BACKGROUND: Left ventricular (LV) torsion is emerging as a sensitive parameter of LV systolic myocardial performance. The aim of the present study was to explore the effects of acute myocardial infarction (AMI) on LV torsion and to determine the value of LV torsion early after AMI in predicting LV remodeling at 6-month follow-up. METHODS AND RESULTS: A total of 120 patients with a first ST-segment elevation AMI (mean+/-SD age, 59+/-10 years; 73% male) were included. All patients underwent primary percutaneous coronary intervention. After 48 hours, speckle-tracking echocardiography was performed to assess LV torsion; infarct size was assessed by myocardial contrast echocardiography. At 6-month follow-up, LV volumes and LV ejection fraction were reassessed to identity patients with LV remodeling (defined as a > or =15% increase in LV end-systolic volume). Compared with control subjects, peak LV torsion in AMI patients was significantly impaired (1.54+/-0.64 degrees /cm vs 2.07+/-0.27 degrees /cm, P<0.001). By multivariate analysis, only LV ejection fraction (beta=0.36, P<0.001) and infarct size (beta=-0.47, P<0.001) were independently associated with peak LV torsion. At 6-month follow-up, 19 patients showed LV remodeling. By multivariate analysis, only peak LV torsion (odds ratio=0.77; 95% CI, 0.65-0.92; P=0.003) and infarct size (odds ratio=1.04; 95% CI, 1.01-1.07; P=0.021) were independently related to LV remodeling. Peak LV torsion provided modest but significant incremental value over clinical, echocardiographic, and myocardial contrast echocardiography variables in predicting LV remodeling. By receiver-operating characteristics curve analysis, peak LV torsion < or =1.44 degrees /cm provided the highest sensitivity (95%) and specificity (77%) to predict LV remodeling. CONCLUSIONS: LV torsion is significantly impaired early after AMI. The amount of impairment of LV torsion predicts LV remodeling at 6-month follow-up.
BACKGROUND: Left ventricular (LV) torsion is emerging as a sensitive parameter of LV systolic myocardial performance. The aim of the present study was to explore the effects of acute myocardial infarction (AMI) on LV torsion and to determine the value of LV torsion early after AMI in predicting LV remodeling at 6-month follow-up. METHODS AND RESULTS: A total of 120 patients with a first ST-segment elevation AMI (mean+/-SD age, 59+/-10 years; 73% male) were included. All patients underwent primary percutaneous coronary intervention. After 48 hours, speckle-tracking echocardiography was performed to assess LV torsion; infarct size was assessed by myocardial contrast echocardiography. At 6-month follow-up, LV volumes and LV ejection fraction were reassessed to identity patients with LV remodeling (defined as a > or =15% increase in LV end-systolic volume). Compared with control subjects, peak LV torsion in AMI patients was significantly impaired (1.54+/-0.64 degrees /cm vs 2.07+/-0.27 degrees /cm, P<0.001). By multivariate analysis, only LV ejection fraction (beta=0.36, P<0.001) and infarct size (beta=-0.47, P<0.001) were independently associated with peak LV torsion. At 6-month follow-up, 19 patients showed LV remodeling. By multivariate analysis, only peak LV torsion (odds ratio=0.77; 95% CI, 0.65-0.92; P=0.003) and infarct size (odds ratio=1.04; 95% CI, 1.01-1.07; P=0.021) were independently related to LV remodeling. Peak LV torsion provided modest but significant incremental value over clinical, echocardiographic, and myocardial contrast echocardiography variables in predicting LV remodeling. By receiver-operating characteristics curve analysis, peak LV torsion < or =1.44 degrees /cm provided the highest sensitivity (95%) and specificity (77%) to predict LV remodeling. CONCLUSIONS: LV torsion is significantly impaired early after AMI. The amount of impairment of LV torsion predicts LV remodeling at 6-month follow-up.
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