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

A continuing theme in our laboratory has been the use of echocardiographically-measured systolic myocardial wall thickening to demonstrate and evaluate the consequences of regional myocardial ischemia. This presentation focuses on two areas: the immediate mechanical consequences of induced myocardial ischemia in two experimental models: canine and human; the correlation between persistent regional myocardial dysfunction and morphologic infarction after sequences of coronary artery occlusion and reperfusion. Many experiments using animal models have demonstrated that acute myocardial ischemia produces almost immediate replacement of normal systolic myocardial wall thickening by systolic thinning. Less is known about the immediate mechanical response of human myocardium to acute ischemia. This was studied in 5 open-chest humans undergoing various cardiac operations. Wall thickening was continuously displayed by a 7 MHz M-mode echocardiographic transducer coupled to the epicardium by suction to maintain constant position. Coronary flow velocity was displayed by a pulsed Doppler device coupled to an epicardial coronary artery by suction. Ischemia was induced by the surgeon who manually occluded the coronary artery with a soft-tipped Kitner dissector or vascular forceps for 30 seconds. It was found that cessation of coronary flow was accompanied by reductions in normal systolic thickening but systolic thinning or expansion only rarely occurred. In contrast, when the identical techniques were used in 5 dogs, systolic thinning always occurred immediately after coronary arterial occlusion. This suggests that there are important species differences between canine and human myocardium in the immediate mechanical response to myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transient myocardial ischemia: experimental echocardiographic demonstration and evaluation of myocardial contraction abnormalities. 375 77

Resetting of arterial and arteriolar wall structural components have been studied in the white rat kidney glomeruli after experimental ischemia (30 min, 1-3 h) without blood flow recovery and with the following recirculation for 3-30 days. The experiments have established that acute renal ischemia caused by the vascular leg ligation for 30-60 min without the following blood flow recovery results in slight microstructural alterations of arterial and arteriolar wall elements. With increased ischemia duration (2-3 h) pathological changes become more prominent and separation of vascular endothelial cells and defibering of the internal elastic membrane take place. In transitory (30-60 min) ischemia of the remaining kidney (one kidney is removed) three days later desquamation of endothelial cells occurs in some arteries. Thinning of arterial walls and overstrain of internal elastic membrane are observed. However, later on (in 30 days) short-term ischemia (30 min) is followed by complete recovery of structural components of arterial and arteriolar walls. In more durable ischemia (2-3 h) of the remaining kidney the recovered blood flow causes marked destructive life-threatening changes in vascular walls.
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PMID:[Morphological evaluation of the state of the structural elements of arterial and arteriolar walls in experimental kidney ischemia]. 394 24

Using a new computed tomographic (CT) scanner design that uses a rapidly moving focused electron beam, 50-ms CT scans were obtained at 2 axial levels simultaneously through the hearts of 6 dogs in order to analyze left ventricular (LV) wall thickness and cross-sectional chamber area after acute occlusion of the left anterior descending coronary artery (LAD). Ten or fifteen 50-ms CT scans (rate of 17 scans/s through the middle of the left ventricle were performed in 1 second (cine acquisition) during intravenous administration of contrast medium at rest, 60 seconds after acute occlusion of the LAD, and 60 seconds after release of the occlusion. The percent extent of systolic wall thickening of the potentially ischemic anterior segment was 37 +/- 15% (+/- standard deviation) in the control state and -5 +/- 6.5% during LAD occlusion (p less than 0.01). There was no significant difference in the percent change in LV luminal area from end-diastole to end-systole between the control state (50 +/- 19%) compared with LAD occlusion (47 +/- 21%). There were no significant differences in the extent of systolic wall thickening or LV luminal area between the control state and 60 seconds after release of occlusion. The alterations in regional myocardial function during acute ischemia are characterized by wall thinning during systole in the jeopardized segment and no significant change in global LV function. These features can be assessed by cine computed tomography during a solitary heart cycle.
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PMID:In vivo assessment of left ventricular wall and chamber dynamics during transient myocardial ischemia using cine computed tomography. 396 99

The relationship between epicardial and transmural function (measured with sonomicrometers) was examined in 13 anesthetized open-chest dogs. Systolic wall thickening was used as a standard of integrated transmural function to compare with epicardial function measured as segment shortening parallel to surface fibers. Three levels of coronary inflow restriction were produced by using decrements in systolic wall thickening as an index of changes in the transmural distribution of myocardial blood flow (microspheres) in myocardium perfused by the left anterior descending artery (anterior-apical group, n = 7) or circumflex artery (posterior-basal group, n = 6). Levels 1 and 2 were characterized by reductions in systolic wall thickening of 35% and 80%, respectively, and marked decreases in deep myocardial blood flow. In the subepicardium, myocardial blood flow was minimally affected at levels 1 and 2 and there was no change in posterior-basal epicardial segment shortening, but anterior segment shortening decreased significantly (by 21% and 37%, respectively). At level 3 myocardial blood flow was reduced transmurally, producing systolic wall thinning and marked epicardial dysfunction in both groups. Parallel epicardial segment shortening underestimated the extent of transmural dysfunction in both groups at levels 1 and 2 but the degree of underestimation was greatest in the posterior-basal group. Anterior-apical segment shortening was impaired at levels 1 and 2, whereas posterior-basal segment shortening was unaffected, suggesting that significant regional variability exists in the epicardial response to nontransmural ischemia.
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PMID:Dissociation between epicardial and transmural function during acute myocardial ischemia. 399 16

With the onset of ischemia, the length of myocardial segments increases rapidly, distorting ventricular geometry. Permanent stretching and thinning of infarcted zones have been termed infarct expansion. Although these changes are noted within minutes in vivo, infarct expansion may not be seen for days in postmortem preparations. The apparent postmortem reversal of early infarct expansion suggests that early expansion may be a functional phenomenon, reversible in the early hours of infarction. Alternatively, reversal of expansion may be a postmortem artifact, concealing the importance of underlying structural abnormalities. Myocardial infarction was produced in five dogs by occluding the left anterior descending coronary artery. Ultrasound sonomicrometers were used to measure myocardial segment end-diastolic length in the infarct and normal zones. After 3 hours of ischemia, the heart was arrested in diastole and biopsy specimens were taken from the normal and infarct zones. Sarcomere length was measured from electron photomicrographs, and myofiber width was measured from light photomicrographs. After 3 hours of ischemia, infarct zone segment length had increased significantly more than normal zone length (116 +/- 11 [SD] versus 103 +/- 4% of control length, p less than 0.05), whereas 2 minutes after cardiac arrest, both the infarct and normal zones returned to preischemic segment length, demonstrating apparent reversibility of early infarct expansion. However, histologic study revealed that the infarct zone myofibers were significantly thinner than normal zone myofibers (7.9 +/- 0.3 versus 9.4 +/- 0.3 micron, p less than 0.001) and sarcomere length in the infarct zone was significantly longer than that in the normal zone (1.9 +/- 0.2 versus 1.5 +/- 0.2 micron, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early infarct expansion: structural or functional? 403 Dec 98

In view of clinical interest in the efficacy of beta-adrenergic blockade during acute myocardial infarction (AMI), we have determined the long-term effect of therapy on scar formation after experimental myocardial ischemia. Intact anesthetized dogs underwent acute occlusion of the left anterior descending coronary artery, by means of a balloon catheter, which permitted monitoring of the aortic-peripheral coronary artery pressure gradient during the 4-hour period of balloon inflation. Practolol administration was begun 15 minutes after the onset of ischemia in group A. Control animals (group B) received procainamide to approximate the antiarrhythmic action of beta blockade. Only group A exhibited significant reduction in the ST segments during acute ischemia. Chronic therapy was maintained for 1 month and the mature scar formed in the myocardium was assessed after 4 months. The extent of subendocardial scar was similar in both groups but subepicardial scar formation was significantly less in group A. There was also a significant decrease in the percentage of total myocardium involved with scar in this treatment group. Although thinning of the left ventricular wall was similar for both groups in the central scar region, this process was significantly reduced at the lateral margin in group A. Thus, specific beta-receptor blockade during acute myocardial ischemia and sustained during the repair process can result in a reduced quantity and altered distribution of mature scar.
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PMID:Effects of beta-adrenergic inhibition on scar formation after myocardial infarction. 614 52

The pathophysiologic events in optic nerve axons have recently been recognized as crucial to an understanding of clinically significant acquired alterations in the ophthalmoscopic appearance of the optic disc. Stasis and related abnormalities of axonal transport appear to explain most aspects of optic nerve head swelling, including optic disc drusen and retinal cottonwool spots. Loss of axoplasm and axonal death can be invoked to interpret optic disc pallor, thinning and narrowing of rim tissue, changes in the size and outline of the optic cup, laminar dots, atrophy of the retinal nerve fiber layer, and acquired demyelination and myelination of the retinal nerve fiber layer. It is speculated that the axons may also play a role in the mechanical support of the lamina cribrosa in resisting the pressure gradient across the pars scleralis of the optic nerve head. Axons and their associated glial cells may be involved in those cases where "reversibility" of cupping of the optic disc has been reported. The structure, physiology, and experimental pathologic findings of the optic nerve head have been reviewed. Many aspects concerning the final anatomic appearance of the optic nerve head have been explained. However, many questions remain concerning the intermediate mechanisms by which increased intracranial pressure retards the various components of axonal transport in papilledema and by which increased IOP causes axonal loss in glaucoma. Investigation of the molecular biology of axonal constituents and their responses to abnormalities in their physical and chemical milieu could extend our understanding of the events that result from mechanical compression and local ischemia. Moreover, we have identified a need to further explore the role of axons in the pathophysiology of optic disc cupping.
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PMID:Optic nerve axons and acquired alterations in the appearance of the optic disc. 620 9

The purpose of this study was to investigate the relation between abnormalities of left ventricular (LV) wall thickening during systole in ischemic regions and the interaction of LV pressure and regional intramyocardial pressure. Wall thickness was measured in 10 open-chest dogs with ultrasonic dimension gauges. LV pressure, aortic pressure, and intramyocardial pressure in the subendocardium were measured with catheter-tip micromanometers. Regional ischemia was produced by occlusion of the left anterior descending coronary artery. During the control period, peak subendocardial pressure exceeded LV pressure by 44 +/- 6 mm Hg. With hypokinesia, defined as a 50% to 89% reduction of systolic wall thickening, peak subendocardial pressure exceeded peak LV pressure but to a lesser extent (15 +/- 1 mm Hg). During akinesia, defined as a 90% to 100% reduction of systolic wall thickening, there was less than 1 mm Hg difference between peak subendocardial pressure and peak LV pressure. During dyskinesia, defined as systolic thinning of the ischemic wall, peak LV pressure exceeded peak subendocardial pressure by 29 +/- 6 mm Hg. These observations indicate that regional changes of LV wall thickness characterized by hypokinesia, akinesia, and dyskinesia are associated with pressure gradients between the LV cavity and the LV wall that are compatible with the abnormalities of wall motion.
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PMID:Relation of intramyocardial and intracavitary pressure to regional myocardial asynergy in the canine left ventricle. 621 65

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. 622 35

Knowledge of left ventricular chamber dynamics is central to our understanding of cardiac physiology. The complicated changes in left ventricular geometry observed in the dog during various phases of the cardiac cycle can be represented as distinct linear relationships between chamber eccentricity and intracavitary volume during diastole and ejection, and probably represent structural properties of the ventricular wall. Chamber geometry of the left ventricle is a major determinant of overall myocardial function. The slope of the radius of curvature (r) to wall thickness (h) relationship is a geometric constant that determines the mural force at any given transmural pressure. Chronic pressure and volume overload produce changes in this geometric relationship as a result of increased mural force resisting ejection. The adaptive mechanism of ventricular hypertrophy in this setting alters the r/h ratio and returns systolic mural force toward normal. Coronary occlusion induces acute changes in regional geometry characterized by holosystolic wall bulging and systolic wall thinning, which shift the r/h relationship upward and to the left. The geometric alteration during ischemia probably increases systolic mural force and could adversely affect myocardial function. Recent studies with patients have shown the r/h ratio to be of value in distinguishing between reversible and irreversible impairment of myocardial performance. Because most myocardial diseases produce major alterations in the structure of the ventricular wall, analysis of dynamic chamber geometry may prove of prognostic value in assessing patients with cardiac disorders.
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PMID:Dynamic geometry of the intact left ventricle. 645 23


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