Abstract 2608: Dyssynchrony Contributes to Left Ventricular Dysfunction after Acute Myocardial Infarction
In patients with acute myocardial infarction (AMI), involved segments may not only show depressed but also delayed contraction, leading to left ventricular dyssynchrony. However, the presence of dyssynchrony in patients with AMI has not been previously studied. Real time 3D echo (RT3DE) is particularly suitable for this purpose due to its ability to evaluate the entire left ventricle (LV) in real time. We aimed to describe the presence of LV dyssynchrony in AMI by correlating it with the degree of LV dysfunction, infarct size and location, and to characterize the presence of dyssynchrony in myocardial segments at risk.
Methods. We prospectively enrolled 29 patients admitted for a first ST elevation AMI. A RT3DE performed within 48hs of admission was analyzed by a reader blinded to the clinical data. Peak systole for each of the 16 segments was defined as the time between the beginning of the QRS and the moment of minimal segmental volume. Dyssynchrony index (DI) was defined as the standard deviation of timing for peak systole in all 16 segments, and reported as percentage of the cardiac cycle length to adjust for different heart rates. Segments with peak systole after the aortic valve closure were considered to have delayed contraction. LV dysfunction was assessed by LVEF and infarct size by peak Troponin I. Myocardial segments at risk for each patient were determined after reviewing each coronary angiogram, based on the location of the culprit lesion, and blinded to RT3DE and clinical data.
Results: 21 patients (72%) were male; age was 60±12 years, LVEF 42.2±8.3% and QRS duration was 87.8±13.4. AMI involved the anterior wall in 41% of patients. DI was 7.6±2.7. DI had a good correlation with LVEF (r=0.5, p=0.005) but not with peak TnI (r=0.27, p=0.15). There was no difference in DI between patients with anterior and non-anterior AMI (p=0.85). Segments at risk had later contraction compared to non-at-risk (peak systole 37.4±6 vs 34.1±4.5%, p=0.03). 60.4±24.5% of the segments at risk showed delayed contraction compared to 38.9±12.9 of those not at risk (p=0.0003).
Conclusion: In patients early after an AMI, LV dysfunction is mostly related to LV dyssynchrony rather than infarct size or location. Dyssynchrony is caused by delayed contraction of segments at risk.