LEFT VENTRICULAR MECHANICS Identification of Viable Myocardium in Acute Anterior Infarction Using Duration of Systolic Lengthening by Tissue Doppler Strain: A Preliminary Study Trond Vartdal, MD, Eirik Pettersen, MD, Thomas Helle-Valle, MD, Erik Lyseggen, MD, PhD, Kai Andersen, MD, PhD, Hans-Jørgen Smith, MD, PhD, Lars Aaberge, MD, PhD, Otto A. Smiseth, MD, PhD, and Thor Edvardsen, MD, PhD, Oslo, Norway Background: The aim of this study was to investigate whether strain Doppler echocardiography before reperfusion therapy could quantify ischemic dysfunction and predict viable myocardium in acute myocardial infarction as determined by magnetic resonance imaging. Methods: Twenty-six patients (mean age, 60 6 12 years; seven women) with acute myocardial infarctions who underwent acute percutaneous coronary intervention were examined using strain Doppler echocardiography immediately before the procedure. Percutaneous coronary intervention was performed 296 6 122 min after the onset of pain. Peak left ventricular systolic longitudinal strain and the duration of systolic lengthening were analyzed. Magnetic resonance imaging was performed 11 6 5 months after therapy. Scarring exceeding 50% of the segment area was considered nonviable. Results: Peak systolic strain fell gradually (becoming less negative) from normal segments to segments with transmural infarction (P < .0001), and the duration of systolic lengthening increased (P < .0001). Myocardial scar- ring was closely correlated with peak systolic strain (R = 0.76, P < .00001) and the duration of systolic lengthening (R = 0.88, P < .00001). There was a significant correlation between the degree of scarring and time to percuta- neous coronary intervention (R = 0.40, P = .045). In segments with systolic lengthening, the improvement in strain after remodeling was significantly higher (5.5 6 5.1%) than in segments with duration of systolic lengthening > 67% of systole (2.2 6 3.7%) (P < .001). Receiver operating characteristic curve analyses showed that duration of systolic lengthening > 67.3% could identify nonviable myocardium (sensitivity, 90%; specificity, 94%). Conclusions: In patients with acute myocardial infarctions in the anterior wall, strain measurements can identify myocardium with nontransmural scarring. The duration of systolic lengthening is a novel, easily implemented variable that may identify ischemic but viable myocardium. Myocardial infarctions in other left ventricular regions should be investigated in future studies. (J Am Soc Echocardiogr 2012;25:718-25.) Keywords: Echocardiography, Magnetic resonance imaging, Myocardial infarction, Ischemia, Myocardial strain The accurate assessment of myocardial function is an important clinical issue in patients with acute myocardial infarctions (AMIs). Revascularization of dysfunctional but still viable myocardium may be of prognostic importance. 1,2 Approximately 40% of regions showing Q waves or dysfunction in chronic myocardial infarction are not irreversibly damaged, and myocardial function in those regions may be improved by revascularization. 3,4 Patients with ST-segment elevation myocardial infarctions (STEMIs) and with chest pain should receive reperfusion therapy according to present guide- lines. However, patients with AMIs are a heterogeneous group, in which up to one third of those with non–ST-segment elevation myo- cardial infarctions have occluded culprit arteries, while some patients with STEMIs have no occlusions. Thus, the correct identification of viable tissue in patients with ischemic heart failure could be of great clinical importance. 5 In a clinical setting, a range of different imaging modalities can be useful in assessing viability. 2,6-12 However, none of these methods is suitable in the acute setting, and there is currently no established method to detect viable myocardium during ongoing ischemia. Electrocardiography is currently the only method for the detection of transmural injury in AMI. Q waves, however, should be used with care to distinguish transmural from subendocardial infarcts. 13 From the Department of Cardiology (T.V., E.P., T.H.-V., E.L., K.A., L.A., O.A.S., T.E.) and the Department of Radiology (H.-J.S.), Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway. Drs. Vartdal, Lyseggen, and Helle-Valle were recipients of a research fellowship from the Norwegian Council on Cardiovascular Diseases, and Dr. Pettersen was a recipient of a research fellowship from the Norwegian Research Council. Reprint requests: Thor Edvardsen, MD, PhD, Oslo University Hospital, Rikshospi- talet, Department of Cardiology, 0027 Oslo, Norway (E-mail: thor.edvardsen@ medisin.uio.no). 0894-7317/$36.00 Copyright 2012 by the American Society of Echocardiography. doi:10.1016/j.echo.2012.04.016 718