(3S-5S-6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3-5-dihydroxyhept-6-enoic-acid and Coronary-Stenosis

This study sought to assess, by serial computed tomography angiography (CTA), the effect of statin treatment on coronary plaque morphology.. In addition to the assessment of luminal stenosis, CTA also allows characterization of plaque morphology. Large, positively remodeled plaques with large necrotic cores have been reported as indicators of plaque instability.. CTA was performed in 32 patients (26 men, ages 64.3 +/- 8.5 years). Of these, 24 received fluvastatin after the baseline study; 8 subjects who refused statin treatment were followed as the control subjects. Serial imaging was performed after a median interval of 12 months. All vessels were examined in every subject, and a 10-mm-long segment was identified for comparison before and after intervention. Total plaque volume, low attenuation plaque (LAP) volume, lumen volume, and remodeling index were calculated.. In the statin-treated patients, the total plaque volume (92.3 +/- 37.7 vs. 76.4 +/- 26.5 mm(3), p < 0.01) and LAP volume (4.9 +/- 7.8 vs. 1.3 +/- 2.3 mm(3), p = 0.01) were significantly reduced over time; however, there was no change in the lumen volume (63.9 +/- 25.3 vs. 65.2 +/- 26.2 mm(3), p = 0.59). On the other hand, no change was observed in the CTA characteristics in the control subjects, including total plaque volume (94.4 +/- 21.2 vs. 98.4 +/- 28.6 mm(3), p = 0.48), LAP volume (2.1 +/- 3.0 vs. 2.3 +/- 3.6 mm(3), p = 0.91), and lumen volume (80.5 +/- 20.7 vs. 75.0 +/- 16.3 mm(3), p = 0.26). The plaque volume change (-15.9 +/- 22.2 vs. 4.0 +/- 14.0 mm(3), p = 0.01) and LAP volume change (-3.7 +/- 7.0 vs. 0.2 +/- 1.5 mm(3), p < 0.01) were significantly greater in the statin than the control group. The lumen volume (1.3 +/- 15.6 vs. -5.5 +/- 13.1 mm(3), p = 0.24) and remodeling index (-2.4 +/- 6.8% vs. -0.3 +/- 6.5%, p = 0.53) did not show the significant differences between the 2 groups. The decrease in the plaque volume was due to reduction in the LAP volume (R = 0.83, p < 0.01), and was not related to any changes in the lumen volume (R = 0.21, p = 0.24).. This preliminary study suggests that serial CTA evaluation of coronary plaques allows for the assessment of interval change in the plaque morphology. Statin treatment results in decreases in the plaque and necrotic core volume. The features known to be associated with plaque instability.

Topics: Aged; Coronary Angiography; Coronary Stenosis; Fatty Acids, Monounsaturated; Female; Fluvastatin; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Indoles; Male; Middle Aged; Necrosis; Pilot Projects; Predictive Value of Tests; Prospective Studies; Severity of Illness Index; Tomography, X-Ray Computed; Treatment Outcome

Statins are frequently given in conjunction with clopidogrel for prophylaxis and therapy of coronary heart disease. The antiplatelet effect of clopidogrel may be attenuated by lipophilic statins such as atorvastatin. It was the aim of this study to measure the antiplatelet effect of clopidogrel and the incidence of cardiovascular events after stent implantation in patients with coronary artery stenting.. ADP-induced aggregometry was used in 319 patients after coronary artery stent implantation to determine whether added administration of clinically relevant statins would affect the antiplatelet action of clopidogrel. Also a three-month follow-up was undertaken to determine the incidence of cardiovascular events.. There were no significant differences between the statin-receiving subgroups, either in platelet aggregation nor in clinical outcome in our cohort.. No statin-clopidogrel interaction nor any clinically relevant events were documented in the studied cohort. No interaction between CYP3A4 statins and a single loading dose of 600 mg clopidogrel was documented in this cohort.

Topics: Atorvastatin; Clopidogrel; Coronary Disease; Coronary Stenosis; Fatty Acids, Monounsaturated; Fluvastatin; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Indoles; Platelet Aggregation; Platelet Aggregation Inhibitors; Pyrroles; Simvastatin; Stents; Ticlopidine