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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2005.12.017 Byline: Onn Akbar Ali, Ravinay Bhindi, Aisling C. McMahon, David Brieger, Leonard Kritharides, Harry C. Lowe Abstract: Iatrogenic and spontaneous downstream microembolization of atheromatous material is increasingly recognized as a source of cardiovascular morbidity and mortality. Devising ways of reducing this distal embolization using a variety of mechanical means -- distal protection -- is currently under intense and diverse investigation. This review therefore summarizes the present status of distal protection. It examines the problem of distal embolization, describes the available distal protection devices, reviews those areas of cardiovascular medicine where distal protection devices are being investigated, and discusses potential future developments. Author Affiliation: Cardiology Department, Concord Repatriation General Hospital and ANZAC Research Institute, University of Sydney, Concord, Sydney, NSW, Australia Article History: Received 12 August 2005; Accepted 6 December 2005

Background: Transcatheter aortic valve implantation (TAVI) is an effective treatment for severe aortic stenosis in high-risk patients. Several complications related to the TAVI procedure, including aortic regurgitation (AR), cerebrovascular accident (CVA) and the requirement for permanent pacemaker (PPM), are thought to be secondary to balloon aortic valvuloplasty (BAV) before TAVI. The aim of the present review was to evaluate any beneficial role of the direct TAVI approach over BAVTAVI., Methods: A comprehensive search of major databases was performed. Only studies comparing TAVI with and without BAV were included. A total of nine full length articles was included in the analysis., Results: Among 2,650 patients, 1,043 underwent 'direct TAVI' without pre-BAV, while 1,607 underwent TAVI following BAV. Overall, there was no difference between the 30-day all-cause mortality (OR 0.96, 95% CI 0.63-1.47, p = 0.86), CVA (OR 0.81, 95% CI 0.34-1.92, p = 0.63) and PPM implantation (OR 0.84, 95% CI 0.66- 1.05, p = 0.12) between the two approaches. The rate of moderate to severe AR was significantly lower with direct TAVI implantation (OR 0.44, 95% CI 0.20-0.96, p = 0.04). In the case of self-expandable valves, direct TAVI was associated with a lower device success (OR 5.15, 95% CI 1.33-19.9, p = 0.02)., Conclusions: No difference was identified in mortality between direct TAVI and BAV-TAVI. However, direct TAVI is associated with a lower incidence of AR, a finding that would only be confirmed by conducting further randomized studies.

Aortic valve stenosis (AS) is the commonest form of valvular heart disease in the Western world. Its prevalence increases exponentially with age and it is present in 2-7% of all patients over 65 years of age. In view of the considerable cardiovascular morbidity and mortality associated not only with AS, but even its earlier stage, aortic sclerosis, many investigations have been directed towards better understanding of its pathogenesis, with the ultimate objective of developing strategies to retard its progression. Although risk factors and downstream mediators appear similar for AS and atherosclerosis (older age, male sex, hypertension, smoking, hypercholesterolemia, and diabetes, as many as 50% of patients with AS do not have clinically significant atherosclerosis. On the basis both of recent experimental evidence and clinical trials, it appears that atherogenesis is not pivotal to the pathogenesis of AS. On the other hand, there is increasing evidence of active involvement of aortic valve fibroblasts with resultant increased production of reactive oxygen species, active pro-inflammatory and pro-fibrotic processes culminating in calcification. We also discuss the evidence of involvement of the nitric oxide system in the pathogenesis of AS. The renin-angiotensin system has also emerged as a major player in the pathogenesis of AS. Histologically, there is increased ACE expression and elevated angiotensin II levels in stenotic valves, while we have just demonstrated amelioration of AS with the use of ACE inhibitors in an animal model. We further discuss intervention studies aimed at retarding AS progression, including recent failures of statins to retard progression of AS in large randomized clinical studies. Finally, we discuss the special case of bicuspid aortic valve, including its genetics and unique associated features.