UMLS:C0151814 - FACTA Search

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Query: UMLS:C0151814 (coronary occlusion)
3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine whether the extent of the zone at risk for infarction after coronary artery occlusion influences the percentage of the zone that evolves to necrosis in the absence of intervention, 99mTc-labeled albumin microspheres were injected into the left atrium 1 min after coronary occlusion in 34 dogs. Six hours after occlusion, the left ventricle was cut into 3-mm-thick slices for triphenyltetrazolium chloride staining and autoradiography. The extent of myocardial necrosis and hypoperfused zone was measured by planimetry and expressed as a percentage of the total volume of the left ventricle. The extent of myocardial necrosis and hypoperfused zone varied widely from 8 to 40% and 14 to 43% of the left ventricle, respectively. However, there was a close correlation between infarct size (IS, percent of left ventricle) and the extent of hypoperfused zone (HZ, percent of left ventricle): IS = 0.89x (HZ) - 0.21 (r = 0.909, SEE = 3.02, p less than 0.01). The ratio of infarct size to the extent of hypoperfused zone was 87.9 +/- 2.3%. Dogs with large hypoperfused zones (greater than or equal to 30% of the left ventricle) had a significantly greater ratio of infarct size to the extent of the hypoperfused zone (95.3 +/- 2.4%, n = 11, p less than 0.05) than dogs with small hypoperfused zones (less than 30% of the left ventricle; 84.3 +/- 3.0%, n = 23). Moreover, the ratio was greater than or equal to 90% in all but one dog (91%) with large hypoperfused zones, but in only 10 of 23 dogs (43%) with small hypoperfused zones (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does the extent of the zone at risk after coronary artery occlusion influence the percentage of the zone that evolves to infarction? 239 88

To evaluate the potential advantages of thallium-201 (201T1) single-photon emission computerized tomography (SPECT) to assess myocardial infarct size in the experimental animal, six normal dogs and 14 dogs with 6 to 8 hr closed-chest coronary occlusion (eight left anterior descending and six left circumflex) were studied. Ten minutes after intravenous administration of 2 mCi of 201T1, 30 projections were obtained over 180 degrees. The dogs were killed and their hearts sliced and stained by triphenyl tetrazolium chloride (TTC). Pathologic infarct size was calculated for each slice and for the entire left ventricular myocardium as percent weight. Tomograms were quantified by automatically generating maximum-count circumferential profiles, which were compared with normal limit profiles derived from the six normal dogs. Tomographic infarct size was defined as the percentage of circumferential points falling below normal for each tomogram. SPECT and TTC infarct size on 71 slices correlated highly (mean +/- SD 27.9 +/- 23.4% and 26.7 +/- 25.3%, respectively; r = .93, p less than .001, SEE = 9.4%). To determine SPECT infarct size as percent total left ventricular myocardial weight, infarct sizes from each slice were added to one another after each was multiplied by a coefficient that reflected the contribution of that slice to the total left ventricular weight. SPECT and TTC infarct size for the entire left ventricle correlated closely (mean +/- SD 20.5 +/- 7.6% and 19.3 +/- 8.3%, respectively; r = .86, p less than .001, SEE = 4.5%). It is concluded that 201T1 SPECT is a valid method for the noninvasive assessment of experimental myocardial infarct size.
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PMID:Quantification of myocardial infarct size by thallium-201 single-photon emission computed tomography: experimental validation in the dog. 242 40

The current study assessed the capability of ECG-gated MR imaging to quantitate both the percentage of the left ventricle involved by acute myocardial infarction and the mass of acute myocardial infarction at 3 and 21 days after coronary occlusion in dogs. Infarct mass was measured from gated transverse MR images using computer-generated calculated-T2 images. T2 images provided accentuation of the boundary between infarcted and normal myocardium as well as objective, reproducible calculation of image voxels representing infarcted myocardium. Postmortem and in vivo MR infarct mass and percentage correlated closely at 3 days (r = .98, SEE = 0.73 g; r = .97, SEE = 1.2%), and 21 days (r = .94, SEE = 1.54 g; r = .95, SEE = 1.61%). Left ventricular mass, infarct mass, and percentage of infarct were measured on end-diastolic MR images. Infarct mass at 3 and 21 days was not significantly different, with a mean deviation of 0.63 g. There was close intra- and interobserver reproducibility (r = .99 and r = .90, respectively) for measurement of infarct mass. The quantitative technique employed for determining the mass of acute myocardial infarctions, based on the different T2 relaxation times of infarcted and normal myocardium, provides for objective analysis and reproducibility. With this technique, MR provides an accurate method for assessing the mass of acute infarcts and the percentage of the left ventricle involved by the infarct both early and late after coronary occlusion.
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PMID:Measurement of myocardial infarct size at early and late time intervals using MR imaging: an experimental study in dogs. 349 44

This study examined the relation between left ventricular (LV) function and the severity of acute myocardial ischemia in a conscious dog model. The LV ejection fraction (EF) was measured by multigated equilibrium radionuclide angiography, and regional myocardial blood flow was measured with radioactive microspheres before and 10 minutes after distal and then proximal occlusion of the left anterior descending (LAD, 13 dogs) or left circumflex (LC, 13 dogs) coronary artery. Two methods were used to evaluate the extent of ischemia. The first method determined the mass of myocardium that was ischemic based on different degrees of reduced blood flow. The second method estimated the severity of ischemia expressed as blood flow deficit resulting from each coronary occlusion. Global LV function was very sensitive to ischemia, and the relation between change in function and the degree of ischemia were described best by linear functions. The best linear correlation between mass of ischemic myocardium and percent reduction in EF resulted from the ischemic region defined as all tissue with 25% or greater reduction in blood flow, r = 0.84 for LAD (Y = 0.96X + 1.8) and r = 0.75 for LC (Y = 0.53X + 2.0) occlusions. Defining ischemic mass by more severe reduction in blood flow resulted in exclusion of ischemic myocardium that affected function. The myocardial blood flow deficit also correlated linearly with percent reduction in EF, r = 0.89 for LAD (Y = 1.31X + 2.7) and r = 0.81 for LC (Y = 0.83X - 0.1) occlusions. The slope of the regression lines using both analyses of ischemia were significantly greater (p less than 0.01) for LAD than LC occlusions, indicating that for comparable degrees of ischemia LAD as compared to LC occlusion decreased EF to a greater extent. Calculation of EF from attenuated corrected volumes resulted in small changes in LAD, but not LC, EF and did not account for the disproportionate effects of LAD and LC ischemia. In a separate group of studies (n = 18) EF measured by radionuclide angiography after LAD or LC occlusions correlated well with biplane contrast angiography r = 0.93, SEE 5.1. These data suggest that disproportionately greater effects of LAD compared to LC ischemia on global EF in the dog are due primarily to different pathophysiologic responses to ischemia.
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PMID:Relation between myocardial perfusion and left ventricular function following acute coronary occlusion: disproportionate effects of anterior vs. inferior ischemia. 356 88

Acute myocardial infarction progresses radially from endocardium to epicardium within the ischemic area. The amount of progression is highly variable, but depends largely on the transmural distribution of myocardial blood flow. Recent contrast echocardiographic observations indicate that slowly appearing low levels of contrast enhancement are often seen in the ischemic region, particularly in the epicardial level, and that ischemic regions which show these low levels of contrast have significantly more blood flow than those that do not. This study was designed to determine whether the transmural distribution of this delayed contrast enhancement can sufficiently discriminate between regions of high and low flow to serve as an in vivo predictor of the transmural extent of acute infarction. Twenty-four dogs had acute circumflex coronary ligation which was maintained for 6 hours. Contrast echocardiographic studies were performed at the level of the mitral chordae 2 hours after occlusion using a dilute hydrogen peroxide and blood solution as a contrast agent. Comparison was made with the pathologic infarct measured by triphenyltetrazolium chloride staining. The mean transmural extent of infarction ranged from 0 to 89% and was predicted in vivo by the transmural extent of the delayed contrast defect (r = 0.92; infarction [percent transmural] = 0.74 contrast [percent transmural] + 11%; SEE = 10%). Reproducibility for the transmural extent of delayed contrast defects was good (r = 0.89 to 0.98.) These data further support the concept that the transmural distribution of delayed contrast enhancement parallels blood flow and indicate that the mean transmural extent of acute infarction can be predicted in vivo 2 hours after coronary occlusion from the residual contrast defect.
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PMID:In vivo prediction of the transmural extent of experimental acute myocardial infarction using contrast echocardiography. 371 9

To define the in vivo relation between abnormal wall motion and the area at risk for necrosis after acute coronary occlusion, 11 open chest dogs were studied. Five dogs underwent left anterior descending coronary artery occlusion and six underwent left circumflex artery occlusion. Area at risk was defined at five short-axis levels (mitral valve, chordal, high and low papillary muscle and apex) using myocardial contrast echocardiography. Wall motion was measured in the cycles preceding injection of contrast medium. Two observers used two different methods to measure wall motion. In method A, end-diastolic to end-systolic fractional radial change for each of 32 endocardial targets was determined. The extent of abnormal wall motion was then calculated using three definitions of wall motion abnormality: akinesia/dyskinesia, fractional inward endocardial excursion of less than 10%, and fractional inward endocardial excursion of less than 20%. In method B, the information from the entire systolic contraction sequence was analyzed and correlated with a normal contraction pattern. The best linear correlation between area at risk (AR) and abnormal wall motion (AWM) was achieved using method B and expressed by the following linear regression: AWM = 0.92 AR + 3.0 (r = 0.92, p less than 0.0001, SEE = 1.7%). Of the three definitions of abnormality used in method A, the best correlation was achieved between area at risk and less than 10% inward endocardial excursion and was expressed by the following polynomial regression: AWM = -0.01 AR2 + 1.5 AR -0.14 (r = 0.92, p less than 0.001, SEE = 1.7%). These data demonstrate that there is a definite relation between area at risk and abnormal wall motion but that this relation varies depending on the method used to analyze wall motion. However, wall motion during acute ischemia is also influenced by the loading conditions of the heart. Because these may vary in a manner that is independent of the ischemic process, measurement of both risk area and abnormal motion may provide a more comprehensive assessment of cardiac function in myocardial ischemia than is provided by the measurement of either alone.
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PMID:Contrast echocardiography in acute myocardial ischemia. III. An in vivo comparison of the extent of abnormal wall motion with the area at risk for necrosis. 394 58

Myocardial contrast echocardiography has been shown recently to accurately assess the "area at risk" for necrosis after acute coronary occlusion in the experimental model. Risk area quantitation, however, has been studied primarily from single tomographic planes. Because the three-dimensional extent of myocardial necrosis depends on the total volume of myocardium at risk, the total left ventricular "area at risk" was determined in 11 dogs (Group A) with either left anterior descending or left circumflex artery occlusion using contrast echocardiography and compared with risk area determined by technetium autoradiography. An excellent correlation was found between the two methods (r = 0.96%, y = 0.91x + 1.5, p less than 0.001, SEE = 3.17). A comparison of risk area for individual levels of the left ventricle using both methods, however, showed some variation in the degree of correlation, with the poorest fit being apparent at the apex. To identify the source of the variation, errors caused by data registration were minimized in six additional dogs (Group B) by implanting epicardial markers at a single level and measuring "area at risk" at this level using both methods. When no registration error was present, the correlation between the two methods was excellent (r = 0.99, y = 0.92x + 2.6, p less than 0.001, SEE = 0.55). In conclusion, the "area at risk" for infarction after acute coronary occlusion can be determined accurately for the entire left ventricle as well as for a single tomographic slice using myocardial contrast echocardiography. This was validated using technetium autoradiography, which is an established method of determining "area at risk" in the experimental setting.
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PMID:Contrast echocardiography in acute myocardial ischemia: I. In vivo determination of total left ventricular "area at risk". 609 39

During sustained coronary occlusion in canine preparations, the extent of regions that fail to show contrast enhancement when imaged by supra-aortic hydrogen peroxide contrast echocardiography (SHPCE) has been shown to correlate well for single cross sections with the extent of malperfused myocardium "at risk" of infarction. In the present study, SHPCE was investigated as a means of determining the fraction of total left ventricular mass at risk during occlusion. Since necrotic tissue has low blood flow even when reperfused, we also investigated the potential of quantitating the extent of infarcted myocardium by measuring the extent of contrast defects seen with SHPCE performed during reperfusion. In 20 dogs the fraction of the left ventricle showing a contrast defect during coronary occlusion correlated well with the fraction of the left ventricular mass "at risk" by an autoradiographic technique (autoradiography = 0.83 echocardiography + 8.6%; r = .89, SEE = 4.5%). SHPCE was also performed after 3 hr of reperfusion following occlusions varying in duration from 60 to 150 min. The fraction of the ventricle showing a contrast defect during reperfusion predicted the infarcted portion of the left ventricle as shown by triphenyl tetrazolium chloride staining (% left ventricle infarcted = 0.81 echocardiography + 3.3%; r = .84, SEE = 5.3%). Observer variability for the fraction of the ventricle showing a contrast defect was excellent during both occlusion and reperfusion. The ratio of the left ventricular extent of contrast-negative regions during reperfusion and occlusion was used to calculate a necrosis-to-risk index in vivo that correlated relatively well with the myocardial necrosis-to-risk ratio determined morphologically (r = .77, SEE = 16%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hydrogen peroxide contrast echocardiography: quantification in vivo of myocardial risk area during coronary occlusion and of the necrotic area remaining after myocardial reperfusion. 673 85

Regional left ventricular function was studied serially by quantitative two-dimensional echocardiography (2-D echo) in 20 dogs after left anterior descending coronary artery ligation. Normal values for regional myocardial thickening were established in 20 healthy dogs and used as a standard to recognize abnormally contracting segments (ACS). In normal hearts, the mean percent thickening tended to increase from base (25.8%) to apex (34.0%), but showed considerable diversity from segment to segment (range 20.0-40.0%); nevertheless, at least some degree of thickening was seen in every segment. After coronary occlusion, myocardial segments either thinned or failed to thicken. At the papillary muscle level, there was an improvement in function between 2 and 48 hours, with thinning at 2 hours and thickening at 48 hours. Tissue infarct size (IS) determined at 48 hours was related to IS derived from a weighted summation of ACS at 2, 24 and 48 hours. At 2 hours, ACS considerably overpredicted and correlated poorly with tissue IS (25.3% vs 13.4%; r = 0.60); by 48 hours, IS predicted by ACS had decreased to 15.3% (p less than 0.05) and had an improved, but only fair correlation with tissue IS (r = 0.73, SEE = 4.9%). We conclude that there is considerable heterogeneity to myocardial thickening by 2-D-echo, but failure to thicken is not seen in the normal dog heart. In many dogs, the extent of myocardial dysfunction 2 hours after coronary ligation exceeds that seen later. Tissue IS is difficult to predict accurately from ACS. Since the amount of muscle dysfunction is not necessarily equivalent to the amount of tissue necrosis in acute myocardial infarction, ACS may be more appropriate used to tract the course of infarction rather than to predict IS.
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PMID:Serial evaluation of myocardial thickening and thinning in acute experimental infarction: identification and quantification using two-dimensional echocardiography. 708 4

Quantitative assessment of perfusion defects with myocardial contrast echocardiography can be a valuable tool in the evaluation of patients with coronary artery disease. However, the use of 2-dimensional echocardiography for this purpose is limited to a restricted number of imaging planes. Real-time 3-dimensional echocardiography (RT3D) is a novel technique that provides instantaneous volumetric images. The aim of this study was to validate the use of RT3D for the quantitative assessment of myocardial perfusion defects in a model of acute coronary occlusion. To this end, 20 sheep underwent acute ligation of the left anterior descending (n = 14) or the posterior branch of the circumflex (n = 6) artery under general anesthesia. The RT3D images were obtained after left atrial injection of the contrast agent EchoGen (perflenapent emulsion; 0.8-1 mL). Evans blue dye was injected into the occluded coronary artery for subsequent anatomic identification of underperfused myocardium. The mass of the entire left ventricle and of the underperfused myocardial region were measured after death. Blinded off-line calculation of left ventricular (LV) mass and perfusion-defect mass from RT3D images were performed using an interactive aided-manual tracing technique. Total LV mass ranged from 68 to 141 g (mean plus minus SD: 92 +/- 24 g). The mass of the perfusion defect ranged from 0 to 43 g (mean +/- SD: 16 +/- 9 g) or 0 to 36% of total LV mass (mean +/- SD: 18% +/- 9%). The RT3D estimation of total LV mass strongly correlated with the anatomic measurement (r = 0.91; y = -2.54 + 1.04x; standard error of the estimate [SEE] = 11.9 g). The RT3D calculation of the mass of underperfused myocardium also strongly correlated with the anatomic measurement, both in absolute terms (r = 0.96; y = 2.01 + 0.87x; SEE = 2.2 g) and when expressed as percentage of total LV mass (r = 0.96; y = 0.11 + 1.02x; SEE = 2.8%). Hence, RT3D with myocardial contrast opacification accurately predicts the amount of underperfused myocardium in an animal model of acute coronary occlusion. This technique may therefore be useful for the quantitative assessment of myocardial perfusion defects in patients with coronary artery disease.
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PMID:Quantitative assessment of left ventricular perfusion defects using real-time three-dimensional myocardial contrast echocardiography. 1187 82

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