Postoperative RAS blockade therapy is associated with greater LV mass index regression and reduced all-cause mortality. These data need to be confirmed by a prospective randomised controlled outcome trial.

No abstract

Background-We recently developed a 4F child catheter that can be inserted into 6F or larger conventional guiding catheters.The use of 4F mother-child technique may improve the delivery of coronary stents to complex lesions. Accordingly, we sought to determine the potential of using a 4F mother-child technique to treat complex coronary lesions. Methods and Results-The support power and the trackability of the mother-child technique of 4-in-6 were evaluated using a coronary artery tree model. In addition, the results of 51 lesions treated by using a 4F child catheter were retrospectively analyzed. The in vitro experiment demonstrated that backup support of the 4-in-6 system was increased when the child catheter was advanced into the coronary tree Ն5 cm (PՅ0.01); further, the 4F child catheter was associated with superior trackability as compared with a 5F child catheter (15.0 cm [15.0 to 15.0] versus 13.0 cm [12.8 to 13.0], PϽ0.005). A total of 51 lesions, in which conventional techniques had been unsuccessful, were treated using the 4F mother-child technique. Lesion success was achieved in 48 (94%) lesions. Stent deployment was attempted in 44 (86%) and was successful in 40 of 44 (91%). There were 2 instances of stent dislodgment. Conclusions-With the superior trackability of the 4F child catheter and with increased backup support of the mother-child system, the 4F mother-child system provided Ͼ90% success rate for lesions in which conventional techniques had failed. The 4F mother-child system may become a viable alternative to conventional techniques in treating complex coronary lesions. (Circ Cardiovasc Interv. 2011;4:155-161.)

In patients with severe AS, a good correlation exists between iFR and FFR. Both the iFR and FFR values exhibit good correlation with perfusion scintigraphy-identified myocardial ischemia. The iFR could be a safe diagnostic tool for patients with severe AS. (The Impact of FFR and iFR in Patients with Severe Aortic Stenosis; UMIN000024479).

Coronary atherosclerosis progresses both as slow, gradual enlargement of focal plaque and also as a more dynamic process with periodic abrupt changes in plaque geometry, size, and morphology. Systemic vasculoprotective therapies such as statins, angiotensin-converting enzyme inhibitors, and antiplatelet agents are the cornerstone of prevention of plaque rupture and new adverse clinical outcomes, but such systemic therapies are insufficient to prevent the majority of new cardiac events. Invasive imaging methods have been able to identify both the anatomic features of high-risk plaque and the ongoing pathobiological stimuli responsible for progressive plaque inflammation and instability and may provide sufficient information to formulate preventive local mechanical strategies (eg, preemptive percutaneous coronary interventions) to avert cardiac events. Local endothelial shear stress (ESS) triggers vascular phenomena that synergistically exacerbate atherosclerosis toward an unstable phenotype. Specifically, low ESS augments lipid uptake and catabolism, induces plaque inflammation and oxidation, downregulates the production, upregulates the degradation of extracellular matrix, and increases cellular apoptosis ultimately leading to thin-cap fibroatheromas and/or endothelial erosions. Increases in blood thrombogenicity that result from either high or low ESS also contribute to plaque destabilization. An understanding of the actively evolving vascular phenomena, as well as the development of in vivo imaging methodologies to identify the presence and severity of the different processes, may enable early identification of a coronary plaque destined to acquire a high-risk state and allow for highly selective, focal preventive interventions to avert the adverse natural history of that particular plaque. In this review, we focus on the role of ESS in the pathobiologic processes responsible for plaque destabilization, leading either to accelerated plaque growth or to acute coronary events, and emphasize the potential to utilize in vivo risk stratification of individual coronary plaques to optimize prevention strategies to preclude new cardiac events.