Defining the Transmurality of a Chronic Myocardial Infarction by Ultrasonic Strain-Rate Imaging

Abstract

Background— In a correlative functional/histopathologic study, we investigated the regional deformation characteristics of both chronic nontransmural and transmural infarctions before and after a dobutamine challenge. Methods and Results— After stenosing copper-coated stent implantation to produce circumflex artery endothelial proliferation, 18 pigs were followed up for 5 weeks. Posteuthanasia histology showed 10 to have a nontransmural and 8 a transmural infarction. Eight nonstented animals served as controls. Regional radial function was monitored by measuring ultrasound-derived peak systolic strain rates (SR _SYS ) and systolic strains (ε _SYS ) (1) before stent implantation and (2) at 5 weeks, at baseline (bs) and during an incremental dobutamine infusion. In controls, dobutamine induced a linear increase in SR _SYS (dobutamine: bs, 4.8±0.4 s ⁻¹ ; 20 μg · kg ⁻¹ · min ⁻¹ , 9.9±0.7 s ⁻¹ ; P SYS at low dose (bs, 58±5%; at 5 μg · kg ⁻¹ · min ⁻¹ , 78±6%; P SYS and ε _SYS were significantly lower than prestent values (SR _SYS , 2.9±0.5 s ⁻¹ and ε _SYS , 32±6%, P SYS increased slightly at 5 μg · kg ⁻¹ · min ⁻¹ (4.7±0.6 s ⁻¹ , P SYS showed no change. For nontransmural infarctions, transmural scar extension correlated closely with ε _SYS at bs ( r =0.88). For transmural infarctions, SR _SYS at bs was significantly reduced and ε _SYS was almost not measurable (SR _SYS , 1.8±0.3 s ⁻¹ ; ε _SYS , 3±4%). Both deformation parameters showed no further change during the incremental dobutamine infusion. Conclusions— Ultrasonic deformation values could clearly differentiate chronic nontransmural from transmural myocardial infarction. The transmural extension of the scar could be defined by the regional deformation response.