Background-We studied whether lipid-lowering therapy with atorvastatin (target LDL cholesterol [LDL-C] Ͻ100mg/dL) compared with a moderate treatment regimen that used other lipid-lowering drugs led to a lesser progression of atherosclerosis and to different changes in plaque echogenicity in patients with coronary artery disease. Methods and Results-This study was a 12-month, open-label, randomized, multicenter trial, which used serial 3D intracoronary ultrasound to calculate plaque volume and plaque echogenicity. After transcatheter therapy, 131 patients were randomized (atorvastatin nϭ65, usual care nϭ66). The target plaque had to be a minor lesion (ie, a diameter stenosis of Ͻ50% on angiography). After 12 months, mean LDL-C was reduced from 155 to 86 mg/dL in the atorvastatin group and from 166 to 140 mg/dL in the usual care group. Mean absolute plaque volume showed a larger increase in the usual care group compared with the atorvastatin group (usual care 9.6Ϯ28.1 mm 3 , atorvastatin 1.2Ϯ30.4 mm 3 ; Pϭ0.191). The hyperechogenicity index of the plaque increased to a larger extent for the atorvastatin group than for the usual care group, with a significant treatment effect for the percent change (atorvastatin 42.2%, usual care 10.1%; Pϭ0.021). Conclusions-One year of lipid-lowering therapy to Ͻ100 mg/dL LDL-C most likely led to a slowdown of plaque growth of minor lesions. The significantly larger increase in plaque hyperechogenicity is most likely due to a change in plaque composition. (Circulation. 2001;104:387-392.)

Background-Recent clinical trials have suggested that intensive versus standard lipid-lowering therapy provides for additional benefit. Electron-beam computed tomography provides the opportunity to quantify the progression of coronary artery calcification (CAC) in serial measurements. Methods and Results-In a multicenter, randomized, double-blind trial, 471 patients (age 61Ϯ8 years) who had no history of coronary artery disease and no evidence of high-grade coronary stenoses (Ͼ50% diameter reduction) were randomized if they had Ն2 cardiovascular risk factors and moderate calcified coronary atherosclerosis as evidenced by a CAC score Ն30. Patients were assigned to receive 80 mg or 10 mg of atorvastatin per day over 12 months. Progression of CAC volume scores could be analyzed in 366 patients. After pretreatment with 10 mg of atorvastatin for 4 weeks, 12 months of study medication reduced LDL cholesterol from 106Ϯ22 to 87Ϯ33 mg/dL in the group randomized to receive 80 mg of atorvastatin (PϽ0.001), whereas levels remained stable in the group randomized to receive 10 mg (108Ϯ23 at baseline, 109Ϯ28 mg/dL at the end of the study, PϭNS). The mean progression of CAC volume scores, corrected for the baseline CAC volume score, was 27% (95% CI 20.8% to 33.1%) in the 80-mg atorvastatin group and 25% (95% CI 19.1% to 30.8%) in the 10-mg atorvastatin group (Pϭ0.65). CAC progression showed no relationship with on-treatment LDL cholesterol levels. Conclusions-We did not observe a relationship between on-treatment LDL cholesterol levels and the progression of calcified coronary atherosclerosis. Over a period of 12 months, intensive atorvastatin therapy was unable to attenuate CAC progression compared with standard atorvastatin therapy. The possibility remains that the time window was too short to demonstrate an effect. (Circulation. 2006;113:427-437.)

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Enhanced platelet activation is strongly associated with the development and progression of transplant vasculopathy. Understanding the underlying pathophysiological mechanisms might contribute to the development of treatment strategies to prevent transplant vasculopathy.

Myocardial infarction is the result of acute thrombotic occlusion of a coronary artery secondary to rupture of an atherosclerotic plaque. Intracoronary ultrasonic examinations (ICUS) were performed in patients with acute myocardial infarction in order to describe intraluminal ultrasonic findings at the site of an acute coronary occlusion. Coronary angiography and ICUS studies were performed consecutively within 6 h after the onset of chest pain in 50 patients with acute myocardial infarction (AMI) prior to percutaneous coronary angioplasty (PTCA). Following angiographic documentation of a proximal occlusion, a 3.5 mechanical ultrasound catheter (30 MHz) was advanced successfully through the lesion in 42 of 50 patients (84%). In 37 of the 42 patients (88.1%), ICUS differentiated between pulsatile, low echogenic, intraluminal material suggesting thrombus, and mural more highly echogenic atherosclerotic plaque. A negative imprint of the ICUS catheter was documented within the low echogenic material in 25 of 42 (60%) patients with AMI. Low echogenic intraluminal material was found in 31 of 42 (73.4%) segments proximal to the highly echogenic plaque and in 28 of 42 (66.7%) segments distal to it, indicating pre- and post-stenotic thrombus in AMI. The plaque appeared eccentric in 32 of 42 patients (76.2%) with AMI. Cross-sectional area stenosis due to highly echogenic plaque averaged 48 +/- 14%. Calcification of plaque was evident in 35 of 42 patients (83.3%) and the surface of the plaque was rough in 30 of 42 (42.4%). Fissures were found in 10 (23.8%) and a dissection was detected in four (9.5%) cases.

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An intravenous infusion of 40 mg of recombinant tissue-type plasminogen activator (t-t-PA) was given intravenously over 90 minutes to 123 patients with acute myocardial infarction (AMI) of less than 4 hours' duration. A coronary angiogram was recorded at the end of the infusion in 119 patients. Central assessment of the angiograms revealed a patent infarct-related artery in 78 patients (patency rate 66%, 95% confidence limits 57 to 74%). Patients with a patent infarct-related artery at the first angiogram were randomized in a double-blind manner to receive a subsequent B-hour infusion of either 30 mg of rt-PA or placebo. All patients had received an initial bolus of 5,000 IU of heparin and then 1,000Ill/hour until a second angiogram was recorded 6 to 24 hours after the start of the second perfusion. At central assessment of the second coronary angiogram the reocclusion rate was 2 of 36 patients who received II-PA at the second infusion and 3 of 37 patients not receiving this drug (or the 2 groups combined 7%, 95% confidence limits 2 to 15%). Three of 60 patients (5%, 95 % confidence limits 1 to 14 % ) with patent arteries on both previous angiograms had a later occlusion as judged on the angiogram recorded at hospital discharge.No difference in late reocclusion rates between the 2 treatment groups was observed.( Am J Cardiol 1987;60:231-237) A cute coronary thrombolysis with recombinant human tissue-type plasminogen activator (rt-PA] has been shown to be practicable and effective,*-5 but uncertainty persists about the most effective dosage schedule, both in terms of total dosage and distribution in timeeG To be clinically relevant, thrombolysis requires not only early recanalization, but also long-term maintenance of patency of the infarct-related artery. Different studies have shown widely varying rates of coronary reocclusion during the first hours or days after thrombolysis as documented by repeat angiography.7-2J The present trial was performed to determine the early and late predischarge reocclusion rates after patency of the infarct-related artery had been shown by coronary angiography in patients with acute myocardial infarction [AMI) treated with intravenous rt-PA. Because reocclusion was reported to occur within 1 hour after cessation of the rt-PA infusion6 an early repeat catheterization was planned at the end of the second infusion: 6 hours after start of the second infusion, the latest after 24 hours. A second aim was to assess whether a continued infusion with rt-PA over 6 hours could prevent early and late reocclusion and further reduce residual stenosis as measured by quantitative coronary angiography. The results of the quantitative angiography, performed with a computer-assisted cardiovascular angiography analysis system (CAAS], are reported separately.25 Methods Patients and management:Inclusion and exclusion criteria were the same as for the first 2 European 231