Background-Pulmonary vein isolation with radiofrequency catheter ablation techniques is used to prevent recurrences of human atrial fibrillation. Visualization of the architecture at the venoatrial junction could be crucial for these ablative techniques. Our study assesses the potential for intravascular ultrasound to provide this information. Methods and Results-We retrieved 32 pulmonary veins from 8 patients dying from noncardiac causes. We obtained cross-sectional intravascular ultrasound (IVUS) images with a 3.2F, 30-MHz ultrasound catheter at intervals on each vein. Histological cross-sections at the intervals allowed comparisons with ultrasonic images. The pulmonary venous wall at the venoatrial junction revealed a 3-layered ultrasonic pattern. The inner echogenic layer represents both endothelium and connective tissue of the media (mean maximal thickness, 1.4Ϯ0.3 mm). The middle hypoechogenic stratum corresponds to the sleeves of left atrial myocardium surrounding the external aspect of the venous media. This layer was thickest at the venoatrial junction (mean maximal thickness, 2.6Ϯ0.8 mm) and decreased toward the lung hilum. The outer echodense layer corresponds to fibro-fatty adventitial tissue (mean maximal thickness, 2.15Ϯ0.36 mm). We found a close agreement among the IVUS and histological measurements for maximal luminal diameter (mean difference, Ϫ0.12Ϯ1.3 mm) and maximal muscular thickness (mean difference, 0.17Ϯ0.13 mm) using the Bland and Altman method. Conclusions-Our

The understanding of cardiac anatomy is crucial for the interventional arrhythmologist. In spite of the introduction of several nonfluroscopic navigational tools, some of them capable of reconstructing a computer-based surrogate of the endocardial surface of the heart cavities, simple fluoroscopy with or without the aid of angiographic techniques is still the most widely used method to guide mapping and ablation procedures. In some instances, fluoroscopic and angiographic methods have no possible replacement to unravel certain arrhythmologically useful anatomic landmarks. New interpretations of cardiac architecture show the need to challenge some traditional anatomic views, like the concept of septums within the heart. The fluoroscopic anatomy also needs to be reconsidered in the light of the new attitudinally oriented nomenclature. This article presents an overview of the fluoroscopic anatomy of the heart. When pertinent, some anatomical concepts are discussed in more detail like the triangle of Koch, the pyramidal space, and the interatrial groove. In the sections on the atria and on the ventricles, the authors focus on the anatomic information that is relevant for mapping and ablation from a fluoroscopic viewpoint, providing some hints on how best to depict the morphological features from the stance of the interventional arrhythmologist. The Visible Human Slice and Surface Server using data sets from the Visible Human Male and Female Project, has been used to facilitate the understanding of the fluoroscopic anatomy.

In vitro studies have suggested that losartan interacts with the thromboxane (TxA2)/ prostaglandin H2 (PGH2) receptor in human platelets, reducing TxA2-dependent platelet activation. The aim of this study was to evaluate the effect of different angiotensin II type 1 receptor antagonists in stroke-prone spontaneously hypertensive rats (SHRSP). The level of platelet activation was assessed by determining P-selectin expression in platelets by flow cytometry. The ex vivo adhesion of platelets was also analyzed. The number of platelets that expressed P-selectin in SPSHR was significantly increased (% P-selectin expression: WKY 4 +/- 0, 4%; SHRSP 15.5 +/- 0, 8% [n = 8], p < 0.05). In SHRSP receiving losartan (20 mg/kg body weight per day) the percentage of platelets expressing P-selectin fell to levels close to that observed in WKY. The number of platelets from SHRSP treated with valsartan and candesartan (20 mg/kg body weight per day for 14 days) that expressed P-selectin was not significantly different from those from untreated SPRHR. Only losartan treatment reduced ex vivo platelet adhesion to a synthetic surface. The antiplatelet effect of losartan does not appear to be related to the level of blood pressure reduction. In ex vivo experiments, losartan significantly reduced the binding of the radiolabeled TxA2 agonist U46619 to platelets obtained from SHRSP in a dose-dependent manner. Treatment with losartan reduced the number of activated platelets in SHRSP independently of its blood pressure effects. TxA2-receptor blockade is proposed as a mechanism by which losartan can prevent platelet activation.