Atrial selective effect of amiodarone to increase threshold of excitation.

Increases of pacing threshold stimulation are well documented with different antiarrhythmic drugs, but not with amiodarone. We report a case of a patient with dual-chamber pacing, with stable thresholds on repeated measurements on the last year, who presented severe increase of atrial pacing threshold resulting in loss of atrial capture after a year of treatment with amiodarone. Thresholds were normalized once amiodarone was removed. Ventricular thresholds were not affected.

Ultrasonic characterization of the pulmonary venous wall: echographic and histological correlation.

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, 1.4+/-0.3 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, 2.6+/-0.8 mm) and decreased toward the lung hilum. The outer echodense layer corresponds to fibro-fatty adventitial tissue (mean maximal thickness, 2.15+/-0.36 mm). We found a close agreement among the IVUS and histological measurements for maximal luminal diameter (mean difference, -0.12+/-1.3 mm) and maximal muscular thickness (mean difference, 0.17+/-0.13 mm) using the Bland and Altman method. CONCLUSIONS: Our experimental study demonstrates for the first time that IVUS images of the pulmonary veins can provide information on the distal limits and thickness of the myocardial sleeves and can be a valuable tool to help accurate targeting during ablative procedures.

Nitric oxide production by neutrophils obtained from patients during acute coronary syndromes: expression of the nitric oxide synthase isoforms.

OBJECTIVES: To analyze the differences in the nitric oxide (NO) forming system between neutrophils obtained from patients during unstable angina (UA) and during acute myocardial infarction (AMI). BACKGROUND: Neutrophils are involved in the regulation of thrombus formation through the release of active substances such as NO. Acute myocardial infarction is the result of an occlusive thrombus; unstable angina is attributed to intermittent thrombus formation. METHODS: We studied 49 patients admitted to hospital within 24 h after the onset of chest pain: 31 experienced AMI and 18 experienced UA. Acute myocardial infarction was defined as CK greater than two-fold the upper limit of normal value of biochemical laboratory, with CK-MB >10% total CK. Unstable angina was defined as transient ST segment changes without significant increases in CK and CK-MB. RESULTS: The amount of NO generated by neutrophils from AMI patients was significantly higher than that generated by neutrophils from UA patients. Neutrophils from UA and AMI patients showed low levels of endothelial-like NO synthase protein expression and a marked expression of the inducible NO synthase (iNOS) isoform. Although neutrophils from patients during acute coronary syndromes generated high amounts of NO, they did not demonstrate an increased ability to stimulate cyclic guanosine monophosphate (cGMP) synthesis in platelets. This lack of activity to release NO by neutrophils from patients during AMI was unrelated to a defect in the platelet cGMP-forming system; sodium nitroprusside, an exogenous NO donor, similarly increased cGMP levels in platelets from AMI patients and healthy donors. CONCLUSIONS: Neutrophils from patients during AMI and UA showed an increased production of NO and a marked expression of the iNOS isoform. However, NO released from these neutrophils showed a deficient functionality. These findings could have clinical implications because they show differences in thrombus growth in patients with UA versus patients with AMI.

Fluoroscopic cardiac anatomy for catheter ablation of tachycardia.

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.

Doxazosina y guanilato ciclasa soluble en un modelo de ratas hipertensas / Doxazosin and Soluble Guanylate Cyclase in a Rat Model of Hypertension

Introducción. Aunque existen diferentes estudios sobre la capacidad del endotelio de generar óxido nítrico en la disfunción endotelial asociada a la hipertensión, el sistema de la guanilato ciclasa soluble (GCs) ha sido menos estudiado. Objetivo. Analizar en ratas espontáneamente hipertensas que desarrollan accidentes cerebrovasculares (SHRSP) el nivel de expresión de la GCs en la pared vascular. También se estudió el efecto del tratamiento con doxazosina, antagonista 1-adrenérgico, sobre la expresión de la GCs en la pared vascular de estos animales. Métodos. Se utilizaron ratas SHRSP (edad, 20 semanas; n = 24). Un grupo de estas ratas fue tratado con doxazosina (10 mg/kg peso/día; n = 12) durante 2 semanas, y se comparó con ratas Wistar-Kyoto (WKY) normotensas (n = 12).Resultados. Segmentos aórticos aislados de ratas SHRSP presentaron una disminución de la respuesta vasodilatadora al nitroprusiato sódico. La respuesta al nitroprusiato sódico mejoró en las ratas SHRSP tratadas con doxazosina respecto de las SHRSP sin tratamiento. La expresión de la 1-GCs determinada por Western blot e inmunohistoquímica estaba disminuida en las ratas SHRSP respecto a las WKY. La administración de doxazosina aumentó la expresión de GCs, particularmente en la capa media cuando se comparara con ratas SHRSP no tratadas. Conclusiones. En las ratas SHRSP existe una disminución de la expresión de 1-GCs en la pared vascular y una reducción en la respuesta a nitroprusiato sódico que mejora tras la administración de doxazosina cuando se compara con SHRSP no tratadas. Estos resultados sugieren la importancia que también puede tener el sistema de la GCs en el tratamiento global de la disfunción endotelial (AU)