Influence of Statin Therapy on Aneurysm Sac Regression after Endovascular Aortic Repair.

PURPOSE: To determine whether statin therapy is associated with abdominal aortic aneurysm (AAA) sac regression after endovascular aneurysm repair (EVAR). MATERIALS AND METHODS: A total of 109 patients treated with EVAR were retrospectively analyzed (no-statin group, n = 45; statin group, n = 64). The primary endpoint was the incidence of AAA sac regression. To investigate independent predictors of AAA sac regression, regression analysis was performed. The mean age was 74 years (range, 55-90 y), and 87.2% of patients were men. RESULTS: The no-statin group had higher rates of AAA sac regression than the statin group at 1 year (no-statin group, 66.7%; statin group, 45.3%; P = .028). The incidence of AAA sac regression increased over time in the statin group, and no statistical difference was seen between the two groups at 2 years (no-statin group, 66.7%; statin group, 57.8%; P = .350). The difference between the changes in maximum AAA diameter was significant between groups at 1 year (no-statin group vs statin group, -4.9 mm ± 5.9; P = .041), but the difference did not reach statistical significance at 2 years (no-statin group, -10.0 mm ± 10.1; statin group, -8.0 mm ± 9.6; P = .306). Statin therapy was not associated with AAA sac regression on univariate (odds ratio [OR], 0.685; 95% confidence interval [CI], 0.310-1.516; P = .351) and multivariate analyses (OR, 0.617; 95% CI, 0.215-1.772; P = .369). CONCLUSIONS: Statin therapy had no effect on AAA sac regression at 2 years. There is insufficient evidence to recommend statin therapy for AAA sac regression.

Effects of Percutaneous Transluminal Angioplasty on Diastolic Function in Patients With Chronic Occlusion of Lower-Extremity Artery.

OBJECTIVE: We investigated whether successful revascularization of total occlusion of a large lower-extremity artery is associated with improvement of left ventricular (LV) diastolic function. BACKGROUND: Total occlusion of a large lower-extremity artery might affect the systemic vascular resistance and increase the afterload, because the left ventricle must work harder to eject blood into a smaller vascular bed. Chronic elevation of afterload is a cause of LV diastolic dysfunction. METHODS: This is a single-center retrospective analysis of 20 patients (10 men, age 69.6 ± 12.3 years) with chronic total occlusions (CTOs) of the aorto-iliac and femoropopliteal segments who underwent a successful endovascular revascularization. Baseline and postprocedural evaluation of diastolic function was performed, and the primary endpoint was improvement in LV diastolic function, which was defined as any decrease of the baseline E/E' ratio or any increase of the baseline E' velocity after the index procedure. RESULTS: There was a significant effect of successful revascularization on the E/A ratio (from 1.5 ± 1.1 to 1.0 ± 0.3; P=.046) because of a significant increase of A velocity (from 86.3 ± 30.4 cm/s to 98.3 ± 21.8 cm/s; P=.03). The E' velocity (from 7.4 ± 2.0 cm/s to 8.3 ± 2.3 cm/s; P=.07) did not show a significant increase, but there was a significant reduction in E/E' ratio (from 14.6 ± 3.9 to 12.4 ± 3.3; P=.02). Logistic regression analysis did not identify possible predictors of improvement in LV diastolic function. CONCLUSION: Our results showed that a successful revascularization was associated with improvement in the echocardiographic parameters of LV diastolic function in patients with CTO of large lower-extremity artery, and these changes may be related to the afterload reduction.

The Influence of Statin Therapy on Restenosis in Patients Who Underwent Nitinol Stent Implantation for de Novo Femoropopliteal Artery Disease: Two-Year Follow-up at a Single Center.

PURPOSE: To determine whether statin therapy is associated with reduced restenosis following nitinol stent implantation for de novo femoropopliteal artery disease. MATERIALS AND METHODS: A total of 135 limbs in 135 patients (mean age, 72 y) implanted with nitinol stents in femoropopliteal occlusions were analyzed (statin arm, n = 91; nonstatin arm, n = 44). The patients were treated with one type of nitinol stent. RESULTS: At baseline, lesions and procedural characteristics were comparable between groups, except that the statin group had more hypertension, coronary artery disease, and hyperlipidemia. There were significant differences in the incidence of binary restenosis between groups at 1 year (45.5% for nonstatin group vs 28.6% for statin group; P = .05) and 2 years (56.8% for nonstatin group vs 38.5% for statin group; P = .04). Primary patency rates at 1 year were 50.5% in the nonstatin group and 72.5% in the statin group (P = .01). Two-year target lesion revascularization rates were 54.5% in the nonstatin group and 35.2% in the statin group (P = .03). On univariate analysis, statin therapy was associated with decreased relative risk of binary restenosis at 1 year (odds ratio [OR], 0.480; 95% confidence interval [CI], 0.227-1.014; P = .050). On multivariate analysis, statin therapy did not significantly affect the odds of binary restenosis (OR, 0.415; 95% CI, 0.071-2.437; P = .330). CONCLUSIONS: The incidence of binary restenosis was significantly lower in the statin group than in the nonstatin group following nitinol stent implantation for de novo femoropopliteal artery disease.