The impact of gender on in-hospital outcomes after carotid endarterectomy or stenting.

AIM: We sought to better define the impact of sex on 'in-hospital outcomes' after carotid endarterectomy (CEA) or stenting (CAS). METHODS: Hospital discharge databases for all carotid interventions obtained from the New York State (NYS) Department of Health, Statewide Planning and Research Cooperative System between 2000 and 2009 (29,917 women, 39,771 men) were analysed. Mortality, stroke and composite event (stroke/death) were compared between procedures after matching of patients by propensity score. Acute myocardial infarction (AMI) was our secondary 'end' point. RESULTS: More than 90% of patients in both sexes were asymptomatic (27,439 women and 36,295 men). Compared to men, asymptomatic women experienced more strokes after CEA (women: 1.38%, men: 1.16%, P = 0.03) and higher AMI rates after both procedures (CEA; women: 0.75%, men: 0.51%, P = 0.0009, CAS; women: 0.96%, men: 0.28%, P = 0.01). Between procedures, symptomatic women undergoing CAS showed higher rates of mortality (CAS: 4.19%, CEA: 0.47%, P = 0.01) and combined (stroke/mortality) events (CAS: 12.09%, CEA: 6.05%, P = 0.02). In all other cohorts, no statistically significant difference was found between the procedures. CONCLUSIONS: Compared to CEA, CAS led to inferior in-hospital outcomes only in symptomatic women in the last decade in NYS. Men and asymptomatic women showed comparable outcomes after both procedures, whereas asymptomatic females were more prone to AMI after both interventions. These sex-associated differences should be taken into account for the treatment of carotid artery disease.

Value of drug-eluting stents after failed percutaneous transluminal angioplasty in the infrapopliteal vessels for the treatment of critical limb ischemia: favorable mid-term patency and limb salvage results.

AIM: The endovascular treatment of infrapopliteal arterial disease in the setting of critical limb ischemia (CLI) is increasing in use. In patients in whom percutaneous transluminal angioplasty (PTA) resulted in suboptimal angiographic results, flow limiting dissection or re-coil is thought to limit clinical success. This single-center experience examines the angiographic and clinical results when Drug-Eluting Stents (DES) were placed in a large cohort of patients with CLI after immediate infrapopliteal PTA failure. METHODS: A retrospective review of a prospectively collected single-center endovascular database was performed. Sixty-seven Rutherford grade 4, 5, and 6 patients were treated between October 2005 and February 2010 with PTA because lack of an acceptable autologous vein for bypass-grafting or severe medical comorbidities precluded them from surgical bypass. The study cohort had suboptimal angiographic results immediately after PTA that was subsequently treated with DES. Patients were then placed on clopidogrel and aspirin indefinitely. Angiographic, clinical, and the results of noninvasive vascular examinations were collected. RESULTS: In total, 123 stents (94 sirolimus, 27 everolimus, 2 paclitaxel) were placed in 67 patients to treat a total of 84 angiographic lesions. Simultaneous femoral-popliteal intervention was performed in 66% of the patients while 45% of the treated lesions were total occlusions. Lesion length ranged from 17 mm-142 mm (mean 50 mm). Initial technical success was 100%, with all 84 lesions being treated successfully with less than 10% stenosis after stent implantation. Mean follow-up was 20 months (1-42 months) with 6, 12, and 24-month primary patency rates of 90%, 86%, and 72% respectively. Freedom from major amputation was 91.1% (61/67) with all six amputations occurring in the Rutherford grade 6 group (6/11). Overall mortality rate was 19% (13/67) with one death occurring within 30 days. CONCLUSION: The use of drug-eluting stents following suboptimal PTA for the treatment of infrapopliteal arterial disease in this cohort of patients with CLI produced high primary patency and limb salvage rates supporting the efficacy of this treatment strategy.

The role of type I collagen in aortic wall strength with a homotrimeric.

PURPOSE: Elastin and collagen (types I and III) are the primary load-bearing elements in aortic tissue. Deficiencies and derangements in elastin and type III collagen have been associated with the development of aneurysmal disease. However, the role of type I collagen is less well defined. The purpose of this study was to define the role of type I collagen in maintaining biomechanical integrity in the thoracic aorta, with a mouse model that produces homotrimeric type I collagen [alpha1(I)]3, rather than the normally present heterotrimeric [alpha1(I)]2 alpha2(I) type I collagen isotype. METHODS: Ascending and descending thoracic aortas from homozygous (oim/oim ), heterozygous (oim /+), and wildtype (+/+) mice were harvested. Circumferential and longitudinal load-extension curves were used as a means of determining maximum breaking strength (Fmax) and incremental elastic modulus (IEM). Histologic analyses and hydroxyproline assays were performed as a means of determining collagen organization and content. RESULTS: Circumferentially, the ascending and descending aortas of oim /oim mice demonstrated significantly reduced Fmax, with an Fmax of only 60% and 23%, respectively, of wildtype mice aortas. Oim/oim descending aortas demonstrated significantly greater compliance (decreased IEM), and the ascending aortas also exhibited a trend toward increased compliance. Reduced breaking strength was also demonstrated with longitudinal extension of the descending aorta. CONCLUSION: The presence of homotrimeric type I collagen isotype (absence of alpha2(I) collagen) significantly weakens the aorta. This study demonstrates the integral role of type I collagen in the biomechanical and functional properties of the aorta and may help to elucidate the role of collagen in the development of aneurysmal aortic disease or dissection.

The caput medusae of hypercoagulability.

Thrombosis may be the most common cause of death in the United States. Virchow postulated, approximately 150 years ago, that intravascular thrombosis was caused by changes of the vessel wall, by reduction in blood flow, and by alteration of the chemical composition of the blood. The hypercoagulability component of the Virchow triad has, until recently, been poorly defined. During the past 40 years, a number of acquired and congenital hypercoagulable disorders have been described so that currently the cause for thrombotic events can be determined in many patients. The hypercoagulable-related thromboses are usually venous but may, less often, be arterial, and the thromboses often are the cause of significant morbidity and mortality. The vascular surgeon often participates in the management of hypercoagulable disorders. This review of hypercoagulable disorders is presented with the hope that the early recognition of these disorders will lead to the appropriate diagnosis and proper management of hypercoagulable-related thromboses.

Ambient pulsatile pressure modulates endothelial cell proliferation.

Many studies over the last decade have indicated that circulatory forces such as shear stress and cyclic strain can influence the endothelial cell (EC) phenotype. However, very little is known about the in vitro effects of pressure on EC. To study this, cultured bovine aortic EC were grown in custom designed pressure chambers with carefully regulated CO2/air environment. EC were exposed to either atmospheric, static (135 mmHg) or pulsatile pressure (160/110 mmHg). A pulsed pressure frequency of 60 cycles/min was maintained by computer-controlled solenoid valves, placed in series with pressure lines. EC proliferation was determined both by cell count after trypsin release on days 1,3 and 5 and by 3H-thymidine incorporation. By day 5, a significant decrease in cell number occurred in both pressure groups, confirmed by the thymidine studies. No changes were observed in cell morphology and cell viability as assessed by LDH activity studies. To investigate the mechanism of this effect, EC conditioned media from the three pressure conditions were transferred to non-exposed, control EC. Significant cell growth inhibition was demonstrated in the control EC group treated with conditioned media from EC cultured under pulsatile pressure conditions. This finding suggests that EC exposed to pulsatile pressure secrete an autocrine factor with growth inhibitory properties. This effect was not mediated by the growth factors TGFbeta and IL-1 as shown by Northern blot analysis and antibody-neutralization studies.