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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rigid stainless steel osteosynthesis plates (DCP/ASIF) were attached bilaterally onto the intact tibio-fibular bone in 40 rabbits. Axial compression was used on the right side, neutral plate fixation on the left. The radiographic appearances of the bone were analysed 1 day, and 1, 3, 12, 24 and 36 weeks postoperatively. The changes in the bone were progressive, related to the time of fixation, and similar in the right and left leg. The main alterations were a progressive thinning of the cortical bone under the plate and a progressive cancellous transformation of the tubular bone.
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PMID:Radiographic abnormalities in tubular bone after rigid plate fixation in rabbits. 64 75

Early in the acute phase of myocardial infarction the phenomenon of expansion may occur, with regional thinning and dilatation of necrotic region. This complication may be detected by echocardiography since the first hours of infarction. During the two subsequent weeks, an additional increase of left ventricular volume may occur, due to an increase of length of the infarcted segments and, as well, of the contractile segments which suffer a "volume overload hypertrophy". This is the phenomenon of remodeling. Finally during the first year post infarction, a progressive left ventricular dilatation may develop. This late dilatation seems to be due to an increase of perimeter of the contractile regions only. By the time this topographic changes have occurred, the left ventricle assumes a more spheric configuration. Left ventricular dilatation affects adversely cardiac function, with higher incidences of heart failure and death. Experimental and clinical studies show that, in selected patients, remodeling and ventricular dilatation may be attenuated by the administration of angiotensin-converting-enzyme inhibitors, with better indices of left ventricular function. Final results of several on-going multicenter studies are awaited for; they will allow a better definition of the role of ACE inhibitors on prevention and treatment of left ventricular dysfunction after myocardial infarction.
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PMID:[Expansion of infarction, dilatation and ventricular remodelling. Therapeutic potential of angiotensin-converting enzyme inhibitors]. 161 Jun 13

An acute myocardial infarction, particularly one that is large and transmural, can produce expansion and alterations in the topography of both the infarcted and non-infarcted regions or the ventricle. This remodelling can importantly affect the function of the ventricle and the prognosis. Side-to-side slippage of myocytes in the myocardium occurring in association with ventricular dilatation is responsible for wall thinning. The increased internal load that is sustained through the cardiac cycle is thought to promote further stress, dilatation and hypertrophy of the non-infarcted area. The collagen network has been showed to be high responsible for the remodelling of the interstitium and therefore for the scar formation involved in the expansion. The process for ventricular enlargement can be influenced by infarct size, healing end ventricular wall stresses. The process of scarification can be interfered with during the acute infarct period by the administration of glucorticosteroids and non-steroidal anti-inflammatory agents, which results in thinner infarct and further expansion. A most effective way to prevent or minimize the increase in ventricular size is to limit the initial insult. Acute thrombolytic reperfusion therapy may work in this way. Finally early and long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions of the left ventricle, reducing progressive enlargement with a prolongation in survival.
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PMID:[Left ventricular remodelling]. 184

An important antecedent to the development of late congestive heart failure is left ventricular dilatation and remodeling following myocardial infarction, which occurs in 30-40% of acute anterior transmural infarcts. Dilatation and remodeling commence within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and uninfarcted regions of the myocardium are equally involved in the process. The remodeling process comprises left ventricular wall thinning (mainly due to cell slippage), chamber dilatation, and compensatory hypertrophy of the uninfarcted segment of the myocardium. The hypertrophy may initially be physiologic but may ultimately become a pathologic process, and thereby contribute to pump dysfunction. The possible reasons why the ventricular hypertrophy may ultimately be dysfunctional include alterations in local architecture and their sequelae alone or in concert with local changes in the beta-adrenergic, alpha-adrenergic, or renin angiotensin systems. At the present time, there are encouraging data to suggest that nitroglycerin, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process.
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PMID:Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions. 214 59

Left ventricular dilation and remodelling occur in 35-40% of anterior transmural myocardial infarcts and these events are important antecedents to the development of late congestive heart failure. This process commences within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and the uninfarcted regions of myocardium are equally involved in the process. Thinning of the left ventricular wall occurs mainly as a result of cell slippage. In addition, compensatory hypertrophy occurs in the uninfarcted segment of the myocardium. While this hypertrophy may initially be physiological, it ultimately appears to become a pathological process and thereby contributes to pump dysfunction. At the present time there are encouraging data to suggest that nitroglycerin, administered in the setting of the acute infarction, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process. Whether a patent infarct related artery further limits dilation is uncertain and is currently under investigation.
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PMID:The prevention of congestive heart failure: left ventricular dilation and its management. 215 39

The enlarged heart has long been recognized as an important sign of systolic dysfunction of many different etiologies. Regardless of etiology, cardiac enlargement is associated with decreased survival. Cardiac enlargement after acute myocardial infarction (AMI) may be a progressive process. Early after AMI, the process of infarct expansion, or thinning and stretching of the infarct region leads to early volume enlargement detectable within 3 days of the infarct. During the next 2 weeks, volume enlargement takes place which includes lengthening of both the infarcted and the non-infarcted regions. Finally, additional left ventricular enlargement occurs during the next year after the infarction. Both experimental and clinical studies have demonstrated that such progressive LV enlargement may be halted by angiotensin converting enzyme inhibition with captopril. A large scale randomized trial is currently under way to determine whether captopril improves survival after infarction (Survival and Ventricular Enlargement, SAVE).
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PMID:Left ventricular dilatation following myocardial infarction: clinical course and potential for therapy. 252 55

A collagen network, composed largely of type I and III fibrillar collagens, is found in the extracellular space of the myocardium. This network has multiple functions which includes a preservation of tissue architecture and chamber geometry. Given its tensile strength, collagen is a major determinant of tissue stiffness. Its disproportionate accumulation, in the form of either a reactive or a reparative fibrosis, further increases stiffness. A degradation of collagen tethers, on the other hand, is an anatomic requisite for a distortion in tissue architecture and a reduction in stiffness that can lead to chamber dilatation, wall thinning, and even rupture of the myocardium. Collagen turnover in the myocardium is dynamic. When synthesis exceeds degradation, an adverse accumulation of collagen appears to distort tissue structure. This is true for either the hypertrophied and/or nonhypertrophied ventricle. Factors that contribute to the appearance of myocardial fibrosis are largely different from those that promote cardiac myocyte growth. Included amongst these fibrogenic factors are effector hormones of the reinin-angiotensin-aldosterone system (RAAS). Studies conducted both in intact animals (relative to dietary sodium intake) and in cultured adult cardiac fibroblasts have pointed toward the association between collagen accumulation and chronic elevations in circulating angiotensin II and aldosterone. A tissue hormonal system involving angiotensin II, endothelins and bradykinin, may likewise regulate fibrogenesis. In this regard, angiotensin converting enzyme is found in connective tissue of the normal heart, including the matrix of heart valves and the adventitia of the intramural coronary arteries, and fibrous tissue that forms following infarction or with chronic RAAS activation. The importance of ACE in the regulation of local angiotensin II and bradykinin levels and their contribution to collagen turnover is a fruitful area of research with important clinical implications. The myocardium also contains a proteolytic system, including collagenase. The characteristics and regulation of matrix metalloproteinases and their tissue inhibitors in various cardiovascular disease states requires further investigation.
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PMID:Collagen network of the myocardium: function, structural remodeling and regulatory mechanisms. 802 11

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P < .05). In the surviving rats (18 SHR, 19 WKY, 18 SHRD), both left ventricular cavity area (LCVA) and the infarct segment length per the noninfarct segment length (FW/IVS), measured as indices of left ventricular dilation, were significantly less in SHR and SHRD than in WKY, and the thickness of the left ventricular free wall (Wth), used as an index of left ventricular thinning, was significantly higher in both SHR and SHRD than in WKY (P < .01). However, there was no significant difference in FW/IVS, LCVA, and Wth between SHR and SHRD. Hemodynamic findings 1 week after coronary occlusion demonstrated that all rats were in heart failure, and there were no significant differences in hemodynamics among the three groups. In conclusion, our findings showed that hypertrophy with hypertension reduced infarct expansion, but that reduction of blood pressure by ACE inhibitor did not reduce infarct expansion more than hypertrophy did. However, this finding suggest that an ACE inhibitor may improve the rate of survival of patients with left ventricular hypertrophy with hypertension.
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PMID:Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats. 886 21

Progressive changes typically occur in left ventricular (LV) architecture following moderate- to large-sized myocardial infarction (MI). These changes include early expansion and thinning of the infarct zone and subsequent increase in myocardial mass within the non-infarcted zone, with LV dilatation and loss of the normal elliptical configuration of the LV cavity. These changes are accompanied by impaired myocyte function and advancing clinical expression of heart failure. Numerous animal and human studies have documented inhibition of LV remodeling post-MI by angiotensin converting enzyme (ACE) inhibitors. Although the ideal timing for initiating treatment remains uncertain, evidence exists that benefit persists long after the time of initial injury. Mechanisms for the effects of ACE inhibitors on LV remodelling may be dependent on changes in myocardial load, may be load independent, or both. These effects are likely to be mediated by reductions in circulating and local tissue concentrations of angiotensin II and in bradykinin degradation. Regardless of the exact mechanism or mechanisms by which ACE inhibitors exert their favourable influence on LV remodelling, it is likely that this effect is a key mediator of the documented clinical benefits afforded by treatment with this class of agents.
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PMID:Role of angiotensin converting enzyme inhibitors in preventing left ventricular remodelling following myocardial infarction. 886 35

Infarct scar, a requisite to the rebuilding of necrotic myocardium following myocardial infarction (MI), has long been considered inert. Earlier morphologic studies suggested healing at the infarct site was complete within 6-8 weeks following MI and resultant scar tissue, albeit necessary, was acellular and simply fibrillar collagen. Utilizing molecular and cellular biologic technologies, recent studies indicate otherwise. Infarct scar is composed of phenotypically transformed fibroblast-like cells, termed myofibroblasts (myoFb) because they express alpha-smooth muscle actin (alpha-SMA) and these microfilaments confer contractile behavior in response to various peptides and amines. These cells are nourished by a neovasculature and are persistent at the MI site, where they are metabolically active expressing components requisite to angiotensin (Ang) peptide generation, including converting enzyme, receptors for AngII and transforming growth factor (TGF)-beta1. They continue to elaborate fibrillar type I collagen. Their generation of these peptides contribute to ongoing scar tissue collagen turnover and to fibrous tissue formation of noninfarcted myocardium. Infarct scar contraction accounts for its thinning and its tonus may contribute to abnormal ventricular chamber stiffness with diastolic dysfunction. Infarct scar is a dynamic tissue: cellular, vascularized, metabolically active and contractile. Pharmacologic interventions with angiotensin converting enzyme inhibitor or AT1 receptor antagonist has proven effective in attenuating scar tissue metabolic activity and minimizing adverse accumulation of fibrous tissue in noninfarcted myocardium.
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PMID:Infarct scar: a dynamic tissue. 1077 28


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