Infrarenal Abdominal Aortic Aneurysm Endovascular Treatment: Long-term Results From a Single-Center Experience in an Unselected Patient Population.

BACKGROUND: The aim of the present study was to evaluate early-, mid-, and long-term outcomes in an unselected population of patients treated for abdominal aortic aneurysms (AAAs) by endovascular aneurysm repair (EVAR) with different commercially available off-the-shelf devices. MATERIALS AND METHODS: A retrospective study was conducted on a prospectively compiled computerized database on patients presenting an infrarenal AAA treated between January 2008 and December 2015 in a high-volume Italian tertiary referral Center. Demographic, clinical, and specific morphological features were considered as potentially influencing the outcomes and the type of the implanted device. Outcome measures were procedure-related reintervention, AAA-related, and all-cause mortality rates at 30-day, 12-month, and long-term follow-up. Reinterventions considered for the analysis were AAA rupture, graft infection, type I or III endoleaks, type II endoleaks with sac enlargement > 5 mm, graft stenosis or occlusions, procedures related to renal or visceral ischemia, and reintervention for access vessel injury. RESULTS: Of 498 EVAR procedures performed for elective infrarenal AAA treatment during the entire study period, 479 patients were enrolled, the mean age was 73.5 ± 7.34 years (range 51-91), and 416 (86.84%) were men. The mean maximum AAA diameter was 52.02 ± 8.04 mm (range 39-90.2), a maximum AAA diameter ≥59 mm was recorded in 107 patients (22.33%), and an aortic neck length was <10 mm in 137 (28.60%). Technical success was achieved in all patients. At a mean follow-up of 52.97 ± 26.16 months (range 1-120), overall reintervention and death rates were 8.14% and 20.04%, respectively, without AAA-related deaths. At univariate analysis, hypertension was the only demographical variable found to be associated with higher risk of reintervention, P = 0.04 (OR: 2.34; CI 95%: 1.00-5.42). Furthermore, male sex (P = 0.02; OR: 2.62; CI 95%: 1.09-6.27) and chronic renal insufficiency (P = 0.003; OR: 2.08; CI 95%: 1.27-3.42) were associated with higher mortality rates. AAA diameter ≥59 mm was statistically associated with a higher rate of both reintervention and mortality: P < 0.001 (OR: 9.05; CI 95%: 4.52-18.11) and <0.001 (4.00; 2.46-6.49), respectively. CONCLUSIONS: Our experience seems to suggest that EVAR could be safely and effectively performed in an unselected patients' population, with encouraging results up to a ten-year follow-up.

Increased FGF23 serum level is associated with unstable carotid plaque in type 2 diabetic subjects with internal carotid stenosis.

BACKGROUND: The object of this study was to investigate the potential role of FGF23 on plaque stability in type 2 diabetic patients with internal carotid artery stenosis. METHODS: In this retrospective observational study, we analyzed FGF23 serum level in 361 type 2 diabetic patients with internal carotid artery stenosis undergoing carotid endarterectomy and in 598 diabetic controls without carotid atherosclerosis. RESULTS: We found that FGF23 median serum levels was significantly higher in patients than in diabetic controls [67.7 (59.5-77.8) pg/mL and 43.89 (37.5-50.4), P < 0.001] and was significantly and independently associated with unstable plaque in patients with internal carotid artery stenosis [OR, 5,71 (95% CI, 2.09-15.29]. CONCLUSIONS: We have found, for the first time, that FGF23 could be associated with unstable plaque in type 2 diabetic patients with internal carotid artery stenosis.

TNFRSF11B gene polymorphisms increased risk of peripheral arterial occlusive disease and critical limb ischemia in patients with type 2 diabetes.

AIMS: Osteoprotegerin (OPG) is a secretory glycoprotein that belongs to the tumor necrosis factor receptor family and plays a role in atherosclerosis. OPG has been hypothesized to modulate vascular functions; however, its role in mediating atherosclerosis is controversial. Epidemiological data in patients with cardiovascular disease (CVD) indicate that OPG serum levels are associated with several inflammatory markers, myocardial infarction events, and calcium scores, suggesting that OPG may be causative for CVD. METHODS: The present study aimed to evaluate whether the OPG gene (TNFRSF11B) polymorphisms are involved in the development of peripheral arterial occlusive disease (PAOD) and critical limb ischemia (CLI) in patients with type 2 diabetes. This genetic association study included 402 diabetic patients (139 males and 263 females) with peripheral arterial occlusive disease and 567 diabetic subjects without peripheral arterial occlusive disease (208 males and 359 females). The T245G, T950C, and G1181C polymorphisms of the OPG gene were analyzed by polymerase chain reaction and restriction fragment length polymorphism. RESULTS: We found that the T245G, T950C, and G1181C gene polymorphisms of the OPG gene were significantly (27.9 vs. 12.2 %, P < 0.01; 33.6 vs. 10.4 %, P < 0.01 and 24.4 vs. 12.7 %, P < 0.01, respectively) and independently (adjusted OR 4.97 (3.12-6.91), OR 7.02 (4.96-11.67), and OR 2.85 (1.95-4.02), respectively) associated with PAOD. We also found that these three polymorphisms act synergistically in patients with PAOD and are associated with different levels of risk for PAOD and CLI, depending on the number of high-risk genotypes carried concomitantly by a given individual. CONCLUSION: The TNFRSF11B gene polymorphisms under study are associated with PAOD, and synergistic effects between these genotypes might be potential markers for the presence and severity of atherosclerotic disorders.

Association between TNFRSF11B gene polymorphisms and history of ischemic stroke in Italian diabetic patients.

Osteoprotegerin (OPG) is a secretory glycoprotein that belongs to the tumor necrosis factor receptor family and plays a role in atherosclerosis. The present study aimed to evaluate whether OPG gene (TNFRSF11B) polymorphisms are involved in ischemic stroke in an Italian population with diabetes. Participants in a retrospective case-control study included 364 diabetic patients (180 males, 184 females) with history of ischemic stroke and 492 diabetic subjects without history of ischemic stroke (252 males, 240 females). The T245G, T950C, and G1181C polymorphisms of the OPG gene were analyzed by polymerase chain reaction and restriction fragment length polymorphism. We found that the T245G, T950C, and G1181C gene polymorphisms of the OPG gene were significantly (34.1 vs. 9.5 %, P < 0.0001; 30.8 vs. 6.3 %, P < 0.0001 and 26.4 vs. 11.6 % P < 0.0001, respectively) and independently (adjusted OR 5.15 [3.46-7.68], OR 6.63 [4.26-10.31], and OR 3.03 [2.04-4.50], respectively) associated with history of ischemic stroke. We also found that these three polymorphisms act synergistically in patients with stroke history. The TNFRSF11B gene polymorphisms studied are associated with history of ischemic stroke and synergistic effects between these genotypes might be potential markers for cerebrovascular disorders.