Desarom Teso

Laminar shear stress stimulates vascular smooth muscle cell apoptosis via the Akt pathway.

Vascular smooth muscle cells (SMC) may be directly exposed to blood flow after an endothelial‐denuding injury. It is not known whether direct exposure of SMC to shear stress reduces SMC turnover and contributes to the low rate of restenosis after most vascular interventions. This study examines if laminar shear stress inhibits SMC proliferation or stimulates apoptosis. Bovine aortic SMC were exposed to arterial magnitudes of laminar shear stress (11 dynes/cm2) for up to 24 h and compared to control SMC (0 dynes/cm2). SMC density was assessed by cell counting, DNA synthesis by 3[H]‐thymidine incorporation, and apoptosis by TUNEL staining. Akt, caspase, bax, and bcl‐2 phosphorylation were assessed by Western blotting; caspase activity was also measured with an in vitro assay. Analysis of variance was used to compare groups. SMC exposed to laminar shear stress had a 38% decrease in cell number (n = 4, P = 0.03), 54% reduction in 3[H]‐thymidine incorporation (n = 3, P = 0.003), and 15‐fold increase in TUNEL staining (n = 4, P < 0.0001). Akt phosphorylation was reduced by 67% (n = 3, P < 0.0001), whereas bax/bcl‐2 phosphorylation was increased by 1.8‐fold (n = 3, P = 0.01). Caspase‐3 activity was increased threefold (n = 5, P = 0.03). Pretreatment of cells with ZVAD‐fmk or wortmannin resulted in 42% increased cell retention (n = 3, P < 0.01) and a fourfold increase in apoptosis (n = 3, P < 0.04), respectively. Cells transduced with constitutively‐active Akt had twofold decreased apoptosis (n = 3, P < 0.002). SMC exposed to laminar shear stress have decreased proliferation and increased apoptosis, mediated by the Akt pathway. These results suggest that augmentation of SMC apoptosis may be an alternative strategy to inhibit restenosis after vascular injury. J. Cell. Physiol. 216: 389–395, 2008.

Do vascular surgeons improve the outcome of carotid endarterectomy? An analysis of 12,618 elective cases in the state of Connecticut.

Because cardiac complications may predict long-term survival after carotid endarterectomy (CEA), this study evaluates contemporary outcome, including cardiac complications, after CEA. Patients in Connecticut hospitals undergoing CEA between 1991 and 2002 were identified using the state discharge database (Chime, Inc.; ). Of the 12,618 CEAs performed, there were 53 (0.4%) deaths, 155 (1.2%) neurologic complications, and 300 (2.4%) cardiac complications. Despite an increase in patient age (p < .0001, Kruskal-Wallis test) over time, there were decreases in mortality (p = .0001, chi-square), postoperative stroke ( p = .001), and cardiac complications (p = .0003). Vascular surgeons performed a minority of the procedures in the state (11%), but there were fewer cardiac complications after CEA performed by vascular surgeons than general surgeons (0.8% vs 3.0%; p < .0001). Multivariable logistic regression demonstrated that the risk of a cardiac complication was elevated in patients operated on by a nonvascular surgeon, patients with previous heart disease or stroke, and the elderly. In a state with very high performance of CEA by general and nonvascular surgeons, postoperative mortality and neurologic complications remain low. However, there were fewer cardiac complications when a vascular surgeon performed the procedure. These results suggest that increased referral to vascular surgeons could improve procedural safety.