of positive or negative exercise stress echocardiography for predicting coronary events in ensuing twelve months. Am J Cardiol 1993;71:64&651. 11. Diamond GA, Forrester JS. Analysis of probability as an aid in the clinical diagnosis of coronary-artery disease. N Engl J Med 1979;300:135f&1358. 12. Dymond DS, Foster C, Grenier RD, Carpenter J, Schmidt DH. Peak exercise and immediate post exercise imaging for the detection of left ventricular function- al abnormalities in coronary artery disease. Am Heart .I 1984;53:1532-1537. 13. Armstrong WF, O’Donnell fA, Ryan T, Feigenbaum H. Effect of prior rnyo- cardial infarction and extent and location of coronary artery disease on accuracy of exercise echocardiography. JAm CM Cardiol 1987;10:531-538. infarction, and in asymptomatic individuals. Ani Heart J 1988:116:523-535. 15. Ryan T, Armstrong WF, O’Dobnell JA, Feigenbaum H. Risk stratification after acute myocardial infarction by means of exercise two-dimensional echocardiog- raphy. Am HeartJ 1987;114:1305-1316. 16. Brown KA. Prognostic value of thallium-201 myocardial perfusion imaging: a diagnostic tool comes of age. Circulation 1991;83:363-381, 17. Pamelia FX, Gibson RS, Watson DD, Grziddock GB, Sirowatka J, Belier GA. Prognosis with chest pain and normal thallium-201 scintigrams. Am J Cardiol 1985;55:92&926. 14. Goldschlager N, Sax HC. The diagnostic and prognostic value of the treadmill 18. Gal RA, Gunasekera J, Massardo T, Shalev Y, Port SC. Long-teim prognostic value of a normal dipyridamole thallium-201 perfusion scan. Chin Cardiol 1991;14: exercise test in the evaluation of chest pain, in patients with recent myocardial 911-914. Effect of Serum Lipid Concetitratibns on Restenosis After Successful de Novo Percuianeous l’ransluminal Coronary Angiopiasiy in Patients with Total Cholesterol 160 to 240 *g/d! and Triglycerides ~350 mg/dl Vladimir Dzavik, MD, Koon K. Teo, MB, PhD, Shinji Yokoyama, MD, PhD, Renuca Modi, Alison Dinwoodie, MD, Jeffrey R. Burton, MD, Wayne J. Tymchak, MD, and Terrence J. Montague, MD T he efficacy of successful percutaneoustransluminal center study evaluating the effect of simvastatin and coronary angioplasty (PTCA) continues to be limit- ed by a late restenosis rate, ashigh as45%.’ This process enalapril on coronary artery disease progression and regression in patients with a total serum cholesterol lev- is likely due to a responseto injury causedby balloon- induced intimal disruption.2 Several growth factors are el of 160 to 240 mg/dl (4.1 to 6.2 mmol/L) and a tri- glyceride level ~350 mg/dl (4.0 mmol/L). No patient believed to play a role in initiating and propagating took lipid-lowering medication between the time of neointimal smooth cell proliferation and gradual reduc- tion in the arterial luminal diameter after PTCA.3 PTCA and subsequent SCAT baseline angiography.This study design using the SCAT population servedto elim- Whether or not abnormalities of lipoprotein metabolism inate the noise caused by a high LDL cholesterol, and contribute to restenosis remains a matter of controver- SY.~ Although some investigators have found no corre- lation between the level of serum lipids and restenosis,5 evidence from other small studies using clinical mark- ers for restenosis and visual or caliper angiographic assessment suggests that low high-density lipoprotein (HDL) cholesterol, high triglycerides, and high lipopro- tein(a) (Lp[a]) may be associated with an increasedrisk of restenosis after PTCA.&* The purpose of this study was to further evaluate the effect of HDL cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, and Lp(a) on restenosis after successful PTCA of de novo nonocclusive coronary lesions in patients with nor- mal or mildly elevated total serum cholesterol (1240 mg/dl or 6.2 mmol/L) using quantitative computerized analysis. . . . The study group consistedof 52 consecutivepatients who had previous successfulPTCA of a de novo nonoc- eluded stenotic lesion of a native coronary artery, and who were to be enrolled in the Sim+astatin/Enalapril Coronary Atherosclerosis RegressionTrial (SCAT), out of 270 total patients enrolled in that trial. SCAT is a prospective randomized 2 X 2 factorial design, multi- From the Division of Cardiolo y, University of Alberta Hospitals, Uni- versity of Alberta Edmonton, A berta, Canada TG6 287. Manuscript 9 received January 26, 1995; revised manuscript received and accept- ed February 13, 1995. TABLE I Baseline Characteristics of the 52 Study Patients With de Nova PTCA Variables Age (yrl 57 f 9 Men/women (%) 87/13 Reason far PTCA (%) Stable angina 9 (17) Unstable angina 12 (23) After AMI (-xl year) 26 (50) Acute AMI 1 PI Silent ischemia 2 (4) Primary artery dilated Left anterior descending 29 left circumflex 14 Right 9 Time from PTCA to fallow-up (ma) 15 * 11 Mean pre-PTCA % diameter stenosis 67.0 i 11.6 Mean past-PTCA % diameter stenosis 30.8 i- 8.2 Mean fallow-up % diameter stenosis 39.0 * 17.6 % of patients with iestenasis (~50%) 21 Total cholesterol in mg/dl (mmal/L) 205 i 27 (5.3 e 0.7) LDL cholesterol in mg/dl (mmal/L) 132 i 27 (3.4 * 0.7) HDL cholesterol in mg/dl (mmal/L) 39 zt 8 (1 .O * 0.2) Triglycerides in mg/dl (mmal/L) 158 it 79 (1.9 * 0.9) Tatal/HDL cholesterol ratio 5.5 f 1.2 Lipoprotein(a) (g/L) 0.11 f 0.13 Values ore expressed as mean t SD. AMI = acute myocordiol infarction; HDL = highdensity lipoprotein; LDL = low-density lipoprotein; PTCA = percutaneous transluminal coronary ongim plosly. 936 THE AMERICAN JOURNAL OF CARDIOLOGY@ VOL. 75 MAY 1, 1995