Safety, clinical outcome, and fracture rate of femoropopliteal stenting using a 4F compatible delivery system.

OBJECTIVE: To determine the safety, clinical outcome, and fracture rate of femoropopliteal interventions using 4F stents. METHODS: Between January 2010 and December 2011, 112 symptomatic patients were treated by stent implantation. Ten patients were lost to follow up; therefore, 102 patients (62 men; mean age 66.4 ± 10.1 years) were retrospectively analyzed. The indication for femoropopliteal revascularization was severe claudication (Rutherford-Becker score = 3) in 63 (62%) patients and chronic critical limb ischemia (Rutherford-Becker score = 4-6) in 39 (38%). Follow up included palpation of peripheral pulses and measurement of ankle brachial index. In patients with suspected in-stent restenosis duplex ultrasonography was performed. In 2013, patients were asked to return for a fluoroscopic examination of the stents. RESULTS: 114 lesions (Trans-Atlantic InterSociety Consensus-C and D, n = 45) were treated with 119 stents (Astron Pulsar, n = 42; Pulsar-18, n = 77). Lesions were long (≥100 mm) in 49 cases and heavily calcified in 35. Stents were long (≥120 mm) in 46 cases. Ten stents were partially overlapped. The technical and clinical success rates were 100%. Two puncture related complications were noted, neither of which required surgical repair. Eleven patients died (myocardial infarction, n = 4; stroke, n = 2; cancer, n = 5) and nine patients underwent major amputation (above knee, n = 4). The primary patency rate was 83% at 6 months and 80% at 12 months. The primary assisted patency rate was 97% at 6 months and 94% at 12 months. The secondary patency rate was 86% at 6 months and 85% at 12 months. The prevalence of fractures was 26% (type III and IV, 10%) after an average follow up of 25 months. CONCLUSION: Femoropopliteal stenting using a 4F compatible delivery system can be accomplished with a low complication rate, acceptable fracture rate, and with similar 12 month patency and revascularization rates as their 6F counterparts.

Serum fetuin-A levels inversely correlate with the severity of arterial calcification in patients with chronic lower extremity atherosclerosis without renal disease.

AIM: Fetuin-A is a hepatic glycoprotein that inhibits extraosseous calcification. Lower serum fetuin-A concentration was associated with severe arterial calcification in patients with end stage renal disease. We evaluated the association of serum fetuin-A levels and the severity of atherosclerosis in patients with peripheral vascular disease having normal renal function. METHODS: In this cross-sectional study among 93 chronic atherosclerotic patients with lower extremity vascular disease, systemic atherosclerosis and calcification was assessed by ultrasound (carotid intima-media thickness/IMT/, calcification at the abdominal aorta, carotid and femoral bifurcations, aortic and mitral valves) and angiography (Bollinger score). Standard serum markers of inflammation, diabetes, renal function, ankle-brachial indexes and traditional risk factors for atherosclerosis were noted and Fontaine classification was applied for the severity of symptoms. RESULTS: The patients mean (SD) age was 59.95 (7.61) years, 78% were men, 35% had diabetes. Serum fetuin-A level showed significant negative correlation with ultrasound calcification score (P=0.018, r=-0.257) and Bollinger angiographic score (P=0.035, r=-0.347). Fetuin-A did not correlate with IMT or Fontaine classification. Fetuin-A also showed significant correlation with albumin, transferrin and hemoglobin A1c (r=0.287, 0.305 and 0.219, respectively at P<0.05). Logistic regression analysis confirmed the association between fetuin-A and calcification score (OR: 3.03, CI: 1.05-8.7), P=0.039) independent of traditional risk factors. CONCLUSION: Our data show that serum fetuin-A levels inversely correlate with the severity of atherosclerosis in nonuremic patients with symptomatic chronic lower limb ischemia. These data support a putative protective role for fetuin-A in the development of arterial calcification.