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

The diastolic portion of the cardiac cycle can be divided into sequential phases: isovolumic ventricular relaxation; rapid ventricular filling; slow, or passive, ventricular filling; and atrial contraction. Contraction and relaxation are to some extent interrelated; however, relaxation is not simply a passive reversal of events during systole. Rather, relaxation is an energy-consuming process which involves dissociation of calcium from the actin-myosin-complex and reuptake of calcium by the sarcoplasmic reticulum. Left ventricular diastolic function is determined by the interrelationship of several/factors, including some intrinsic to the left ventricular chamber (completeness of left ventricular relaxation, time course of left ventricular contraction, and elastic and viscous properties of the myocardium) and others extrinsic to the left ventricle (pericardial and pleural pressure, right ventricular contraction, and coronary perfusion pressure). Acute ischemia alters diastolic left ventricular function by: slowing isovolumic relaxation, delaying left ventricular filling and altering passive elastic properties of the myocardium. Slowing of isovolumic relaxation is measured as a fall in the maximal rate of left ventricular pressure decline (peak negative dP/dt) and as an increase in the time constant (T) of left ventricular pressure fall. Delayed left ventricular filling is manifested regionally as a reduced rate of septal and posterior wall thinning (by echocardiography) and globally as a reduced rate of chamber filling (by gated radionuclide angiography).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamics in ischemia: diastolic phase]. 652 97

To explore possible mechanisms of left ventricular early segmental relaxation, complete occlusion of the left anterior descending coronary artery (LAD) was produced in seven open-chest dogs and partial occlusion of the LAD was produced in six open-chest anesthetized dogs. Regional wall thickness was measured both in an ischemic and a normally perfused zone using implanted ultrasonic crystals. Two to three seconds following complete LAD occlusion, thinning of the ischemic wall occurred prematurely during isovolumic relaxation. The extent of premature thinning became more prominent 5 to 10 sec following LAD occlusion. Early thinning of the ischemic wall preceded thinning of the normally perfused wall by 110 +/- 10 msec. Partial occlusion of the LAD produced a 33 +/- 6% reduction of coronary flow and a 23 +/- 4% reduction of systolic wall thickening in the ischemic region. Systolic thickening of the nonischemic wall was unchanged relative to the preocclusion period. Premature early thinning of the mildly ischemic wall preceded thinning of the normally perfused segment by 90 +/- 8 msec. The observation that ischemia can produce segmental early thinning of the ventricular wall may have implications in understanding the mechanism of the angiographic observation of the segmental early relaxation phenomena in patients with coronary artery disease.
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PMID:Early segmental thinning of the left ventricular wall following regional ischemia. 664 Jun 63

To determine if there is a quantitative relationship between systolic contraction abnormalities (demonstrated by two-dimensional echocardiography) and reduced myocardial perfusion in a setting of moderate and severe coronary stenosis, we created 70% or 90% reduction in circumflex coronary artery diameter in open-chest dogs. Transient ischemia was induced by superimposing increased myocardial oxygen requirements (i.v. isoproterenol, aortic constriction) in the presence of the stenosis or by decreased coronary perfusion (lowering arterial pressure with i.v. nitroprusside, nitroglycerin, or hemorrhage). Acute systolic wall thinning show by two-dimensional echocardiography or by implanted myocardial sonomicrometers was taken as functional evidence of myocardial ischemia. Myocardial perfusion was determined by radiolabeled microspheres when wall thinning was apparent. Systolic wall thinning could not be induced by these interventions when the degree of coronary stenosis was only 70%. Systolic wall thinning occurred only when increased myocardial oxygen requirements or decreased aortic pressure were superimposed on 90% coronary stenosis. Under these conditions, myocardial perfusion was reduced to 28 +/- 27 ml/100 g/min (mean +/- SD), 15--25% of control. Aortic diastolic pressure was a major determinant of ischemia in that contraction abnormalities produced by a 90% stenosis and vasodilators or hemorrhage could be acutely reversed by superimposing acute aortic constriction, which elevated arterial pressure; myocardial perfusion increased correspondingly. Thus, the demonstration of transient systolic wall thinning by two-dimensional echocardiography during a stressful intervention indicated that severe coronary stenosis was present, and that the perfusion of the acutely dyskinetic myocardial area was 25% of control or less.
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PMID:Two-dimensional echocardiography in experimental coronary stenosis. II. Relationship between systolic wall thinning and regional myocardial perfusion in severe coronary stenosis. 680 69

Seven dogs were evaluated with prospective ECG-gated computerized transmission tomography (CTT) to analyze left ventricular (LV) wall thickness and cross-sectional chamber area after acute occlusion of the left anterior descending coronary artery (LAD). ECG-gated CTT scanning during i.v. administration of contrast material was performed over the mid-left ventricle at rest, after acute occlusion of the LAD and 30 minutes after release. The extent of systolic wall thickening (EWTh) of the anterior (potentially ischemic) segment was 39.8 +/- 8.8% (SEM) in the control state and -26.0 +/- 4.7% during LAD occlusion (p less than 0.01). The nonischemic septum demonstrated a compensatory increase in EWTh, from 28.6 +/- 3.5% to 46.4 +/- 6.1% during LAD occlusion (p less than 0.05). The end-diastolic LV luminal area (LVA) increased from 17.4 +/- 0.8 cm2 in the control state to 21.0 +/- 1.1 cm2 during LAD occlusion (p less than 0.01). End-systolic LVA also increased, from 11.0 +/- 0.9 to 15.2 +/- 1.1 cm2 (p less than 0.01). In addition, the percent change in LVA from end-diastole to end-systole declined from 37.4 +/- 3.8% during control to 28.0 +/- 2.6% during LAD occlusion (p less than 0.02). In conclusion, gated CTT demonstrates that the alterations in acute ischemia are characterized by changes in regional wall thickening dynamics, consisting of wall thinning during systole in the jeopardized segment and compensatory increase in the extent of systolic thickening in the normal segment, and changes in global LV function, consisting of an increase in the LVA and a decrease in the percent change of LVA during systole. Gated CTT may be useful for monitoring regional and global effects of ischemia when subjects can be studied in the supine position and with respiration suspended for 45 seconds.
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PMID:In vivo assessment of left ventricular wall and chamber dynamics during transient myocardial ischemia using prospectively ECG-gated computerized transmission tomography. 685 Oct 18

A technique for epicardial mapping of segmental myocardial function at multiple sites over both right and left ventricles was developed using a high-resolution, 7.5-MHz, short-focus, miniaturized, M-mode echocardiographic transducer worn on the fingertip. Myocardial function was determined from the extent and time course of systolic thickening and diastolic thinning at each site mapped. The technique was characterized in an open-chest canine model of myocardial ischemia. Ischemia was induced by transient or permanent coronary occlusion in 17 dogs. Acute occlusions produced reduced segmental thickening within 10-15 seconds and, often, overt systolic thinning of ischemic myocardium. Rhodamine fluorescence perfusion maps were compared with echocardiographic maps in nine dogs. Segmental thickening was reduced in perfused segments adjacent to, but not involved by, ischemia, as well as ischemic segments. Reproducibility appeared satisfactory for quantitative analysis of grouped data on multiple segments, and qualitative analysis in individual segments. Initial human studies performed during coronary bypass surgery in 11 subjects showed echocardiographic abnormalities in the six patients with ventriculographic abnormalities and in four with normal ventriculograms. Transmural infarctions were akinetic, showing no change in thickness throughout the cardiac cycle. Hypokinetic segments distal to high-grade coronary stenosis were common, although most segments distal to stenosis contracted normally. Reversal of segmental contraction abnormalities by coronary bypass grafting was shown in three subjects, while worsening of function was seen in previously abnormal segments in two and in a previously normal segment in one subject. Epicardial echocardiographic mapping is a practical method for intraoperative assessment of myocardial function during coronary surgery in man that may enhance our understanding of the pathophysiology of coronary disease and the effects of coronary surgery.
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PMID:Epicardial mapping of segmental myocardial function: an echocardiographic method applicable in man. 698 15

The purpose of this study was to assess the sensitivity and specificity of two-dimensional echocardiography in detecting ischemia-induced transient myocardial dyskinesis. We prepared an open-chest dog model of severe coronary stenosis (90% reduction of circumflex coronary artery diameter) and induced ischemia by acutely raising myocardial oxygen requirements with i.v. isoproterenol and acute aortic constriction. The changes observed with echocardiography were compared with those obtained by intramyocardial sonomicrometers placed side by side or in an endocardial-epicardial orientation. Ischemia was defined as systolic wall expansion or thinning on sonomicrometers and two-dimensional echocardiography. We found complete agreement between sonomicrometers and two-dimensional echocardiography in all control tracings and after ischemia was induced; whenever dyskinesis occurred it was seen by both techniques. Although there was qualitative agreement between echocardiographic and sonomicrometric techniques, there were quantitative differences in the assessment of wall thickening. Such differences may be related to malalignment of the sonomicrometers, echocardiographic resolution limitations or other technical factors. We conclude that two-dimensional echocardiography is a sensitive and specific technique for detecting transient myocardial ischemia, and therefore should be useful for demonstrating exercise-induced ischemia in patients with coronary artery disease.
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PMID:Two-dimensional echocardiography in experimental coronary stenosis. I. Sensitivity and specificity in detecting transient myocardial dyskinesis: comparison with sonomicrometers. 709 70

The effects of step-wise reduction in left circumflex coronary blood flow on: 1) posteroinferior wall dynamics; 2) normally-perfused anterior wall dynamics; and 3) cavity function were assessed simultaneously by roentgen videometric analysis of left ventricular angiograms in open-chest dogs during normal and increased afterload. At control coronary flow with normal afterload, peak rates of systolic thickening and diastolic thinning of the posteroinferior and anterior walls were similar. Step-wise reduction in circumflex coronary flow resulted in a progressive fall in systolic and diastolic posteroinferior wall dynamics. Increased LV afterload resulted in a decrease in posteroinferior wall dynamics even at control coronary flow, and reduction in flow resulted in even greater deterioration than occurred with normal afterload. The decrease in posteroinferior wall dynamics with reduction in circumflex coronary flow was accompanied by an increase in peak rates of systolic thickening and diastolic thinning of the normally perfused anterior wall. The level of coronary blood flow at which this increase in anterior wall dynamics occurred, varied with LV loading conditions, occurring earlier when afterload was increased. There was no earlier or greater decrease in diastolic than systolic wall dynamics with progressive reduction in coronary flow with either normal or increased afterload. Left ventricular end-diastolic volume, end-diastolic pressure and ejection fraction changed little until coronary blood flow was reduced to 50% of control; by contrast, stroke-work was exquisitely sensitive to changes in coronary flow. There was no correlation between changes in regional and cavity systolic or diastolic function. The delay in onset of LV cavity dysfunction with ischemia may have been partly due to the "compensatory increase" in anterior wall dynamics, counterbalancing the impaired posteroinferior wall dynamics.
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PMID:Effects of progressive reduction in coronary blood flow on regional and global left ventricular contraction and relaxation during normal and increased afterload: a roentgen videometric study. 717 76

This study examined the relationships between the left ventricular (LV) regional function, regional myocardial blood flow (RMBF), and myocellular necrosis after sudden proximal occlusion of the left anterior descending coronary artery (LAD) in 36 awake, unsedated dogs. Net wall thickening during systole (NET) was used to assess regional LV function, was expressed as percent control, and was measured with chronically implanted ultrasonic crystals. RMBF was measured with 8- to 10-micrometer radioactive microspheres. In regions with a moderate degree of functional loss, NET fell to 35.3 +/- 2.2% of control at 5 minutes when RMBF fell from 1.9 +/- 0.08 to .086 +/- 0.09 ml/g per min (P less than 0.05). No significant change occurred in midwall or epicardial RMBF. The relationship between endocardial flow and NET was non-linear (r = 0.69, P less than 0.0001). In these segments, subsequent changes in RMBF were unrelated to corresponding functional alterations through 24 hours. In segments with paradoxic systolic wall thinning RMBF fell in endocardial, midwall, and epicardial layers; endocardial ischemia was most severe (0.30 +/- 0.05 ml/g per min). Segmental myocellular necrosis was most severe in the endocardial layer and correlated significantly with both RMBF and segmental function. Myocellular necrosis increased in severity as flow was reduced below 70-75% of normal. Thus, in this model of LV ischemia, (1) regional LV functional loss is most sensitive to reductions in endocardial RMBF; (2) subsequent increases in RMBF are largely unassociated with functional recovery; (3) transmural ischemia results in paradoxical systolic wall thinning.
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PMID:Interrelationships between regional left ventricular function, coronary blood flow, and myocellular necrosis during the initial 24 hours and 1 week after experimental coronary occlusion in awake, unsedated dogs. 723 98

To detect abnormal interventricular septal (IVS) motion during exercise-induced ischemia, ergometer exercise echocardiography was performed using a specially devised transducer in 12 patients (pts) with effort angina (left anterior descending artery disease) and 10 normal subjects (N) at rest, and during exercise and recovery. During exercise, percent systolic IVS thickening (% delta T) and IVS excursion (Ex) increased from 52 +/- 13% at rest to 73 +/- 19% and from 7.0 /- 1.3 mm at rest to 10.6 +/- 1.9 mm, respectively, in N, and also from 52 +/- 23% to 67 +/- 36% and from 7.3 +/- 1.9 mm to 9.7 +/- 2.1 mm in all of 3 pts with distal left anterior descending artery disease. On the other hand, in 9 pts with proximal left anterior descending artery disease, % delta T and Ex during exercise decreased from 41 +/- 17+ at rest to 26 +/- 25% and from 7.7 +/- 1.2 mm to 5.1 +/- 4.6 mm. The late systolic wall thickening of IVS was observed during peak exercise in 2 of the 9 pts, one of whom exhibited systolic IVS thinning and a decrease in diastolic thickness (from 6 mm to 4.5 mm). In 5 pts with IVS asynergy during exercise diastolic IVS thickness increased maximally from 10.2 +/- 3.3 mm at rest to 11.4 +/- 3.5 mm during recovery (reactive hyperemia). Exercise echocardiography is useful to predict the location of left anterior descending artery disease and to evaluate IVS performance during exercise-induced ischemia.
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PMID:[Exercise echocardiography: interventricular septal thickness and motion in patients with effort angina during ergometer exercise (author's transl)]. 726 97

Experimental myocardial infarction was reproduced in large random-bred dogs by ligation of the left descending coronary artery. After 24 hours of ischemia, subendocardial Purkinje cells showed accumulations of lipid drops, development of foci of myofibril overcontraction with simultaneous accumulation in the cells of large lysosomes, disappearance of the external layer of sarcolemma, thinning of glycocalyx, and intact plasmalemma. Most contractile cardiomyocytes were changed irreversibly. Among them, however, there was a portion of viable cells with marked signs of lipid infiltration. These contractile cells lacked the external layer of sarcolemma, had thinned glycocalyx, plasmalemma in a number of cases was penetrable for colloid lanthanum. The ischemized cells with maximally thinned external layers of sarcolemma and intact plasmalemma may apparently be regarded as potential sources of ectopic activity. Overcontracted Purkinje cells are primarily among them.U
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PMID:[Ultrastructure of the subendocardiac cardiomyocytes of the dog heart in acute experimental myocardial infarct]. 729 64


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