Impact of Left Ventricular Dyssynchrony Early on Left Ventricular Function After First Acute Myocardial Infarction

The impact of left ventricular (LV) dyssynchrony after acute myocardial infarction (AMI) on LV ejection fraction (EF) is unknown. One hundred twenty-nine patients with a first ST-elevation AMI (58 ± 11 years, 78% men) and QRS duration <120 ms were included. All patients underwent primary percutaneous coronary intervention. Real-time 3-dimensional echocardiography and myocardial contrast echocardiography were performed to assess LV function, LV dyssynchrony, and infarct size. LV dyssynchrony was defined as the SD of the time to reach the minimum systolic volume for 16 LV segments, expressed in percent cardiac cycle (systolic dyssynchrony index [SDI]). Myocardial perfusion at myocardial contrast echocardiography was scored (1 = normal/homogenous; 2 = decreased/patchy; 3 = minimal/absent) using a 16-segment model; a myocardial perfusion index, expressing infarct size, was derived by summing segmental contrast scores and dividing by the number of segments. SDI in patients with AMI was 5.24 ± 2.23% compared to 2.02 ± 0.70% of controls (p <0.001). Patients with AMI and LVEF <45% had significantly higher SDI compared to patients with LVEF ≥45% (4.29 ± 1.44 vs 6.95 ± 2.40, p <0.001). At multivariate analysis, SDI was independently related to LVEF; in addition, the impact of SDI on LV systolic function was incremental to infarct size and anterior location of AMI (F change 16.9, p <0.001). In conclusion, LV synchronicity is significantly impaired soon after AMI. LV dyssynchrony is related to LVEF and has an additional detrimental effect on LV function, beyond infarct size and the anterior location of AMI. The impact of left ventricular (LV) dyssynchrony after acute myocardial infarction (AMI) on LV ejection fraction (EF) is unknown. One hundred twenty-nine patients with a first ST-elevation AMI (58 ± 11 years, 78% men) and QRS duration <120 ms were included. All patients underwent primary percutaneous coronary intervention. Real-time 3-dimensional echocardiography and myocardial contrast echocardiography were performed to assess LV function, LV dyssynchrony, and infarct size. LV dyssynchrony was defined as the SD of the time to reach the minimum systolic volume for 16 LV segments, expressed in percent cardiac cycle (systolic dyssynchrony index [SDI]). Myocardial perfusion at myocardial contrast echocardiography was scored (1 = normal/homogenous; 2 = decreased/patchy; 3 = minimal/absent) using a 16-segment model; a myocardial perfusion index, expressing infarct size, was derived by summing segmental contrast scores and dividing by the number of segments. SDI in patients with AMI was 5.24 ± 2.23% compared to 2.02 ± 0.70% of controls (p <0.001). Patients with AMI and LVEF <45% had significantly higher SDI compared to patients with LVEF ≥45% (4.29 ± 1.44 vs 6.95 ± 2.40, p <0.001). At multivariate analysis, SDI was independently related to LVEF; in addition, the impact of SDI on LV systolic function was incremental to infarct size and anterior location of AMI (F change 16.9, p <0.001). In conclusion, LV synchronicity is significantly impaired soon after AMI. LV dyssynchrony is related to LVEF and has an additional detrimental effect on LV function, beyond infarct size and the anterior location of AMI.