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

Surgical occlusion of the left coronary artery of the rat is a relatively simple, economical technique for producing experimental myocardial infarction (MI). Histologic study of 1- to 21-day-old MI in rats showed that following a mild and brief acute inflammatory response at the margins of the necrotic myocardium, there is chronic inflammation, vascular and collagenous proliferation, and resorption of necrostic tissue which progresses until scar formation is complete, usually by 21 days. From Day 1 to Day 21 the volume of infarcted myocardium decreases from 45.9 +/- 5.9% (mean +/- SEM) to 26.1 +/- 3.2% of the left ventricle and infarct thickness decreases from 1.30 +/- 0.06 mm to 0.47 +/- 0.02 mm. Concomitantly, the percent of the surface area of the left ventricle which is infarcted decreases insignificantly from 55.7 +/- 7.2% to 48.3 +/- 4.2%, indicating that the decrease in volume of the infarcted tissue occurs primarily as a result of thinning of the MI. This study provides qualitative and quantitative information on the natural history of MI in rats, which should be useful as a baseline for future studies.
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PMID:Experimental myocardial infarction in the rat: qualitative and quantitative changes during pathologic evolution. 61 96

Ventricular aneurysm is usually a complication of acute transmural myocardial infarction. The development of cardiac aneurysm represents a process of continued thinning and fibrosis of the necrotic tissue of the ventricular wall. Survival allows the development of a solid fibrous scar which of itself does not affect global ventricular function substantially. Hence, ventricular aneurysms can be present for up to 18 years without production of serious symptoms. The cases were reviewed of 45 patients in whom aneurysmectomy and myocardial revascularization were carried out. Surgical mortality was low (6.6 percent, 30 days); survival one year after operation was 76 percent, but at three years had fallen to 47 percent. Cause of late death was dominantly cardiac. In 19 patients post-operative study was done; although graft patency was observed in 98 percent, substantive improvement in ventricular performance was seen in a minority of patients. The outcome in patients with ventricular aneurysm is primarily related to the status of the residual myocardium and to the status of the vessels which supply it. The mechanism of clinical improvement after aneurysmectomy has not been clarified. However, the long-term results appear to be similar to those in patients with extensive myocardial infarction.
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PMID:Aneurysm of the cardiac ventricle. Its management by medical and surgical intervention. 68 66

To assess the early topographic changes after acute transmural myocardial infarction, we studied 28 patients during the first two weeks after infarction by serial two-dimensional echocardiography. Regional end-diastolic segment lengths and wall thicknesses for anterior and posterior left ventricular walls were calculated. Eight patients showed infarct expansion, with disproportionate dilatation and transmural thinning in the infarcted zone, that was significantly different (P less than 0.005) from changes in non-infarcted regions. This regional expansion led to an overall left ventricular dilatation in these eight patients of 25 per cent compared to 5 per cent in the 20 patients without infarct expansion. Although the eight patients with regional expansion did not have significantly higher peak creatine kinase or Killip classification, they had a significantly greater eight-week mortality (four of eight versus none of 20, P less than 0.004). Thus, regional cardiac dilatation may be an early, lethal consequence of transmural infarcts, and appears to be an important mechanism of acute cardiac dilatation after myocardial infarction.
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PMID:Regional cardiac dilatation after acute myocardial infarction: recognition by two-dimensional echocardiography. 75 78

An in vitro study of computed tomographic (CT) scanning of experimental myocardial infarction (MI) was performed by studying isolated canine hearts 18 to 48 yrs. post-infarction. CT scanning does not detect histologically present calcification in the area of an MI, but can be used to identify wall thickness changes in these areas. Decreased attenuation coefficients are found infarcted myocardium where thinning is present. The potential CT scanning to detect areas of MI is confirmed.
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PMID:Computed tomography: in vitro evaluation of myocardial infarction. 83 4

The primary goal of the current study was to assess in situ, using magnetic resonance imaging, the effect of a new angiotensin-converting enzyme inhibitor, cilazapril, in reducing left ventricular remodeling after acute myocardial infarction. Three groups of animals were investigated: (1) sham-operated rats (n = 19); (2) infarcted rats receiving no treatment (n = 23); and (3) infarcted rats receiving cilazapril (100 mg/L drinking water, n = 20). Treatment with cilazapril began on the third day postocclusion and continued for 3 to 4 months. Myocardial infarction was produced by ligation of the left coronary artery, and electrocardiographic (ECG)-gated short-axis images were acquired 3 to 4 months later. Sham-operated animals were subjected to the same procedure but the left coronary artery was not ligated. From the image acquired in the middle of the left ventricle (equatorial slice), left ventricular wall thicknesses, chamber diameters, and surface area measurements of the cavities were determined. At autopsy examination, infarct size and tissue water content were determined. The results demonstrate that magnetic resonance imaging has the potential to assess in situ the alterations of left ventricular dimensions and mass after acute myocardial infarction and can be used to document the influence of therapeutic interventions. Cilazapril provided protection against the deleterious remodeling changes such as ventricular dilation and wall thinning consequent to acute myocardial infarction.
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PMID:Effect of cilazapril on regional left ventricular wall thickness and chamber dimension following acute myocardial infarction: in vivo assessment using MRI. 153 34

To assess the ability of magnetic resonance imaging (MRI) to identify the anatomic and functional abnormalities associated with completely scarred myocardium, 20 patients with chronic transmural myocardial infarction confirmed by electrocardiography and cineventriculography were examined by gradient echo MRI. Myocardial perfusion at rest was assessed in corresponding transverse sections using 99mTc-methoxyisobutyl-isonitrile single-photon emission computed tomography (MIBI-SPECT). MRI scar was defined as diastolic wall thickness (DWT) 2.5 SD below corresponding normal values or systolic wall thickening (delta WT) less than or equal to 1 mm. For MIBI-SPECT images, scar was defined as a MIBI uptake less than 2.5 SD below normal values. By MIBI-SPECT, 152 segments contained normal tissue and 88 contained scarred myocardium. In 226 of 240 (94%) segments, MRI gradings by DWT and MIBI-SPECT gradings were identical. DWT by MRI was higher in normal than in scarred MIBI-SPECT segments (10 +/- 1 versus 4 +/- 2 mm, p less than 0.001). In 230 of 240 (96%) segments, MRI gradings by delta WT and MIBI-SPECT gradings were identical. Segments graded normal by MIBI-SPECT showed higher delta WT by MRI than scar segments (5 +/- 1 versus 0.3 +/- 1 mm, p less than 0.001). MIBI-SPECT perfusion defect size and regions with reduced DWT on MRI tomograms correlated well (r = 0.85). This study indicates that myocardial regions fulfilling electrocardiographic and ventriculographic criteria for transmural myocardial scar are clearly depicted by regional diastolic wall thinning and delta WT less than or equal to 1 mm on gradient echo MR images.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic myocardial infarction: assessment of morphology, function, and perfusion by gradient echo magnetic resonance imaging and 99mTc-methoxyisobutyl-isonitrile SPECT. 153 15

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

LV enlargement is an important determinant of survival after AMI. Pathophysiologic mechanisms leading to LV dilatation after an AMI include early thinning and stretching of the infarcted segment (e.g., infarct expansion) and hypertrophy of the noninfarcted myocardium. Such LV dilatation may adversely affect subsequent cardiac function, leading to heart failure and death. Experimental data in animals and preliminary studies in humans have demonstrated that early administration of captopril, an angiotensin-converting enzyme inhibitor, may limit infarct expansion and will attenuate progressive LV dilatation. This article discussed the clinical importance of the dilated left ventricle and reviewed advances and ongoing research in the use of angiotensin-converting enzyme inhibitors in the chronic phase after AMI.
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PMID:Left ventricular remodeling after acute myocardial infarction: clinical course and beneficial effects of angiotensin-converting enzyme inhibition. 182 84

To evaluate the feasibility of detecting denervated myocardium in the infarcted canine heart, the distribution of sympathetic nerve endings using I-123 metaiodobenzylguanidine (MIBG) was compared with the distribution of perfusion using thallium-201, with the aid of color-coded computer functional map in 16 dogs. Twelve dogs underwent myocardial infarction by injection of vinyl latex into the left anterior descending coronary artery (transmural myocardial infarction, n = 6), or ligation of the left anterior descending coronary artery (nontransmural myocardial infarction, n = 6). Four dogs served as sham-operated controls. Image patterns were compared with tissue norepinephrine content and with histofluorescence microscopic findings in biopsy specimens. Hearts with transmural infarction showed zones of absent MIBG and thallium, indicating scar. Adjacent and distal regions showed reduced MIBG but normal thallium uptake, indicating viable but denervated myocardium. Denervation distal to infarction was confirmed by reduced norepinephrine content and absence of nerve fluorescence. Nontransmural myocardial infarction showed zones of wall thinning with decreased thallium uptake and a greater reduction or absence of MIBG localized to the region of the infarct, with minimal extension of denervation beyond the infarct. Norepinephrine content was significantly reduced in the infarct zone, and nerve fluorescence was absent. These findings suggest that 1) MIBG imaging can detect viable and perfused but denervated myocardium after infarction; and 2) as opposed to the distal denervation produced by transmural infarction, nontransmural infarction may lead to regional ischemic damage of sympathetic nerves, but may spare subepicardial nerve trunks that course through the region of infarction to provide a source of innervation to distal areas of myocardium.
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PMID:Scintigraphic assessment of sympathetic innervation after transmural versus nontransmural myocardial infarction. 201 61

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


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