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 the impact of greater infarct transmurality on changes in left ventricular remodeling and function after acute anterior myocardial infarction, serial topographic and functional parameters (two-dimensional echocardiograms) and hemodynamics over 6 weeks, and postmortem topography (planimetry) at 6 weeks, were measured in chronically instrumented dogs randomized to standard coronary artery ligation (group 1) or a modified lower ligation plus collateral obliteration to decrease collateral inflow and increase transmurality (group 2). At 6 weeks, postmortem scar size and collagen were similar in the two groups, but group 2 had greater transmurality associated with more necrosis relative to area at risk, Q waves, infarct expansion, thinning, regional bulging, and cavity dilatation. Over the 6 weeks, group 2 showed more early expansion, late thinning and regional bulging in the short axis, larger diastolic and systolic volumes, and more apical aneurysmal bulging in the long-axis, reflecting more topographic deterioration. More important, group 2 showed greater regional and global left ventricular dysfunction over 6 weeks, lower ejection fraction at 2 days with further decrease over 6 weeks, and more left ventricular thrombus, ventricular arrhythmias, and deaths. In addition, transmurality correlated with the severity of remodeling and dysfunction. The findings indicate that transmurality is a major determinant of remodeling and left ventricular dysfunction during healing after anterior infarction.
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PMID:Impact of increased infarct transmurality on remodeling and function during healing after anterior myocardial infarction in the dog. 145 Oct 32

To determine whether the long-term reduction of preload and afterload by captopril during healing after acute anterior myocardial infarction might attenuate left ventricular remodeling and improve function, 30 chronically instrumented dogs with infarction produced by left anterior descending coronary artery ligation were randomized 2 days later to oral therapy with placebo (n = 15) or captopril, 50 mg twice daily (n = 15), for 6 weeks. Serial hemodynamic as well as topographic and functional variables (two-dimensional echocardiography) were measured over 6 weeks. Scar topography (planimetry), occluded bed size (coronary arteriography) and collagen (hydroxyproline) content were measured at 6 weeks. Between 2 days and 6 weeks, captopril decreased (p less than 0.001) mean arterial pressure and mean left atrial pressure more than did placebo, but it did not influence heart rate. Infarct scar mass, transmurality and collagen content at 6 weeks were similar in the two groups but scars showed less (p less than 0.001) thinning and expansion with captopril than with placebo. Echocardiograms showed similar infarct expansion and thinning in the two groups at 2 days but less aneurysm with captopril at 6 weeks. Between 2 days and 6 weeks, expansion index (infarct-/noninfarct-containing segment length) decreased (p less than 0.001) with captopril but increased (p less than 0.001) with placebo. Also, thinning ratio (infarct/normal wall thickness) decreased (p less than 0.001) with placebo but did not change (p = NS) with captopril. By 6 weeks, left ventricular asynergy and volumes showed a greater decrease (p less than 0.01) and global ejection fraction a greater increase (p less than 0.05) with captopril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of long-term captopril therapy on left ventricular remodeling and function during healing of canine myocardial infarction. 153 34

To assess the usefulness of X-ray computed tomography (CT) and magnetic resonance imaging (MRI) in detecting and evaluating ischemic heart disease, conventional and enhanced CT were performed for 180 patients (150 with transmural infarction, 12 with subendocardial infarction, and 18 with angina pectoris). MRI examinations were performed for 38 patients (31 with transmural infarction, three with subendocardial infarction, and four with angina pectoris). With enhanced CT, two findings in the myocardium were direct evidence of myocardial infarction: 1. filling defects on the early scans, and 2. late enhancement of the myocardium on the delayed scans. The former were observed mainly at the sites of recent anterior myocardial infarction and the latter were seen in about half of the patients with recent and remote anterior myocardial infarctions. However, these findings were inadequately imaged in patients with inferoposterior infarction and subendocardial infarction. Among 137 patients with transmural infarction, enhanced CT revealed left ventricular aneurysms in 51 (37%) and ventricular thrombi in 26 (19%). ECG-gated MRI apparatus having a superconducting magnetic operating at 0.25 Tesla was used, and data for this study were collected using the single-slice spin echo technique. In eight of nine patients with acute myocardial infarction, gated MRI demonstrated the infarcted myocardium as regions of high signal intensity relative to that of the adjacent normal myocardium. Such a difference in MRI signal intensity was scarcely recognized in the chronic stage of myocardial infarction, but the indirect findings of infarction, such as regional wall thinning, wall motion disturbances, left ventricular aneurysms, and ventricular thrombi were easily detected using MRI. No characteristic finding was obtained by CT or MRI in patients with angina pectoris.
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PMID:[Diagnostic evaluation of ischemic heart disease by X-ray computed tomography and magnetic resonance imaging]. 342 26

Infarct expansion, defined as an alteration in the ventricular topography due to thinning and lengthening of the infarcted segment, develops within the first few hours of the acute symptoms, mostly in patients with a large, transmural, anterior myocardial infarction. Shape changes, peculiar to risk region location and due to disparity in regional ventricular architecture, could be posited as the first step in the process of infarct expansion, with various cellular mechanisms contributing to subsequent continued early and late ventricular dilation. Because the increase in left ventricular volume is expected to be linearly dependent on the extent of the infarction, limiting infarct size, by thrombolysis, would proportionally reduce enlargement of the cavity. The effect of thrombolysis on left ventricular volume, however, seems not to be completely accounted for by the lessening effect of reperfusion on infarct size, because data suggest a restraining effect of reperfusion on the process of ventricular dilation in addition to the lessening effect on infarct size. If this turns out to be true, then the achievement of a patent vessel even beyond the time period when that patency may be expected to salvage myocardium would be further justified. Theoretical predictions substantiate the potential effectiveness in restraining ventricular dilation of stiffening of the necrotic region alone, independently of myocardial salvage in infarcted patients. The process of progressive ventricular dilation involves not only a primary alteration in function of the infarcted region, but also a time-dependent secondary change in the noninfarcted tissue itself, finalized to restore stroke volume despite a persistently depressed ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventricular remodeling and infarct expansion. 827 68

A 90-year-old woman was referred to us due to acute extensive anterior myocardial infarction with cardiogenic shock. Echocardiography revealed akinesis of infarct region, associated with wall thinning. She was treated with catecholamines and diuretics because her hemodynamics were classified in Forrester subset IV. On the ninth day after the onset of infarction, she died of free-wall rupture. The postmortem histological study demonstrated eosinophil infiltration in the area of rupture, which may have been a pathological factor.
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PMID:[Eosinophil infiltration in the heart with free-wall rupture following acute myocardial infarction: a case report]. 1219 45

To evaluate multivoxel (31)P-MR spectroscopy (MRS) for assessment of energy metabolism in patients with myocardial infarction (MI) in correlation to left ventricular (LV) wall thickness and the outcome of revascularization. Thirty patients with subacute anterior myocardial infarction and planned revascularization were enrolled. 3D-chemical shift imaging was applied to determine PCr/ATP ratios in two areas: infarcted/anterior and noninfarcted/septal myocardium. MRI was used to evaluate LV function and wall thickness, and was repeated 6 months after revascularization to assess myocardial viability. Fifteen volunteers were controls. Fifteen patients showed normalization of wall motion abnormalities after revascularization (Group 1; viable), 15 not (Group 2; non-viable). Regarding infarcted/anterior myocardium, Group 2 had lower PCr/ATP ratios (0.81 +/- 0.60 vs 1.17 +/- 0.25), and PCr/ATP ratios were reduced in both groups compared to controls (1.45 +/- 0.29). Regarding noninfarcted/septal myocardium, again Group 2 had lower ratios (0.93 +/- 0.53 vs 1.31 +/- 0.38); however, compared to controls (1.51 +/- 0.32) a reduction of PCr/ATP ratios was only found in Group 2. For both myocardial regions, no correlations between PCr/ATP ratios and LV wall thickness were detected. The more severe energetic alteration in irreversibly damaged myocardium is not an effect of differences of wall thinning. Additional alterations of noninfarcted, adjacent myocardium can be detected.
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PMID:Energetic differences between viable and non-viable myocardium in patients with recent myocardial infarction are not an effect of differences in wall thinning- a multivoxel (31)P-MR-spectroscopy and MRI study. 1711 62

Marathon running transiently increases the risk of sudden cardiac death. Some previous studies have suggested that this is due to relatively advanced but asymptomatic atherosclerosis. Other theories suggest that potentiation of inflammation and the coagulation cascade, by extremes of exertion, is more important. We present a clinical case of a young, previously fit athlete who felt chest discomfort eight miles into a marathon but finished the race. Shortly after completion he felt very unwell and had chest pain. Ambulance electrocardiograms showed evidence of an evolving anterior myocardial infarction. Invasive assessment with coronary angiography and intravascular ultrasound was able to show the mechanism of thrombosis. Fissuring of a small rim of atherosclerosis potentiated a large pro-thrombotic response, the patient was also found to have sickle cell trait. Medical treatment with blood thinning drugs was able to restore normality to the vessel over a period of two weeks, without the need for angioplasty or stent implantation.
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PMID:Evading the fate of Pheidippides: acute coronary thrombosis in a young marathon runner with minimal atherosclerosis but sickle cell trait. 2633 Nov 17