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Clinical assessment of left ventricular systolic torsion: Effects of myocardial infarction and ischemia

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DOI: 10.1016/j.echo.2008.01.011

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echocardiography; left ventricular function; torsion; coronary artery disease

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Background: The helical arrangement of myocardial fibers leads to left ventricular ( LV) torsion, a vital contributor to systolic and diastolic function. Rotation and torsion can now be measured; we sought to determine the utility of torsion as a marker of LV function at rest and after stress in patients with myocardial infarctions ( MIs) and ischemia. Methods: Dobutamine echocardiography was performed in 125 patients. After the exclusion of 40 patients with suboptimal images, LV systolic rotation and torsion were measured offline using speckle-tracking echocardiography in 44 patients with and 41 without prior MIs. Hemodynamic findings and the extent of infarction and ischemia were correlated with length-corrected torsion measurements at baseline and at peak-dose dobutamine. Results: Resting global and regional LV systolic torsion were significantly reduced in patients with compared with those without previous MIs ( 1.16 +/- 1.15 degrees / cm vs 3.16 +/- 1.3 degrees / cm, P <.001), and global systolic torsion was an independent correlate of LV ejection fraction ( LVEF) ( P =. 04). There was no difference in global LV systolic torsion in patients with anteroapical or inferoposterior infarcts ( 1.81 +/- 1.13 degrees / cm vs 2.27 +/- 1.18 degrees / cm, P = NS) and no differences in regional torsion. Torsion was most impaired in patients with multiple areas of infarction ( 1.03 +/- 0.89 degrees / cm, P <.001). However, dobutamine-induced ischemia ( 2.59 +/- 1.14 ischemic segments) had no effect on global and regional systolic torsion at peak dose or change in torsion from rest to peak dose. Conclusions: The influence of MI on LV systolic torsion appears to be related to infarct size rather than site, and torsion was an independent determinant of resting function. LV torsion was not significantly influenced by stress-induced myocardial ischemia.

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