Published online before print June 2, 2003, doi: 10.1161/01.CIR.0000072768.80031.74
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(Circulation. 2003;107:2889.)
© 2003 American Heart Association, Inc.
Clinical Investigation and Reports |
Intravascular Ultrasound Analysis of Infarct-Related and Non–Infarct-Related Arteries in Patients Who Presented With an Acute Myocardial Infarction
From the Cardiovascular Research Institute (J.-i.K., M.T.C., E.P., C.O.B., A.B.B., A.D.P., L.F.S., W.O.S., R.W., J.R.L., K.M.K., N.J.W.), Washington Hospital Center, Washington, DC, and the Cardiovascular Research Foundation (G.S.M.), New York, NY.
Correspondence to Neil J. Weissman, MD, Cardiovascular Research Institute, 110 Irving St NW, Suite 4B-1, Washington, DC 20010. E-mail Neil.J.Weissman{at}medstar.net
Background— Previous studies have reported diffuse destabilization of atherosclerotic plaques in acute myocardial infarction (AMI).
Methods and Results— We used intravascular ultrasound (IVUS) to assess 78 coronary arteries (38 infarct-related arteries [IRAs] with culprit and nonculprit lesions and 40 non-IRAs) from 38 consecutive AMI patients. IVUS analysis included qualitative and quantitative measurements of reference and lesion external elastic membrane (EEM), lumen, and plaque plus media (P&M) area. Positive remodeling was defined as lesion/mean reference EEM >1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; P=0.0011). Culprit lesions were predominantly hypoechoic (63.2% versus 37.9% of nonculprit IRA plaques and 28.1% of non-IRA plaques; P=0.0022). Culprit lesions were longer (17.5±10.1, 9.8±4.0, and 10.3±5.7 mm, respectively; P<0.0001), had larger EEM area (15.0±6.0, 11.5±5.7, and 12.6±5.6 mm2, respectively; P=0.0353) and P&M area (13.0±6.0, 7.5±3.7, 9.3±4.3 mm2, respectively; P<0.0001), smaller lumens (2.0±0.9, 4.1±3.1, and 3.4±2.5 mm2, respectively; P=0.0009), and more positive remodeling (79.4%, 59.0%, and 50.8%, respectively; P=0.0155). The frequency of plaque rupture/dissection was greater in culprit, nonculprit IRA, and non-IRA plaques in AMI patients than in a control group of chronic stable angina patients with multivessel IVUS imaging.
Conclusions— Culprit plaques have more markers of instability (thrombus, positive remodeling, and large plaque mass); however, these markers of instability are not typically found elsewhere. This suggests that the vascular event in AMI patients is determined by local pre-event lesion morphologies.
Key Words: myocardial infarction • plaque • ultrasonics
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