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

Infarct expansion, the time-related thinning and dilation of an acute transmural infarct, leads to aneurysm formation and cardiac rupture in humans. In this study, the effect of exercise on acute infarct expansion early after myocardial infarction was examined in 129 rats. Ninety rats were exercised on a treadmill for 1.5 hours daily for 1 week beginning on the day of coronary artery ligation; the remaining 39 rats remained in their cages. There was no effect on the prevalence or extent of expansion; specifically, infarct wall thickness, left ventricular diameter and expansion grade (0 to 4+) were similar in the exercise and control rats. There was no difference in infarct size or the number of animals with aneurysmal shape changes in the exercise and control groups. There was no significant difference between the two groups in the histologic finding of intramural hemorrhage, a feature that has been associated with cardiac rupture, and no complete rupture was seen. However, there was a nonsignificant trend toward higher mortality in the exercised group. Thus, the findings of this study suggest that moderate exercise early after myocardial infarction produces no significant detrimental effect on infarct size or left ventricular topography in the rat model.
J Am Coll Cardiol 1986 Jan
PMID:Effect of exercise on acute myocardial infarction in rats. 394 Nov 99

Temporal changes in infarct collagen and left ventricular topography during healing after myocardial infarction were studied in 132 dogs with coronary artery ligation: 8 sham dogs and 13 with no infarction (controls) and 111 with infarction (3 at 1 day, 54 at 2 days, 25 at 7 days, 3 at 2 weeks, 9 at 4 weeks and 17 at 6 weeks). Myocardial hydroxyproline (a marker of collagen) was measured by spectrophotometry and pathologic infarct size, arteriographic occluded bed size and topography by computerized planimetry of weighed left ventricular rings. Over 6 weeks, hydroxyproline was unchanged in normal regions (average 4.20 mg/g dry weight) but increased progressively between 7 days and 6 weeks (9.94 versus 55.55 mg/g, p less than 0.001) in infarct zones. Progressive infarct contraction occurred over 6 weeks, with infarct size at 6 weeks being 40% less than at 2 days (9.7 versus 16.3% of the left ventricle, p less than 0.001), although total infarct hydroxyproline was directly related to infarct size at each time period (r = 0.73 to 0.81, p less than or equal to 0.05). Significant (p less than or equal to 0.05) left ventricular topographic changes in infarct hearts compared with control hearts included: 1) increase in cavity area (5.0 versus 3.9 cm2), endocardial circumference (8.8 versus 7.4 cm) and expansion index (infarct/normal endocardial segment length, 1.21 versus 1.02) by 7 days; and 2) decrease in thinning ratio (infarct/normal wall thickness, 0.71 versus 0.98) by 6 weeks. Also, compared with 2 day infarcts, by 6 weeks infarct area was decreased (1.8 versus 3.4 cm2) and the noninfarcted segment length increased (6.9 versus 5.4 cm). Changes in hydroxyproline and topography were similar for anterior (n = 54) and posterior (n = 57) infarcts. Thus, healing in canine infarcts is associated with cavity dilation and infarct expansion within 7 days followed by infarct contraction and thinning by 6 weeks, whereas collagen increases between 7 days and 6 weeks. Collagen deposition in expanded and thinned infarct segments explains the permanent regional shape distortion associated with ventricular aneurysms.
J Am Coll Cardiol 1986 Jan
PMID:Healing after myocardial infarction in the dog: changes in infarct hydroxyproline and topography. 394 Dec 23

Nuclear magnetic resonance imaging has emerged in the past few years as a completely noninvasive method for medical imaging of internal organs. Because of the loss of signal intensity by motional nuclei (hydrogen) using most proton imaging techniques, flowing blood within the cardiovascular system generates little or no signal and consequently there is high natural contrast between blood and the walls of blood vessels or cardiac chambers. However, motion during imaging also complicates cardiac imaging because signal is lost from the nuclei in the moving cardiac structures. Consequently electrocardiographic gating of data acquisition is required for nuclear magnetic resonance imaging of the heart. Distinct advantages of nuclear magnetic resonance imaging in relation to other imaging modalities are good contrast between soft tissues and the capability for characterization of specific tissues by estimation of magnetic relaxation times. Early in vitro studies measuring relaxation times of myocardial tissue samples of excised hearts indicate that nuclear magnetic resonance imaging will be capable of discriminating infarcted from normal myocardium. Recent studies using electrocardiographically gated nuclear magnetic resonance imaging of dogs with acute infarction showed the infarct as a region of high intensity on spin-echo images. Initial clinical experience with electrocardiographically gated nuclear magnetic resonance imaging (0.35 tesla) in patients has clearly defined internal cardiac anatomy without the use of contrast media. This technique has demonstrated the consequence of previous myocardial infarction such as regional wall thinning, aneurysm, thrombus and contractile dysfunction, a number of pericardial abnormalities and the morphology of hypertrophic and congestive cardiomyopathies.
J Am Coll Cardiol 1985 Jan
PMID:Assessment of cardiac anatomy using nuclear magnetic resonance imaging. 396 36

Two-dimensional echocardiographic findings in porcine valve dysfunction were compared with pathologic findings in 10 patients (12 valves). Three specific echocardiographic findings were identified in patients with regurgitant lesions: prolapse, fracture and flail leaflets. Prolapse was associated pathologically with thinning of the leaflets, longitudinal tears close to the ring margin and acid mucopolysaccharide accumulation. Valve fracture was seen with and without prolapse and was accompanied pathologically by small pinpoint perforations or tears of the leaflet. A flail leaflet was seen with a linear tear of the free margin and was associated with calcific deposits. Mild degrees of fracture seen pathologically were missed on the echocardiographic study in five patients. Thickening or calcification, when present in moderate or severe amounts, was correctly identified by echocardiography. When all abnormal features were considered collectively, two-dimensional echocardiography correctly identified at least one of them in all patients. Therefore, two-dimensional echocardiography may prove useful in assessing the source of valvular regurgitation in patients with bioprosthetic valves.
J Am Coll Cardiol 1985 Feb
PMID:Correlation of two-dimensional echocardiography and pathologic findings in porcine valve dysfunction. 396 7

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.
Am J Cardiol 1985 Feb 15
PMID:In vivo assessment of left ventricular wall and chamber dynamics during transient myocardial ischemia using cine computed tomography. 396 99

Alterations in afterload may occur during acute myocardial infarction (AMI), but it is unknown whether such alterations cause long-term changes in the left ventricular topography or alter healing of the AMI. AMI was produced by ligation of the left anterior descending coronary artery in open-chest dogs. Eight dogs were randomized to a methoxamine group with an infusion dose of 30 micrograms/kg/min starting 1 hour after ligation for 4 hours to increase systemic systolic pressure by 40 to 50 mm Hg, and 8 were randomized to a saline control group (n = 8). Seven days later the dogs were killed and the hearts examined. The ratio of infarct wall thickness to noninfarct wall thickness was 1.13 +/- 0.03 (mean +/- standard error of the mean) in control dogs and was 0.98 +/- 0.03 in the dogs treated with methoxamine (p less than 0.005). An expansion index was determined as previously reported and expansion was considered to have occurred if this index exceeded 1.09. The expansion index was 0.98 +/- 0.06 in the control group and 1.18 +/- 0.07 in the methoxamine group (p less than 0.05). Histologic analysis suggested a lag in the healing rate in the methoxamine-treated dogs. Thus, early, brief increases in afterload cause infarct expansion and thinning and appears to slow the early healing phase of AMI in dogs.
Am J Cardiol 1985 Feb 15
PMID:Effects of transient increased afterload during experimentally induced acute myocardial infarction in dogs. 396

The magnitude and distribution of mechanical stresses acting on the closed cusps of porcine bioprosthetic valves (PBVs) were estimated using a finite element model. The effects of leaflet stiffening, focal calcium and focal thinning on leaflet stresses were determined. In a normal closed PBV leaflet, stresses increased as pressure was increased. At a pressure of 80 mm Hg, the maximal normal principal stresses were 11 g/mm2 near the center of the leaflet and increased to 19 g/mm2 at a pressure of 160 mm Hg. These observations suggest that the closed valve in the mitral position would experience higher mechanical stresses than the closed valve in the aortic position. Tissue stiffening increased stresses throughout the leaflet and introduced a site of stress concentration near the center of the leaflet. At a pressure of 80 mm Hg, the maximal principal normal stress increased 55% when the leaflet was stiff in comparison to the normal leaflet. Focal calcium and focal thinning caused marked gradients of stress between the sites of calcium or thinning and the immediate surrounding tissue. The magnitude of these stress gradients increased with increasing pressure. These sites of mechanical stress concentration or stress gradients appear to be compatible with sites of leaflet calcification or disruption. Such stresses may contribute to spontaneous degeneration of PBVs.
Am J Cardiol 1985 Apr 01
PMID:Estimation of mechanical stresses on closed cusps of porcine bioprosthetic valves: effects of stiffening, focal calcium and focal thinning. 398 72

Apical left ventricular (LV) wall motion abnormalities have been described in chronic volume overload. To evaluate if these abnormalities are due to an actual hypokinesia we analyzed the percent shortening of apical LV radiants (PS%) by an angiographic computerized method and the endocardial systolic movement (ESM) and thickening (%Th) of the same region using M-mode echocardiographic technique in 11 patients affected by pure aortic regurgitation (AR). In these patients mean apical radii shortening was reduced with respect to normal values. Both %Th and ESM were significantly reduced in AR when compared to normal subjects (24.5 +/- 31.7% vs. 63.8 +/- 35.8%, p less than 0.01 and 4 +/- 7 vs. 10 +/- 3 mm, p less than 0.01, respectively). In addition, %Th and ESM directly correlated with PS% (r = 0.79, p less than 0.01 and r = 0.77, p less than 0.01, respectively). PS% correlated positively with systolic eccentricity and inversely with end-systolic volume index (r = 0.64, p less than 0.05 and r = 0.57, p less than 0.05, respectively). Finally, in AR %Th was related to a normalized peak rate of systolic wall thickening (r = 0.85, p less than 0.01) and to a normalized peak rate of diastolic wall thinning (r = 0.68, p less than 0.05). These results showed that in AR a reduced apical radii percent shortening was associated with a reduced normalized peak rate of systolic wall thickening and of diastolic wall thinning, thus indicating an actual hypokinesis and an impaired contractility. Moreover, the observed abnormalities correlated with an altered LV dynamic geometry linked to chronic volume overload.
Clin Cardiol 1985 May
PMID:Apical left ventricular asynergy in chronic aortic regurgitation. 399 2

The healing phase of acute myocardial infarction (AMI) is initiated by proteolysis of necrotic myocardium, followed by infiltration of fibroblasts and deposition of collagen. To assess whether ibuprofen, a potent antiinflammatory agent, preserves existing collagen and enhances deposition of new collagen during infarct healing, biochemical and morphologic studies were made of experimentally induced myocardial infarcts in untreated rats and in rats treated with ibuprofen. All treated rats received 12.5 mg/kg of ibuprofen at 1, 6 and 18 hours after AMI. Group 1 rats underwent measurement of myocardial hydroxyproline (HP) content at 24 hours after AMI. Group 2 rats received ibuprofen, 12.5 mg/kg, twice a day for 2 additional days, with measurement of myocardial HP at 3 days (group 2a) or 21 days (group 2b) after AMI. Group 3 rats received ibuprofen, 12.5 mg/kg, twice a day for 6 additional days with measurement of HP content, or infarct size and degree of thinning at 21 days after AMI. Compared with untreated rats, ibuprofen-treated rats had significantly greater amounts of HP in the infarct at 24 hours (group 1, 8.9 +/- 2.2 nmol/mg dry weight vs untreated, 7.1 +/- 2.8 nmol/mg dry weight, p less than 0.04) and at 21 days (group 2b, 112 +/- 37 nmol/mg dry weight vs untreated, 91 +/- 39 nmol/mg dry weight, p less than 0.05, and group 3, 125 +/- 51 nmol/mg dry weight vs untreated, 91 +/- 39 nmol/mg dry weight, p less than 0.003). Substantial scar thinning was noted in all rats; no difference in scar thinning was noted between treated and untreated rats at 21 days after AMI.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1985 Jun 01
PMID:Effect of ibuprofen on the healing phase of experimental myocardial infarction in the rat. 400 5

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)
J Am Coll Cardiol 1985 Oct
PMID:Early infarct expansion: structural or functional? 403 Dec 98


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