Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether piroxicam, a widely used, long-acting anti-inflammatory agent, causes scar thinning after acute myocardial infarction (MI), MI was produced in 16 anesthetized, open-chest dogs by ligation of the proximal left anterior descending coronary artery. The dogs were randomized into 2 groups and treated in a blinded fashion, 8 with piroxicam, 1 mg/kg i.v. at 15 minutes and at 3 hours after ligation (Group 1) and 8 with saline solution (Group 2). Two-dimensional echocardiograms were performed 7 days and 6 weeks after ligation. At 6 weeks, the dogs were killed and the hearts examined. Scar thickness was 7.1 +/- 0.3 mm in control dogs and 5.2 +/- 0.4 mm in piroxicam-treated dogs (p less than 0.01). The ratio of scar thickness to noninfarcted wall thickness was 0.87 +/- 0.03 (mean +/- standard error of the mean) in the control group, and was significantly lower (0.62 +/- 0.04) in the piroxicam-treated group (p less than 0.001). Regional function, expressed as the percent change in the area of the left ventricular cavity (% delta A) from short-axis 2-dimensional echocardiograms, was 42 +/- 3% 7 days after occlusion in the control group and was not significantly different in the treated group (34 +/- 5%). At the end of 6 weeks % delta A had improved in the piroxicam-treated group to 44 +/- 3% (p less than 0.05 compared with the value after 7 days), and was similar to % delta A of the control group at 6 weeks (43 +/- 3%). Thus, clinical doses of piroxicam administered early after MI caused moderate scar thinning, which was not associated with impairment of regional left ventricular function 6 weeks later.
Am J Cardiol 1984 Feb 01
PMID:Morphologic and functional effects of piroxicam on myocardial scar formation after coronary occlusion in dogs. 669 91

Two-dimensional echocardiographic measurements of regional left ventricular end-diastolic wall thickness and systolic wall thickening were studied during coronary artery occlusion and early after reperfusion and compared with measurements of regional myocardial infarct size. In 25 closed chest anesthetized dogs with left anterior descending coronary artery occlusion followed by reperfusion, the occlusion period was 3 minutes in group I (n = 4), 20 minutes in group II (n = 4), 60 minutes in group III (n = 5) and 180 minutes in group IV (n = 12). Infarct size in groups III and IV was quantitated using the triphenyltetrazolium chloride technique. After coronary occlusion, wall thickening was replaced by thinning in the center of the ischemic region at the midpapillary echographic short-axis section, and no improvement in function occurred up to 60 minutes after reperfusion, except in group I. Ischemic zone end-diastolic wall thickness did not change significantly from control to the end of the coronary occlusion period, except Group IV. At 60 minutes after reperfusion, end-diastolic wall thickness increased only slightly in groups I and II (by 7.2 and 0.24%, respectively), but a marked increase was observed in groups III and IV (by 41 and 50%, respectively). The percent change in ischemic zone end-diastolic wall thickness from before reperfusion to 60 minutes after reperfusion correlated well with the amount of myocardial necrosis in corresponding segments (r = 0.936, standard error of estimate = 11.4%); an increase in segmental end-diastolic wall thickness of more than 25% was generally associated with 20% or more segmental necrosis. It is concluded that significantly increased regional end-diastolic wall thickness early after reperfusion is associated with irreversibly damaged myocardium, and this might be used as an index of myocardial salvage.
J Am Coll Cardiol 1984 Jun
PMID:Increased regional end-diastolic wall thickness early after reperfusion: a sign of irreversibly damaged myocardium. 671 5

Constrictive pericarditis and restrictive cardiomyopathy are difficult to distinguish at the bedside and occasionally at routine cardiac catheterization. Left ventricular diastolic function was studied by computer analysis of digitized M-mode echocardiograms in four patients with constrictive disease and three with restrictive disease, and the data were compared with those of normal subjects. The respective distinguishing echographic features of constrictive pericarditis and restrictive cardiomyopathy were as follows: the major filling period of the left ventricle was 78 +/- 9% of normal versus 128 +/- 4% (p less than 0.01), minimal left ventricular dimension to peak filling interval was 50 +/- 10 versus 110 ms (p less than 0.05) and the maximal rate of left ventricular posterior wall thinning was -4.9 versus -2.3 seconds-1 (p less than 0.05). This preliminary study suggests that it may be possible to accurately diagnose the two disease entities using this technique at the bedside and to avoid cardiac catheterization.
J Am Coll Cardiol 1983 Feb
PMID:Differentiation of constrictive pericarditis and restrictive cardiomyopathy using digitized echocardiography. 682 63

The factors that determine the thickness of transmural myocardial infarcts are unknown. Therefore, the relation between the size and thickness of transmural infarcts in 67 rats 21 days after occlusion of the left main coronary artery was studied. On examination of histologic sections, infarct size was determined by planimetry and expressed as a percentage of the left ventricular (LV) area, and thickness was expressed as a percentage of noninfarcted ventricular septal wall thickness. The circumferential length of the infarcted ventricle was measured in millimeters, as well as the circumferential length of the noninfarcted ventricular septum. Septal wall thickness was similar in rats with transmural infarcts and in sham-operated rats. No significant correlation was observed between infarct size and thickness (r = 0.10) or between circumferential length of the infarct and infarct thickness (r = 0.17). However, large (greater than or equal to 20% of the left ventricle, n = 37) and small (less than 20% of the left ventricle, n = 30) infarcts which were similarly thin (37 +/- 1% and 34 +/- 2% of septal wall thickness, respectively) affected LV topography differently. Large infarcts resulted in a 23% greater loss of myocardium (p less than 0.001), greater expansion of the LV cavity (18 +/- 9 mm2 compared with 14 +/- 1 mm2 in small infarcts, p less than 0.005), and lengthening of the septal wall (7.2 +/- 1.1 mm and 6.7 +/- 1.0 mm in large and small infarcts, respectively [p less than 0.05], and 6.3 +/- 0.1 mm in shams). Increase in cavity area and septal length in infarcted ventricles suggested a volume overload hypertrophy, which at 3 weeks was nonetheless inadequate to provide as much normal muscle as was present in sham-operated rats. In an additional 9 rats with subendocardial infarctions (involving less than 75% of the LV wall from endocardium to epicardium), the LV walls were thicker (94 +/- 5% of septal wall thickness, compared with 35 +/- 1% for transmural infarcts, p less than 0.001) and an inverse correlation was observed between infarct size and thickness. In conclusion, neither the size of a transmural infarct in rat nor the circumferential length of infarction determines the thickness of the infarct; however, infarct size does affect LV topography by increasing LV cavity area and the length of the noninfarcted septal wall. Subendocardial infarcts result in less myocardial thinning than do transmural infarcts.
Am J Cardiol 1983 Mar 01
PMID:Topographic changes in the left ventricle after experimentally induced myocardial infarction in the rat. 682 45

Although much attention has been directed toward interventions which reduce myocardial infarct size, the effect of such agents on the healing phase of myocardial infarction is not well understood. The present study examines the effect of the nonsteroidal anti-inflammatory agent ibuprofen, previously demonstrated to be able to reduce infarct size, and of aspirin on the healing of experimentally produced myocardial infarcts. Thirty-nine anesthetized, open-chest dogs were subjected to proximal left anterior descending coronary artery occlusions for 6 weeks. Four groups of dogs were studied: (1) a control (untreated) group: (2) ibuprofen, 12.5 mg/kg intravenously 15 minutes and 6, 12, 18, and 24 hours after occlusion (high dose); (3) ibuprofen, 12.5 mg/kg intravenously 15 minutes and 3 hours after occlusion (low dose); (4) aspirin, 30 mg/kg intravenously 15 minutes and 3 hours after occlusion. The average thickness of the transmural scar and of the noninfarcted left ventricular wall was determined from multiple measurements of formalin-fixed left ventricular slices. The ratio of transmural scar to noninfarcted wall thickness was determined. In control animals the ratio was 0.87 with only 1 of 15 animals having a ratio less than 0.60. High-dose ibuprofen-treated animals had an average ratio of 0.59 (difference not significant [NS] compared with control values), with 6 of 9 animals having a ratio less than 0.60 (p less than 0.02 compared with control values). Low-dose ibuprofen-treated animals had an average ratio of 0.66 (p less than 0.05 compared with control values), with 4 of 8 animals having a ratio less than 0.60 (p = NS compared with control values). In the aspirin-treated animals, the ratio was 0.88 (p = NS compared with control values), with 0 of 7 animals having a ratio less than 0.60 (p = NS compared with control values). Although 1 of 22 animals had ratios less than 0.60 in the control and aspirin groups, 10 of 17 had ratios less than 0.60 in the ibuprofen-treated groups (p less than 0.001). Scars in treated animals did not differ from those in control animals histologically or by analysis of hydroxyproline content per unit weight. Thus, ibuprofen, a nonsteroidal anti-inflammatory agent which reduces infarct size, is shown to increase the incidence of scar thinning after myocardial infarction.
Am J Cardiol 1983 Mar 01
PMID:Scar thinning due to ibuprofen administration after experimental myocardial infarction. 682 46

In 19 patients with Duchenne's muscular dystrophy, left ventricular wall thickness in end-systole and end-diastole was determined serially every 12 months by echocardiography and compared with ventricular wall growth in normal subjects. In the normal subjects, left ventricular wall thickness increased linearly with increasing body surface area. A control group of wheelchair-bound patients with a variety of neurologic disorders, although not followed serially, had a distribution of end-diastolic wall thickness values similar to that of the normal subjects. In patients with muscular dystrophy, wall thickness increased linearly with respect to body surface area for some time and then began to thin. The time at which thinning began was not directly related to age, although it was more common in older than in younger patients. Those patients who died demonstrated marked deviation from normal wall growth. Free wall thinning is probably a result of fibrosis and loss of myofibrils.
J Am Coll Cardiol 1983 Jul
PMID:Serial left ventricular wall measurements in Duchenne's muscular dystrophy. 685 8

Myocardial infarction (MI) was produced in 27 dogs by ligation of the left anterior descending coronary artery. Two-dimensional (2-D) echocardiograms were performed through the closed chest before and serially after coronary ligation, in both the acute and healing stages of MI. Two-dimensional echocardiographic studies performed before the animals were killed were analyzed for left ventricular (LV) contraction defects by 2 algorithms--1 involving systolic myocardial thickening and thinning and the other by determining the extent of endocardial motion to derive cavity area shrinkage. Using the thickening algorithm, myocardial dysfunction was detected in 93% of the animals with MI; with the area shrinkage method, contraction abnormalities were detected in 96% of the animals with MI. When the heart was divided from base to apex into 3 short-axis sections, the thickening algorithm showed a trend toward better identification of normal regions than the area shrinkage algorithm. However, in predicting the circumferential extent of MI, the thickening-thinning method of analysis showed no advantage over the endocardial motion method (r = 0.77, standard error of the estimate = 0.16 versus r = 0.76, standard error of the estimate [SEE] = 0.16; p = not significant [NS]). These observations support the concept that either algorithm can be used effectively to detect the presence and quantify the circumferential extent of MI.
Am J Cardiol 1983 Jun
PMID:Quantitative detection of regional left ventricular contraction abnormalities by 2-dimensional echocardiography. Comparison of myocardial thickening and thinning and endocardial motion in a canine model. 685 83

Seven dogs were instrumented with a left ventricular micromanometer and pairs of ultrasonic crystals to measure left ventricular wall thicknesses (control and ischemic regions) and short and long left ventricular axes; cuff occluders were placed around the left circumflex coronary artery and the inferior vena cava. Measurements were performed at rest, after 2 min of partial and complete coronary occlusion, and 1 and 10 min after release of partial and complete coronary occlusion. Left ventricular wall thickness in the ischemic region showed reduced systolic thickening during partial coronary occlusion and systolic thinning during complete coronary occlusion. During diastole, at zero pressure (inferior vena cava obstruction) the left ventricular short axis was unchanged during partial coronary occlusion but significantly increased (creep) during complete coronary occlusion (P less than 0.05), whereas after release of both partial and complete coronary occlusion the short axis at zero pressure decreased significantly (P less than 0.025). Left ventricular wall thickness at zero diastolic pressure in the ischemic region was significantly thinner during complete coronary occlusion than during control and significantly thicker (reactive hyperemia) 1 min after release of both partial and complete coronary occlusion. The long left ventricular axis remained unchanged during the entire experiment. At end-diastole, the long/short axis ratio was normal during partial (1.72; control 1.68; NS) and complete coronary occlusion (1.69; NS), but it decreased significantly from control of 2.10 to 1.99 with partial coronary occlusion and 1.85 with complete coronary occlusion (P less than 0.01). The changes in the L/S ratio during partial and complete coronary occlusion were proportional to changes in left ventricular chamber volume (correlation coefficient 0.94). Our data show that left ventricular shape remains normal at end-diastole during partial and complete coronary occlusion but becomes significantly more spherical at end-systole, with reduction of the normal tendency for the ventricle to become more elliptical during systole. These elliptical and spherical shape changes of the left ventricle during partial and complete coronary occlusion appear to be closely related to the chamber volume.
Int J Cardiol 1982
PMID:Left ventricular geometry during partial and complete coronary occlusion in the conscious dog. 711 5

Cardiac contusion is a potentially fatal complication of blunt chest trauma. The diagnosis is obscured because cardiac contusion usually occurs in a setting of multisystem trauma. Furthermore, the electrocardiographic changes are nonspecific. Experience with 2-dimensional echocardiography in evaluating cardiac trauma has not previously been emphasized. This report examines the results of 2-dimensional echocardiographic examinations in 7 patients after significant blunt chest trauma. Generalized right ventricular dilatation was identified in 4 cases; superimposed segmental areas of right ventricular dilatation occurred in 3. Three patients had localized myocardial thinning, and segmental wall motion abnormalities occurred in 2. Additional abnormalities identified included ventricular thrombi (4 right and 1 left ventricular), fibrinous pericardial effusion (1), ruptured tricuspid chordae with flail leaflet (1), and a small aneurysm of the sinus of Valsalva (1). It is concluded that 2-dimensional echocardiography is useful for diagnosing cardiac contusion, for estimating the extent of myocardial damage, and for identifying accompanying cardiac lesions such as thrombi, pericardial effusion, and valvular disruption.
Am J Cardiol 1982 Nov
PMID:Two-dimensional echocardiographic findings in cardiac trauma. 713 27

Exercise thallium myocardial scintigrams were analyzed in 76 consecutive patients with documented normal coronary arteries to identify the factors associated with abnormal or "false positive" studies. The thallium scintigrams had been judged normal in 60 patients (79 percent) and abnormal in 16 (21 percent). Analysis of the location of thallium defects in the 16 patients with abnormal scintigrams revealed a pattern that was consistent with coronary artery disease in 5, including 4 with an abnormal left ventricle, and a pattern that was inconsistent in the other 11. In 9 of these 11 patients the pattern of defects suggested soft tissue attenuation, by the diaphragm in 2 and breast or adipose tissue in 7, whereas in the other 2 patients isolated apical defects were seen. Among exercise myocardial scintigrams performed in 68 randomly selected patients with abnormal coronary arteries, 6 (9 percent) were reported to be normal. In four patients with abnormal scintigrams, the diagnosis of coronary artery disease was based on an inconsistent pattern. In three of these the pattern was related to isolated apical defects and in one it was related to apparent soft tissue attenuation. "Consistent" scintigraphic defects, seen frequently in patients with normal coronary arteries, in whom they are usually associated with an abnormal left ventricle. In patients with normal coronary arteries, "inconsistent" thallium defects are probably related to soft tissue attenuation or to normal apical thinning. Although defects caused by isolated apical abnormalities and soft tissue attenuation are also seen in patients with coronary diseases and add somewhat to scintigraphic sensitivity, they are a rare cause of diagnostic scintigraphic abnormalities in patients with coronary disease. The incidence of false positive thallium scintigrams could be reduced and overall accuracy improved by careful attention to the pattern of thallium defects.
Am J Cardiol 1981 Aug
PMID:The inconsistent pattern of thallium defects: a clue to the false positive perfusion scintigram. 727 Apr 32


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