Endovascular treatment of coarctation and related aneurysms.

Today, surgical repair has almost doubled the 30-year survival rate in patients with coarctation of the aorta (CoA), and 72% to 98% of patients now reach adulthood. Possible late complications include malignant hypertension, left ventricular dysfunction, aortic valve dysfunction, recurrent CoA, and aneurysm formation with risk of rupture. Treating postoperative CoA-related aneurysms with observation alone is associated with a mortality rate of 36%, compared with 9% for surgical repair. Even in the best surgeons' hands, aortic surgery has associated complications, and the complexity of reoperative surgery makes the risks substantially greater. For patients with CoA-related aneurysm, endovascular treatment constitutes a good alternative to reoperative surgery because it poses a lower risk of morbidity and mortality. Implanting an endograft has been shown to be successful in treating CoA and related aneurysms, producing excellent intermediate outcomes and minimal morbidity and mortality. Despite evidence that using covered stents improves outcomes, the superiority of any particular stent type has yet to be established. With a variety of endografts available, the decision of which stent to use depends on anatomy, availability, and operator preference.

Routine revascularization is unnecessary in the majority of patients requiring zone II coverage during thoracic endovascular aortic repair: a longitudinal outcomes study using United States Medicare population data.

OBJECTIVE: We aimed to evaluate outcomes of thoracic endovascular aortic repair (TEVAR) with left subclavian artery (LSA) coverage without bypass (TEVAR + SUB) to TEVAR with coverage of the LSA with a bypass at the time of the initial procedure or later at a separate procedure (TEVAR + SUB + BYPASS). METHODS: The Centers for Medicare & Medicaid Services inpatient claims for 2006-2007 were queried using Current Procedural Terminology codes for TEVAR, TEVAR + SUB, TEVAR + SUB + BYPASS or later as a separate procedure. RESULTS: A total of 2676 patients underwent TEVAR; 869 (32.5%) underwent TEVAR + SUB and 49 (5.6%) TEVAR + SUB + BYPASS. At the time of the initial procedure, TEVAR + SUB + BYPASS was associated with a higher incidence of stroke compared to TEVAR + SUB (12.8% vs. 3.8 %; p = 0.0033). Among TEVAR + SUB, only 1.93% (50 patients) had a subsequent bypass performed during a one-year follow-up. Overall rates of morbidity (p = 0.004) and mortality (p = 0.011) trended towards significance in favor of TEVAR + SUB. CONCLUSIONS: TEVAR + SUB were associated with lower rates of mortality and complications. Only a small percentage of TEVAR + SUB required a bypass at one year after procedure. Our data suggest that routine LSA bypass during TEVAR is unnecessary and associated with increase morbidity and mortality.

Prolonged vasoconstriction of resistance arteries involves vascular smooth muscle actin polymerization leading to inward remodelling.

AIMS: Inward remodelling of the resistance vasculature is predictive of hypertension and life-threatening cardiovascular events. We hypothesize that the contractile mechanisms responsible for maintaining a reduced diameter over time in response to prolonged stimulation with vasoconstrictor agonists are in part responsible for the initial stages of the remodelling process. Here we investigated the role of vascular smooth muscle (VSM) actin polymerization on agonist-induced vasoconstriction and development of inward remodelling. METHODS AND RESULTS: Experiments were conducted in Sprague-Dawley rat resistance vessels isolated from the cremaster and mesentery. Within blood vessels, actin dynamics of VSM were monitored by confocal microscopy after introduction of fluorescent actin monomers through electroporation and by differential centrifugation to probe globular (G) and filamentous (F) actin content. Results indicated that 4 h of agonist-dependent vasoconstriction induced inward remodelling and caused significant actin polymerization, elevating the F-/total-actin ratio. Inhibition of actin polymerization prevented vessels from maintaining prolonged vasoconstriction and developing inward remodelling. Activation of the small GTPases Rho/Rac/Cdc42 also increased the F-/total-actin ratio and induced inward remodelling, while inhibition of Rho kinase or Rac-1 prevented inward remodelling. Disruption of the actin cytoskeleton reversed the inward remodelling caused by prolonged vasoconstriction, but did not affect the passive diameter of freshly isolated vessels. CONCLUSION: These results indicate that vasoconstriction-induced inward remodelling is in part caused by the polymerization of actin within VSM cells through activation of small GTPases.

Inward remodeling of resistance arteries requires reactive oxygen species-dependent activation of matrix metalloproteinases.

Inward eutrophic remodeling is the most prevalent structural change of resistance arteries in hypertension. Sympathetic and angiotensin (ANG)-induced vasoconstriction has been associated with hypertension and with the production of matrix metalloproteinases (MMPs) and ROS. Therefore, we hypothesize that prolonged exposure to norepinephrine (NE) and ANG II induces arteriolar inward remodeling dependent on the activation of MMPs and the production of ROS. This hypothesis was tested on rat cremaster arterioles that were isolated, cannulated, pressurized, and exposed to either NE (10(-5.5) mol/l) + ANG II (10(-7) mol/l) or vehicle (control) for 4 h. The prolonged exposure to NE + ANG II induced inward remodeling, as evidenced by the reduced maximal arteriolar passive diameter observed after versus before exposure to the vasoconstrictor agonists. NE + ANG II also increased the arteriolar expression and activity of MMP-2 and the production of ROS as determined, respectively, by real-time RT-PCR, gel and in situ zymography, and the use of ROS-sensitive dyes with multiphoton microscopy. Inhibition of MMP activation (with GM-6001) or ROS production (with apocynin or tempol) prevented the NE + ANG II-induced inward remodeling. Inhibition of ROS production prevented the activation of MMPs and the remodeling process, whereas inhibition of MMP activation did not affect ROS production. These results indicate that prolonged stimulation of resistance arterioles with NE + ANG II induces a ROS-dependent activation of MMPs necessary for the development of arteriolar inward remodeling. These mechanisms may contribute to the structural narrowing of resistance vessels in hypertension.