Circulation. 2003;107:883-888
Published online before print February 3, 2003, doi: 10.1161/01.CIR.0000050146.66577.4B
Published online before print February 3, 2003, doi: 10.1161/01.CIR.0000050146.66577.4B
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(Circulation. 2003;107:883.)
© 2003 American Heart Association, Inc.
Basic Science Reports |
Defining the Transmurality of a Chronic Myocardial Infarction by Ultrasonic Strain-Rate Imaging
Implications for Identifying Intramural Viability: An Experimental Study
From the Department of Cardiology (C.D., B.B., P.C., F.v.d.W., I.D., G.R.S.), the Department of Medical Image Computing, ESAT (J.D.), the Department of Nuclear Medicine (P.M., A.M.), and the Department of Pathology, University Hospital Gasthuisberg, Leuven, Belgium (E.V.); and the Department of Cardiology, University Hospital Wuerzburg, Germany (F.W.).
Correspondence to Professor George R. Sutherland, Department of Cardiology, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. E-mail george.sutherland{at}uz.kuleuven.ac.be
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 (SRSYS) and systolic strains (
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 SRSYS (dobutamine: bs, 4.8±0.4 s-1; 20 µg · kg-1 · min-1, 9.9±0.7 s-1; P<0.0001) and an initial increase of SYS at low dose (bs, 58±5%; at 5 µg · kg-1 · min-1, 78±6%; P<0.05) but a subsequent decrease during higher infusion rates. In the nontransmural group, bs SRSYS and SYS were significantly lower than prestent values (SRSYS, 2.9±0.5 s-1 and SYS, 32±6%, P<0.05 versus prestent). During dobutamine infusion, SRSYS increased slightly at 5 µg · kg-1 · min-1 (4.7±0.6 s-1, P<0.05) but fell during higher infusion rates, whereas SYS showed no change. For nontransmural infarctions, transmural scar extension correlated closely with SYS at bs (r=0.88). For transmural infarctions, SRSYS at bs was significantly reduced and SYS was almost not measurable (SRSYS, 1.8±0.3 s-1; 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.
Key Words: infarction • ultrasonics • contractility
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