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The purpose of this study was to use cardiac MRI to define the morphology of the reversibly injured pen-infarct border zone in patients treated with primary percutaneous coronary intervention (PPCI) for acute ST elevation myocardial infarction. In 15 patients, T2-weighted myocardial edema imaging was used to identify the ischemic bed or area at risk (AAR), and late gadolinium enhancement imaging was used to measure infarct size. Images were coregistered, and the boundaries of edema and necrosis were defined using an edge-detection methodology. We observed that infarction always involved the subendocardium but showed variable transmural extension within the AAR. The mean infarct size was 22 ± 19% (range: 8-48%), and the mean AAR was 34 ± 12% (range: 20-57%). The infarcted myocardium was always smaller than the ischemic AAR and involved between 34% and 99% (mean 72 ± 21%) of the ischemic bed primarily due to variation in transmural infarct extension. Although a lateral border zone of potentially viable myocardium was often present, its extent was limited (range: 0-11 mm, mean: 5 ± 4 mm). As a result of this, infarcts occupied the majority (range: 70-100%, mean: 82 ± 13%) of the width of the AAR. The mean fractional wall thickening in the infarcted, pen-infarcted, and remote myocardium was 3.6 ± 16.0%, 40.5 ± 26.4%, and 88.2 ± 39.3%, respectively. These findings demonstrate that myocardial salvage is largely determined by epicardial limitation of the infarct within the ischemic AAR after PPCI. The lateral boundaries of necrosis approximate to the lateral extent of the ischemic bed and systolic wall motion abnormalities extend well beyond the infarct border zone. [ABSTRACT FROM AUTHOR]

This article focuses on a study that explores distinct yet complementary roles of IIb/IIIa inhibitors and heparin during platelet activation with implications for restenosis following percutaneous coronary interventions (PCI). Unfractionated heparin produces significantly greater inhibition of platelet activation and smooth muscle proliferation than LMWH, at least in vitro, thus cautioning against the adoption of LMWH as the standard during PCI before clinical trials are completed. Results of the study are also discussed in the article.