Carotid artery stenting is safe and associated with comparable outcomes in men and women.

OBJECTIVE: Historically, large randomized controlled studies looking at carotid endarterectomy (CEA) have indicated an increased perioperative risk for women when gender subgroup analysis was performed. However, the outcomes of carotid stenting in women as compared to men have not been adequately investigated. We sought to compare the safety and efficacy of carotid angioplasty and stenting (CAS) when performed in women as compared to men. METHODS: Procedures, complications, demographics, co-morbidities, and follow-up data from carotid stenting procedures performed in a bi-campus division were entered into a prospective database and then retrospectively supplemented with stored angiographic image data and reviewed. Arterial anatomic characteristics evaluated using angiographic images were: common carotid/internal carotid lesion length ratio, common carotid/internal carotid diameter, index lesion length, common carotid/internal carotid artery tortuosity, and lesion and aortic arch calcification. Outcomes compared included groin complications, postoperative pressor requirements, length of stay, restenosis, stroke, myocardial infarction (MI), and death. RESULTS: Between 2003 and 2008, 228 patients underwent 238 procedures. Cerebral protection devices and self-expanding stents were placed in all patients. A total of 97 percutaneous interventions performed in 93 women were compared with 141 interventions in 135 men. Mean age in women was 71.8 +/- 9.2 years, in men was 72.2 +/- 9.1 years (P > .99); 44.3% of women and 34.7% of men had symptomatic disease (P = .14). Preoperative demographics and co-morbidities did not differ significantly between genders, with the exception of hypertension (83.0% of males vs 96.7% of females, P = .001), and history of coronary artery bypass grafting (31.8% of males vs 16.1% of females, P = .01). There were no significant differences seen in anatomic arterial characteristics, though there was a trend towards women having larger internal carotid to common carotid diameter ratios (0.65 vs 0.62) and more plaques isolated to the common carotid segment (9.5% vs 6.9%). There were no significant differences seen in overall 30-day peri-procedural stroke rate (2.1% in women and 4.2% in men, P = .48), death rate (0 % vs 0.7%, P > .99), or cardiac events (3.2% vs 0.7%, P = .3). The combined 30-day stroke, death, and MI rate was 5.7% for males compared to 5.4% for females (P > .99). There were no differences observed in the long-term survival, stroke-free survival, or restenosis between genders. CONCLUSION: Despite previous concerns over adverse outcomes in women undergoing carotid endarterectomy, from our data, carotid stenting appears to be a safe modality in women with equivalent outcomes when compared to men.

Novel treatment of patients with lower extremity ischemia: use of percutaneous atherectomy in 579 lesions.

OBJECTIVES: Endovascular options for the treatment of lower extremity peripheral arterial disease are typified with diminished patency. A novel alternative to standard angioplasty and stent is the excision of the obstructing arterial plaque using a minimally invasive technique, the Silverhawk Atherectomy device. METHODS: A prospective database was maintained of SilverHawk procedures from 2004 to 2007. A total of 579 lesions were treated in 275 patients (claudication 101 patients (36.7%) and critical limb ischemia (CLI) in 174 patients (63.3%). Noninvasive laboratory evaluation was performed at 1, 3, and 6 months, and yearly. Stand-alone atherectomy was attempted, and adjunct therapy was used for residual stenosis. RESULTS: Mean age was 70.0 years (range, 37-102) (62.5% male, 46.2% smokers, 67.6% diabetes mellitus). Lesion characteristics were 199 superficial femoral arteries, 110 popliteal, 218 tibials, and 52 multilevel. Thirty-day perioperative mortality was 1.8%. Mean follow-up was 12.5 months (range, 0.5-48.2). 18-month primary and secondary patency for all lesions was 52.7% +/- 2.8 and 75.0% +/- 2.4 (P < 0.0001). Eighteen-month primary and secondary patency for claudicants was 58.0% +/- 4.3 and 82.5% +/- 3.5 (P < 0.0001) and for CLI was 49.4% +/- 3.7 and 69.9% +/- 3.2 (P < 0.0001), respectively. The reintervention rate was 25.3% in claudicants and 30.1% for CLI. Limb salvage was 100% in claudicants and overall limb salvage was 92.4% per patient at 18 months and only 4.4% required bypass. CONCLUSION: This is the largest reported series with the longest follow-up showing the SilverHawk device as an effective endovascular therapy for patients with claudication and CLI with a low mortality, low complications rate, low amputation rate, and rare need for conversion to surgical bypass. The majority of reintervention was performed with endovascular techniques.

Loss of Ca(v)1.3 (CACNA1D) function in a human channelopathy with bradycardia and congenital deafness.

Deafness is genetically very heterogeneous and forms part of several syndromes. So far, delayed rectifier potassium channels have been linked to human deafness associated with prolongation of the QT interval on electrocardiograms and ventricular arrhythmia in Jervell and Lange-Nielsen syndrome. Ca(v)1.3 voltage-gated L-type calcium channels (LTCCs) translate sound-induced depolarization into neurotransmitter release in auditory hair cells and control diastolic depolarization in the mouse sinoatrial node (SAN). Human deafness has not previously been linked to defects in LTCCs. We used positional cloning to identify a mutation in CACNA1D, which encodes the pore-forming α1 subunit of Ca(v)1.3 LTCCs, in two consanguineous families with deafness. All deaf subjects showed pronounced SAN dysfunction at rest. The insertion of a glycine residue in a highly conserved, alternatively spliced region near the channel pore resulted in nonconducting calcium channels that had abnormal voltage-dependent gating. We describe a human channelopathy (termed SANDD syndrome, sinoatrial node dysfunction and deafness) with a cardiac and auditory phenotype that closely resembles that of Cacna1d(-/-) mice.