intramyocardial coronary arteries. In addition to relaxation abnormalities due to impairment of sarcoplasmic Ca(2+)-ATPase activity, this remodelling of the cardiac interstitium represents a major determinant of pathological hypertrophy in that it accounts for abnormal myocardial stiffness, leading to ventricular diastolic and systolic dysfunction and ultimately the progression of symptomatic heart failure. The effector hormones of the RAAS, angiotensin II (AngII) and aldosterone (Aldo), appear to be primarily involved in promoting the adverse structural remodelling of the myocardial collagen matrix. In cultured adult cardiac fibroblasts, AngII and Aldo have been shown to stimulate collagen synthesis while AngII additionally inhibits matrix metalloproteinase I activity, which is the key enzyme for degradation of fibrillar collagen in the cardiac interstitium, leading to excessive collagen accumulation. These findings may serve as rationale as to why angiotensin converting enzyme inhibition or blockade of the RAAS represents such remedial therapy beyond the effect of simply unloading the heart in patients with congestive heart failure.

Adult↗
PubMed1988

Iatrogenic left main coronary artery stenosis following aortic valve replacement.

A case of severe iatrogenic fibrous left main coronary artery stenosis following aortic valve replacement (Hall-Kaster prosthesis) is documented clinically, angiographically and histologically. Reported histological data of this rare complication of valve replacement are reviewed. The onset of ischaemic symptoms in the first six months after valve replacement is highly suggestive of iatrogenic coronary artery stenosis, and urgent coronary angiography is recommended.

Aortic Valve Stenosis↗
PubMed1988

Ventricular dimensions and wall motion assessed by echocardiography in patients with arrhythmogenic right ventricular dysplasia.

Twenty patients with arrhythmogenic right ventricular dysplasia (ARVD) and 20 healthy volunteers underwent cross-sectional echocardiographic examination for the assessment of ventricular dimensions and wall motion. Right ventricular cavity diameters and wall segments were selected from the inflow and outflow tracts and the right ventricular body. The measurement error for measuring cavity dimensions was low throughout and the reproducibility of wall motion scoring was high in both the normal subjects and the patients. All except one patient had increased dimensions and/or abnormal wall motion in the right ventricle. The right ventricular inflow tract was dilated in nine patients, the outflow tract in 11 patients and the short- or long-axis diameters of the right ventricular body were increased in seven patients. Right ventricular wall motion abnormalities, being the most frequent finding, ranged from mild hypokinesia only to dyskinesia or sacculations, and were fairly evenly distributed among the segments studied. Left ventricular abnormalities, found in eight patients, were generally mild. Cross-sectional echocardiography thus provides highly reproducible measurements of right ventricular size and contraction patterns even in patients with wall shape deformities, and is therefore a feasible non-invasive method for the evaluation of right-sided myocardial abnormalities in patients with ARVD. The diagnostic accuracy of this technique warrants further clarification.

Adolescent↗