BACKGROUND: Endovascular repair (EVAR) for abdominal aortic aneurysm (AAA) is widely adopted; however, the procedure may be jeopardized by type 2 endoleak (T2E). Most T2Es regress over time, but their evolution is unpredictable. There is some evidence about the pleiotropic statin effect on AAA and thrombus stabilization, but there are no data on the influence of statins on T2E. The study's aim is therefore to evaluate a possible effect of statins on T2E evolution. METHODS: A retrospective analysis of patients discharged from 2008 to 2013 with T2E after EVAR was performed. Patients were followed up with duplex ultrasound and computed tomography angiography and divided on statin and no statin users. The primary end point was to evaluate the T2E persistence at 6 months and during follow-up. The secondary end points were to compare the shrinkage (median and rate), the sac increasing rate, and reintervention at 6 months and during follow-up. RESULTS: In the period examined, 756 EVARs were performed and 85 (11%) had T2E at discharge. Thirty-two (37%) patients with T2E were on statins. The median follow-up was 19 (interquartile range [IQR] 7) months. Statin and no statin patients had similar clinical and anatomical characteristics, endoprosthesis type, and medical therapy. At 6 months, patients on statins had lower T2E persistence ([26] 81% vs. [49] 93%, P = 0.16), reaching the significance at 36 months (11 ± 9% vs. 64 ± 7%, P = 0.001). By Cox analysis, statins are independently associated with T2E regression (hazard ratio 0.40, 95% confidence interval 0.020-0.81, P = 0.01), other characteristics are: >2 lumbar arteries or inferior mesenteric artery patency or oral anticoagulant therapy did not reduce T2E. At 6 months, statin patients had higher shrinkage rate and diameter reduction compared with no statin patients (18% vs. 3%, P = 0.03 and 11 mm (IQR 4) vs. 6 mm (IQR 4), P = 0.05, respectively). Freedom from growth diameter and reintervention rate were not significantly different (85 ± 9% vs. 81 ± 14%, P = 0.10 and 75 ± 17% vs. 37 ± 16%, P = 0.13, respectively). CONCLUSION: Statin therapy seems to influence T2E regression and aortic sac stabilization after EVAR in the early medium follow-up; however, prospective studies need to confirm the present results.
BACKGROUND: Endovascular repair (EVAR) for abdominal aortic aneurysm (AAA) is widely adopted; however, the procedure may be jeopardized by type 2 endoleak (T2E). Most T2Es regress over time, but their evolution is unpredictable. There is some evidence about the pleiotropic statin effect on AAA and thrombus stabilization, but there are no data on the influence of statins on T2E. The study's aim is therefore to evaluate a possible effect of statins on T2E evolution. METHODS: A retrospective analysis of patients discharged from 2008 to 2013 with T2E after EVAR was performed. Patients were followed up with duplex ultrasound and computed tomography angiography and divided on statin and no statin users. The primary end point was to evaluate the T2E persistence at 6 months and during follow-up. The secondary end points were to compare the shrinkage (median and rate), the sac increasing rate, and reintervention at 6 months and during follow-up. RESULTS: In the period examined, 756 EVARs were performed and 85 (11%) had T2E at discharge. Thirty-two (37%) patients with T2E were on statins. The median follow-up was 19 (interquartile range [IQR] 7) months. Statin and no statin patients had similar clinical and anatomical characteristics, endoprosthesis type, and medical therapy. At 6 months, patients on statins had lower T2E persistence ([26] 81% vs. [49] 93%, P = 0.16), reaching the significance at 36 months (11 ± 9% vs. 64 ± 7%, P = 0.001). By Cox analysis, statins are independently associated with T2E regression (hazard ratio 0.40, 95% confidence interval 0.020-0.81, P = 0.01), other characteristics are: >2 lumbar arteries or inferior mesenteric artery patency or oral anticoagulant therapy did not reduce T2E. At 6 months, statin patients had higher shrinkage rate and diameter reduction compared with no statin patients (18% vs. 3%, P = 0.03 and 11 mm (IQR 4) vs. 6 mm (IQR 4), P = 0.05, respectively). Freedom from growth diameter and reintervention rate were not significantly different (85 ± 9% vs. 81 ± 14%, P = 0.10 and 75 ± 17% vs. 37 ± 16%, P = 0.13, respectively). CONCLUSION: Statin therapy seems to influence T2E regression and aortic sac stabilization after EVAR in the early medium follow-up; however, prospective studies need to confirm the present results.