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

Occlusion of the anterior descending coronary artery was produced in sedated baboons 7-15 days after implantation of a micromanometer and ultrasonic crystals for measurement of regional left ventricular dimensions in ischemic, marginal, and control segments. One minute after coronary occlusion (CO), ischemic segments exhibited a marked systolic bulge with wall thinning, and percent systolic shortening of marginal segments decreased. Over the ensuing weeks, there was a progressive increase of end-diastolic lengths in marginal and ischemic segments, whereas systolic shortening in these segments did not improve significantly. Control segments did not change. In control baboons, the coronary collateral index was 55 +/-25 (SE) compared to 560 +/- 74 in normal dogs. One month after CO, the collateral index was 543 +/- 144 in baboons compared to 6,685 +/- 716 in dogs, regions of normal tissue were seen in the infarct (14.2 +/- 2% of left ventricular mass). Minimal coronary collateral development in the baboon provides a likely explanation for differences from the dog in regional functional responses and in the character of the infarct.
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PMID:Myocardial infarction in the baboon: regional function and the collateral circulation. 10 19

The purposes of this study were to demonstrate that echocardiography can be used to demonstrate the systolic wall thinning of acutely ischemic myocardium, and to compare the effects of nitroglycerin and nitroprusside on systolic thinning, wall stress and perfusion of ischemic myocardium. In 37 dogs, the ratio of end-systolic-to-end-diastolic posterior wall thickness fell from 1.30 +/- 0.02 to 0.88 +/- 0.01 ((p less than 0.001) after circumflex coronary occlusion; perfusion of the area supplied by the occluded artery fell from 98.2 +/- 7.5 ml/100 g/min to 36.5 +/- 2.9 ml/100 g/min (p less than 0.001). Nitroglycerin and nitroprusside were given to lower mean arterial pressure by 7% and 15%. Despite the reduction in coronary perfusion pressure, transmural perfusion, endocardial/epicardial perfusion ratio and systolic thinning remained constant. Both drugs reduced the ischemic "wall stress index" (ventricular pressure x ventricular diameter/wall thickness) by almost 50%. Thus, both nitroglycerin and nitroprusside were equally beneficial in this model of acute myocardial ischemia.
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PMID:Effect of acute ischemia, nitroglycerin and nitroprusside on regional myocardial thickening, stress and perfusion. Experimental echocardiographic studies. 10 33

The thickness of the left ventricular free wall and internal chamber diameter were continuously measured by pairs of ultrasonic crystals together with left ventricular pressure in normal conscious dogs. During the resting state, wall thickness decreased abruptly with the onset of atrial contraction from 10.5 mm to an average end-diastolic valueof9.8 mm. In contrast to most previous studies, there was no change in wall thickness during isovolumic systole, and with ejection the wall thickened by 31.3 percent of end-diastolic wall thickness. Atrial pacing, phenylephrine, isoproterenol and propranolol produced significant changes in chamber size with reciprocal changes in wall thickness. In addition, changes in the extent and velocity of left ventricular chamber shortening in the minor equator were associated with comparable reciprocal changes in the extent and velocity of free wall thickening (correlation coefficients 0.97 to 0.99). During acute coronary occlusion, progressive reductions in the extent and velocity of regional wall shortening with partial ischemia were associated with comparable changes in systolic wall thickening characteristics (r = 0.96 and 0.95), and holosystolic elongation in fully ischemic areas was associated with holosystolic wall thinning. During chronic pressure overload, despite wall thickening, the relation between chamber shortening and wall thickening were retained and direct computation of dynamic wall stress variations was possible. These measurements allowed precise definition of the dynamics of the left ventricular wall during normal and abnormal cardiac states. The demonstration that in the absence of regional dysfunction analysis of wall thickness in a single region of ventricular free wall can be used to describe myocardial and overall left ventricular function, as well as regional function in the presence of ischemia, constitutes a new approach to the assessment of cardiac function that has potential for echocardiographic applications.
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PMID:Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog. 13 93

Prolonged depression of segmental systolic thickening after brief coronary artery occlusion may result principally from events during reperfusion rather than during the ischemic interval. Thus, cellular calcium overload at reperfusion may be a mediator of contractile dysfunction after brief ischemia, and reduction of calcium entry by diltiazem, a calcium channel antagonist, may enhance recovery of systolic thickening after brief periods of ischemia. Thirteen awake unsedated dogs instrumented with hemodynamic catheters, left anterior descending coronary artery occluders and five to six pairs of intramyocardial sonomicrometers underwent two 15 min coronary artery occlusions with 24 h reperfusion. The order of infusion of diltiazem (15 micrograms/kg per min) or saline solution was alternated. Systolic thickening, hemodynamic variables and regional myocardial blood flow were measured serially over 24 h. Despite equally severe ischemic dysfunction during coronary occlusion, diltiazem-treated segments with systolic thinning during ischemia recovered control segmental thickening significantly earlier than saline solution-treated segments (at 30 versus 180 min of reperfusion). Blood pressure was mildly decreased during diltiazem treatment; therefore, a second group of 10 dogs underwent a similar occlusion and reflow period during infusion of nitroprusside to lower mean arterial pressure equivalently. Decreases in blood pressure in this group resulted in some improvement in segmental systolic function; however, this did not reach statistical significance at any time. Regional myocardial blood flows were similar in the saline solution- and diltiazem-treated groups during ischemia and reflow. Thus, it is concluded that 1) diltiazem infusion significantly enhanced recovery of segmental systolic thickening after 15 min of ischemia and 24 h of reperfusion; 2) the enhancement in segmental systolic function could not entirely be attributed to decreased mean arterial pressure; 3) improvement in postischemic segmental ventricular function was seen only in those segments with systolic thinning during ischemia; thus, segments with the most severe ischemic dysfunction benefited most; and 4) there were no important differences in regional myocardial blood flow during ischemia and reperfusion between saline- and diltiazem-treated animals.
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PMID:Differential enhancement of postischemic segmental systolic thickening by diltiazem. 230 44

Although the perfluorochemical Fluosol-DA 20% has been shown to reduce myocardial infarct size, its effect on the evolution of infarct healing has not been determined. Rabbits (n = 91) were randomized to ether-oxygenated Fluosol-DA (20 ml/kg) administered intravenously at the time of reperfusion after 30 min of coronary occlusion or no intervention. Animals were sacrificed at 1, 3, 7, and 14 days after infarction. Infarct size was significantly reduced in Fluosol-DA treated animals when compared with controls at one and three days. Infarct thinning was observed at one and three days in both groups. Left ventricular wall thickness in the infarcted area was greater with Fluosol-DA than control at 7 and 14 days. Increasing amounts of foamy macrophages containing perfluorochemical particles were noted in treated animals at 7 and 14 days. No differences were noted in hydroxyproline content between groups. These studies suggest that Fluosol-DA results in persistence of foamy macrophages without significantly altering infarct topography in the temporary occlusion rabbit model.
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PMID:The effect of perfluorochemical fluosol-DA (20%) on myocardial infarct healing in the rabbit. 233 63

Increased regional left ventricular function frequently occurs in the nonischemic myocardium after acute coronary occlusion. To further define the regional and global effects of this increased remote function in the ischemic left ventricle, 22 dogs were studied with two-dimensional echocardiography before and 1 h after left circumflex coronary artery occlusion. Two groups of dogs were identified with and without compensatory increased regional left ventricular function, defined as regional wall thickening in the nonischemic zone greater than 2 SD above baseline. After coronary occlusion, nonischemic wall thickening was 76 +/- 15% in the hyperfunction group (n = 11) and 45 +/- 14% in the nonhyperfunction group (n = 11) (p less than 0.001). Despite similar left ventricular end-diastolic cavity areas and equivalent degrees of ischemic wall thinning, dogs with increased left ventricular function in the nonischemic myocardium had a smaller extent of circumferential left ventricular dysfunction (136 +/- 33 versus 170 +/- 43 degrees, p less than 0.001) and a higher area ejection fraction (38 +/- 9% versus 27 +/- 6%, p less than 0.001). These functional differences occurred despite similar myocardial areas at risk by autoradiography (41 +/- 6% versus 37 +/- 12%, p = NS). The data suggest that increased left ventricular function in the nonischemic myocardium determines the global functional impact of acute coronary occlusion and, through interaction with adjacent myocardium, modifies the extent of circumferential left ventricular dysfunction.
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PMID:Augmentation of regional function in nonischemic myocardium during coronary occlusion measured with two-dimensional echocardiography. 235 91

Despite the rat heart having very low collateral flow, there are many reports of pharmacological limitation of infarct size in rats with permanent coronary occlusion. Investigating possible artefacts, cardiac function was measured in isolated rat hearts (n = 12/group) 1, 2, 4, 6, 12, 18, 24, or 48 h after permanent coronary occlusion. In sham operated controls, cardiac output was 63.8 +/- 3.8 ml/min; in rats with occlusion this fell to 37.7 +/- 3.3 ml/min after 1 h of occlusion and did not increase during the 48 h of study. Lumen areas, areas of underperfusion, and minimum wall thickness were unchanged after 4 h of occlusion. Between 4 and 12 h, substantial wall thinning occurred (midinfarct wall thickness decreased from 3.69 +/- 0.24 mm to 2.01 +/- 0.16 mm). After 12 h of occlusion, wall thinning and expansion of the infarct increased lumen volume by three- to fourfold. Wall thinning resulted in a progressive decrease in the volume of the zone of underperfusion (which decreased by almost 30% over 48 h). Tetrazolium negative tissue was not evident in the first 4 h of occlusion but by 12 h, 85.0 +/- 2.6% of the underperfused tissue was necrotic. Gross examination of sections often indicated apparently tetrazolium positive tissue within the zone of underperfusion. Microscopic examination of histological sections revealed this tissue to be necrotic but, in contrast to the tetrazolium negative tissue within the zone of underperfusion, not yet subject to white cell infiltration. "Apparent" infarct size limitation in the rat heart might be due to: (1) incorrect designation of tissue as tetrazolium positive within the severely ischaemic zone of underperfusion; (2) inappropriately equating the zone of underperfusion (measured at the end of ischaemia) to the risk zone (measured at the onset of ischaemia); (3) the possibility that some drugs might affect white cell infiltration, tetrazolium staining characteristics, wall thinning, and tissue remodelling.
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PMID:Evolving myocardial infarction in the rat in vivo: an inappropriate model for the investigation of drug-induced infarct size limitation during sustained regional ischaemia. 245 66

We explored the role of polymorphonuclear leukocytes (PMN) in the genesis of contractile dysfunction (myocardial "stunning") and of vascular abnormalities after reversible ischemia. Open-chest dogs underwent a 15-min coronary occlusion and 4 h of reperfusion (REP); treated animals (n = 16) received intravenous goat antiserum against canine PMN, whereas controls received nonimmune goat serum (n = 10) or saline (n = 15). In treated dogs, the average blood PMN levels were 10% of those in saline controls. During ischemia, collateral flow tended to be higher, and paradoxical systolic wall thinning tended to be less in neutropenic dogs, but despite this, recovery of wall thickening after REP was not enhanced in these animals. Similarly, arrhythmias during ischemia or REP did not differ among the three groups. Four hours after REP, both resting and minimal coronary resistance (the latter assessed by adenosine infusion) were higher in the stunned compared with the nonischemic myocardium; these vascular derangements, however, were similar in all three groups. Thus profound neutropenia failed to attenuate mechanical dysfunction, to reduce arrhythmias, and to prevent vascular abnormalities after a 15-min coronary occlusion. Although previous studies have suggested that neutrophils mediate cell death during prolonged ischemia, the present findings suggest that PMN do not contribute importantly to the damage associated with brief, reversible ischemia. The duration of flow reduction may be a critical factor determining whether PMN exacerbate ischemic injury.
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PMID:Influence of neutrophil depletion on myocardial function and flow after reversible ischemia. 291 69

Indexes of global ventricular function such as the ejection fraction (EF) and the peak diastolic filling rate (PDFR) are often used to assess the effects of coronary recanalization in patients with myocardial infarction. In this investigation we assessed the relationship between these global indexes and directly measured indexes of regional function during 15 minutes of coronary occlusion followed by 120 minutes of reperfusion in 22 open-chest dogs. A computerized nuclear cardiac probe was used to assess EF and PDFR. Indexes of regional function were measured by Doppler ultrasonic wall-thickening probes. During coronary occlusion, paradoxical systolic thinning occurred and the EF and PDFR decreased an average of 31.6% and 24.4%, respectively. During reperfusion the EF and PDFR improved rapidly and at 60 minutes were similar to baseline. Systolic wall thickening improved more gradually and remained abnormal throughout reperfusion. Likewise, indexes of diastolic function (mean rate to half end-diastolic thinning and late diastolic thinning fraction) recovered slowly and remained abnormal throughout reperfusion (78% and 69.7%, respectively). The correlation between the rate of change of global and regional function was poor during both coronary occlusion and reperfusion. Thus, during coronary occlusion the global and regional indexes of ventricular function undergo directionally similar changes. However, during coronary reperfusion the global indexes do not reflect the slow recovery of the stunned myocardium.
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PMID:Dissociation between global and regional systolic and diastolic ventricular function during coronary occlusion and reperfusion. 295 31

The detection of regional myocardial dysfunction due to acute ischemic event has been limited almost entirely to experimental animal models. In human subjects, it has been limited to the observations during spontaneously-occurring or exercise-induced ischemic events. Recently, percutaneous transluminal coronary angioplasty (PTCA) provides an opportunity to study such dysfunction as the result of repeated interruptions of coronary blood flow. Echocardiograms and electrocardiograms were simultaneously recorded immediately before, during, and after 21 episodes of complete interruptions of coronary blood flow by PTCA in 11 patients. No patient had asynergy of the left ventricle either by two-dimensional echocardiography (2DE) or angiography. All patients had isolated single coronary artery stenosis including the left anterior descending artery in nine, left circumflex artery in one and right coronary artery in one. Recordings of M-mode and 2DE were successfully obtained in 10 patients. After balloon inflation, regional asynergy in the distribution of the instrumented coronary artery appeared in all 10 patients. Hypokinesis developed 9 +/- 3 (means +/- SD) sec after balloon inflation and progressed rapidly to akinesis or dyskinesis. At the same time, decreased systolic thickening of the left ventricular wall appeared in some patients in relation to the development of regional asynergy. However, systolic thinning of the left ventricular wall was not noted in all. The regional asynergy preceded ischemic electrocardiographic changes and had no relation to chest pain. Left ventricular wall motion began to normalize 12 +/- 3 sec after balloon deflation. Thereafter, transient hyperkinesis of the left ventricle developed. The first ischemic electrocardiographic change was a negative U wave which appeared 13 +/- 7 sec after coronary occlusion and remained 3 to 4 sec. Tall T waves were recorded at 28 +/- 12 sec and significant ST elevations developed 31 +/- 11 sec, after balloon inflation. These electrocardiographic changes invariably occurred only after the onset of wall motion abnormalities. Normalization of T waves was recognized at 17 +/- 16 sec and ST segment deviation were no longer present at 18 +/- 10 sec, after reperfusion. These electrocardiographic changes also preceded normalization of regional myocardial dysfunction. In conclusion, left ventricular wall motion abnormalities after coronary occlusion invariably precede the electrocardiographic changes, and begin to normalize after reperfusion prior to the electrocardiographic recovery.
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PMID:[Mechanical and electrocardiographic sequence of coronary artery occlusion: an echocardiographic study during coronary angioplasty]. 296 73


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