Intravascular ultrasound findings in patients with acute coronary syndromes with and without elevated troponin I level

Abstract

T acute coronary syndromes population is heterogenous, and patients with an elevated troponin I on admission have worse outcomes than those without elevated troponin I. In addition, angiographic studies of patients with unstable angina pectoris show less severe culprit lesion stenosis, more frequent B2/C lesion complexity, and a higher prevalence of intracoronary thrombus in patients with troponin elevation. However, coronary angiography provides limited insights into plaque morphology and distribution. The aim of the present study was to use intravascular ultrasound (IVUS) to determine whether patients with acute coronary syndromes and elevated troponin I have different qualitative and quantitative coronary plaque characteristics than patients with acute coronary syndromes without elevated troponin I. • • • We compared the preintervention IVUS findings of 40 patients with acute coronary syndromes (progressive or worsening angina for 6 weeks, rest angina with or without objective evidence of ischemia such as electrocardiographic and/or hemodynamic changes, and recurrence of angina in 6 weeks after acute myocardial infarction), and elevated troponin I (troponin I 0.15 ng/ml on admission) with 46 patients with acute coronary syndromes and normal troponin I levels. Patients were matched for age, gender, the presence of risk factors for coronary artery disease (diabetes mellitus, hypertension, hypercholesterolemia, and smoking) and for lesion location (Table 1). Patients were excluded from analysis if on admission they had (1) a diagnosis of acute ST elevation myocardial infarction, (2) new pathologic Q waves in at 2 contiguous electrocardiographic leads, and (3) recent ( 3 weeks) acute myocardial infarction. All patients met the following IVUS criteria: (1) high quality IVUS imaging of a native coronary artery target lesion and distal and proximal references, (2) de novo lesion, (3) nonostial lesion location, and (4) single culprit lesion. All IVUS studies were performed before any predilation and after administration of 200 g of intracoronary nitrogycerin using a commercially available imaging system (Boston Scientific/SciMed Corporation, Boston Massachusetts) that incorporated a single-element 30or 40-MHz beveled transducer mounted on the tip of a flexible shaft and rotated at 1,800 rpm within a 3.2 Fr or 2.6 Fr short monorail imaging sheath. The IVUS catheter was advance 10 mm distal to the lesion and the transducer was automatically withdrawn retrograde to the aorto-ostial junction using motorized pullback at 0.5 mm/s. Studies were recorded on high-resolution 0.5-inch s-VHS tape for off-line analysis. Quantitative and qualitative analyses were performed by experienced clinicians blinded to the troponin I level according to the recently published American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of IVUS. Reproducibility of the IVUS area and longitudinal measurements from our laboratory has been reported. Quantitative analysis included: (1) lesion and mean reference external elastic membrane (EEM) area, lumen area, and plaque & media (EEM minus lumen) area; (2) plaque burden (plaque & media divided by EEM area); (3) lumen area stenosis (average reference lumen minus lesion minimal lumen cross-sectional area) divided by (average reference lumen area) ; (4) lesion length; and (5) arcs and lengths of calcium. The lesion site was the IVUS image slice with the smallest lumen area. The reference sites were the most normal-looking cross sections within the same segment as the lesion, but before any major side branch. Qualitative assessment of the entire length of the lesion included: (1) plaque morphology (hypoechoic, hyperechoic, calcified, or mixed); (2) location of calcium; and (3) presence of thrombus, dissection, and/or plaque rupture. These latter findings were considered to represent high-risk morphologic configurations. Statistical analysis was performed using SigmaStat (2.03, SPSS Science, Chicago, Illinois) or StatView 5.0 (SAS Institute, Cary, North Carolina). Quantitative data, presented as mean SD, were compared using an unpaired, 2-tailed Student’s t test. Qualitative (categorical) data, presented as frequencies, were compared using chi-square statistics. A p value 0.05 was considered significant. Patient baseline characteristics are summarized in Table 1. Patients with elevated troponin I levels had (1) more prior myocardial infarctions, (2) a similar rate of elevated admission creatine kinase-MB fracFrom the Cardiovascular Research Institute and the Cardiac Catheterization Laboratories, Washington Hospital Center, Washington, DC; and the Cardiovascular Research Foundation, New York, New York. Dr. Fuch’s address is: Cardiovascular Research Institute, Washington Hospital Center, 110 Irving Street NW, 4B-1, Washington, DC 20010. E-mail: shmuel.fuchs@medstar.net. Manuscript received December 14, 2001; revised manuscript received and accepted January 24, 2002.