Notes: Abstract: This article provides the position of the American Council on Science and Health regarding how breast cancer is defined and classified; the magnitude of the public health problem of breast cancer among women; the implications of variation in incidence of breast cancer internationally and with migration; access to health care as a factor in slight differences in incidence and mortality rates among African-American and white women; and the evidence concerning various proposed human-breast-cancer risk factors. The article classifies risk factors as either established, speculated, or unsupported on the basis of available evidence.Specific genes have been identified that may explain as much as 5–10% of new breast cancer cases. Inherited predispositions may be characterized by family history of breast or ovarian cancer, young age at diagnosis, breast cancer diagnosed in both breasts, and male breast cancer. Benign breast disease (BBD), particularly the subtypes of BBD involving atypical hyperplasia, and exposure early in life to ionizing radiation is an established risk factor for breast cancer. Several reproductive characteristics are established as risk factors for breast cancer: early age at menarche, first full-term pregnancy after age 35 years of late age, and late age of menopause. Obesity and low physical activity are established as risk factors for breast cancer and are modifiable.Speculated risk factors for breast cancer that are gaining scientific support include nulliparity, oral contraceptive use, and postmenopausal estrogen replacement therapy. Speculated risk factors for which there is conflicting or preliminary support include not breast feeding, postmenopausal estrogen/progestogen replacement therapy, prescribed diethylstilbestrol, low consumption of phytoestrogens, specific dietary practices, alcohol consumption, not using nonsteroidal antinflammatory drugs, abortion, and breast augmentation. Unsupported risk factors include higher than average consumption of phytoestrogens, premenopausal obesity, electromagnetic fields, and low-dose ionizing radiation after 40 years of age. There is only limited support for xenoestrogens and large breast size as risk factors for breast cancer.

Notes: Introduction: This study was designed to record global high-density maps of left atrial endocardial activation during sinus rhythm and coronary sinus pacing. Method and Results: Noncontact mapping of the left atrium was performed in nine patients with paroxysmal atrial fibrillation undergoing pulmonary vein ablation procedures. High-density isopotential and isochronal activation maps were superimposed on three-dimensional reconstructions of left atrial geometry. Mapping was repeated during pacing from sites within the coronary sinus. Earliest left atrial endocardial activation occurred anterior to the right pulmonary veins in seven patients and on the anterosuperior septum in two patients. A line of conduction block was seen in the posterior wall and inferior septum in all patients. The direction of activation in the left atrial myocardium overlying the coronary sinus was different from the electrogram sequence in the coronary sinus catheter in 6 of 9 patients. During coronary sinus pacing, activation entered the left atrium a mean (SD) of 41 (13) ms after the pacing stimulus at a site 12 (10) mm from the endocardium overlying the pacing electrode. Lines of conduction block were present in the posterior wall and inferior septum. Conclusion: In patients with paroxysmal atrial fibrillation, lines of conduction block are present in the left atrium during sinus rhythm and coronary sinus pacing. Electrograms recorded in the coronary sinus infrequently correspond to the direction of activation in the overlying left atrial myocardium.

Notes: Introduction: A novel mapping/ablation catheter using a coaxially ablation electrode (E) that is moveable between distal and proximal ring electrodes along its shaft was used to create a linear lesion over the cavotricuspid isthmus (CTI) and bidirectional block in 32 patients (21 men; age 38–79 years) undergoing ablation for counterclockwise atrial flutter. Methods and Results: Two bipolar electrograms (E1 and E2) were recorded: between E and the distal ring electrode and between E and the proximal ring electrode. Interpole distance varied for both as the E traversed the slide shaft. Given the catheter's concept, these bipoles are orientated exactly along the line of lesion creation. Prior to ablation, unitary bipolar electrograms were recorded along the catheter slide shaft position. As the CTI lesion was created (E moved along the catheter slide shaft in 2-mm steps with radiofrequency energy delivered to achieve 65°C for 60 sec at each), double potentials (DP) were observed. Interpotential distance became maximal with completion of the linear lesion and bidirectional block. DPs were noted in all these procedures. With pacing from the low septal right atrium at bidirectional block creation, interpotential timing was 140.9 ± 15 msec and from the low right atrial free wall was 145.13 ± 18 msec. In sinus rhythm, DP interpotential timing was less (35.13 ± 9 msec) as activation fronts arrived from both septal and anterior atrial aspects. Conclusion: Bipolar recordings from the coaxially moveable electrode catheter provide unique electrogram data. DPs recorded during and after linear lesion creation can define conduction block across that lesion without the need for additional mapping catheters or complex mapping technology. (J Cardiovasc Electrophysiol, Vol. 14, pp. 236-242, March 2003)

Notes: Activation Patterns and Coronary Sinus Pacing. Introduction: Anatomic and electrical connections between the left atrium and right atrium (RA) have been described. The relationship between coronary sinus (CS) pacing site and RA activation has not been examined. Methods and Results: Fifteen anesthetized swine underwent high-density noncontact mapping of the RA during pacing from up to five different sites within the CS. Isopotential mapping identified the site of earliest RA depolarization and the pattern of subsequent activation. Hearts were excised and endocardial dissection performed. Earliest RA activation occurred at the CS os with proximal CS pacing sites and at Bachmann's bundle at distal pacing sites. The mean depth at which a shift in earliest RA activation site occurred was 46 ± 13 mm (range 21 to 63 mm). RA activation times following earliest activation at the CS and Bachmann's bundle were 40 ± 4 msec and 51 ± 6 msec (P 〈 0.002). Conduction delay or block was recorded at the lateral cavotricuspid isthmus, terminal crest, and tendon of Todaro. Latest RA activation always occurred in the high anterolateral atrium after ascending the anterolateral wall. The lateral RA was activated by the wavefront that traversed the posterior wall rather than by the wavefront crossing the cavotricuspid isthmus, even with earliest RA activation at the CS os. Conclusion: The site of earliest RA activation during CS pacing is dependent upon the pacing depth within the CS. In the porcine heart, areas of conduction delay influence RA activation patterns and timings. These findings may have implications for patients undergoing assessment of radiofrequency ablation of atrial flutter.

Notes: Right Atrial Activation. Introduction: Previous mapping studies of right atrial (RA) activation during sinus rhythm have been limited by the use of epicardial electrode plaques in open chest subjects or microelectrodes in the excised heart. This study describes global RA endocardial activation patterns using high-density mapping and compares the results with underlying endocardial architecture. Methods and Results: Noncontact mapping of the RA was performed in 21 anesthetized swine. Isopotential and isochronal maps were superimposed upon three-dimensional reconstructions of RA geometry. Hearts were excised and endocardial dissection performed. Two patterns of RA activation were recorded. The site of earliest endocardial activation occurred either laterally at a position consistent with the terminal crest or superiorly at the junction between the superior caval vein and RA appendage. The subsequent spread of depolarization followed the longitudinal orientation of muscle fibers. Areas of conduction delay and block were seen at the junction between the terminal crest and posterior wall, the cavotricuspid isthmus, and around the margins of the triangle of Koch. Endocardial dissection at these sites demonstrated complex fiber orientation. A lateral site of earliest activation demonstrated a more prominent display of conduction delay or block. Conclusion: The spread of the sinus impulse follows endocardial myofiber orientation and is dictated by the site of earliest activation. Even during sinus rhythm, anisotropic conduction results in areas of conduction block or delay. These findings have implications in the development of reentrant arrhythmias and may influence surgical or electrophysiologic procedures.

Notes: A 32-year-old man with idiopathic ventricular fibrillation and an implantable cardioverter defibrillator presented during a ventricular fibrillation storm. Frequent monomorphic ventricular ectopics with left bundle branch block morphology were documented, some of which initiated fibrillation. He underwent noncontact mapping of the right ventricle, during which the ventricular ectopics were mapped to a site in the free wall displaying a diastolic potential 80 ms before ectopic QRS onset. Following three radiofrequency energy applications, the ectopics were abolished. After 11-month follow-up, he has experienced no further arrhythmias. Noncontact mapping may identify ablatable triggers of ventricular fibrillation and lead to successful outcomes even when only single ectopics are present.

Notes: Transcatheter Left Atrial Electrical Disconnection. Introduction: An effective, catheter-based treatment for persistent atrial fibrillation (AF) remains elusive. This study assessed the feasibility of transcatheter left atrial (LA) electrical disconnection and its effect on AF inducibility. Method and Results: Thirteen anesthetized swine underwent noncontact mapping of the right atrium (RA) during coronary sinus (CS) pacing. Sites of earliest RA activation were identified using isopotential maps. An ablation catheter was navigated to these sites and a cluster of radiofrequency (RF) lesions applied until earliest activation shifted to a new site. The procedure was repeated until the atria were electrically disconnected. AF induction was attempted before and after ablation. Earliest RA activation was the CS os during proximal CS pacing and Bachmann's bundle during distal CS pacing. These two sites were successfully ablated in all 13 animals. Earliest activation then shifted to the fossa ovalis. RF energy was applied at a median of 2.5 sites (range 1 to 5) around the fossa, then at sites in the triangle of Koch, septum, cavotricuspid isthmus, and posterior wall. Atrial electrical disconnection was achieved in 10 of 13 animals (5 LA electrical disconnection, 3 RA electrical disconnection, 2 biatrial electrical disconnection with complete heart block). After atrial electrical disconnection, the LA became electrically silent. Before ablation, AF was inducible in every animal. After atrial electrical disconnection, AF was inducible in 3 of 10 animals. Conclusion: Atrial electrical disconnection is feasible using noncontact mapping and RF ablation. Successful electrical disconnection of the atria reduces AF inducibility. This approach is worthy of further evaluation as a management strategy for persistent AF, combined with device therapies.

Notes: In porcine studies anodes in the middle cardiac vein compare favorably with those in the RV. It has not been demonstrated whether the RV and middle cardiac vein or the middle cardiac vein alone anodes are superior when shocking to a conventional SVC and active housing cathode nor whether a bystander middle cardiac vein electrode exerts a passive electrode affect. Twelve pigs were anesthetized and had an active housing implanted in the left pectoral region and defibrillation coils placed at the RV apex and in the SVC. A custom-made defibrillation coil (Ela Medical) was advanced into the middle cardiac vein through a 9 Fr transvenous catheter. The DFT for three anodes (RV; RV and middle cardiac vein; middle cardiac vein) to the SVC and active housing was then assessed by a three reversal binary search, the order of testing was randomized. In seven animals DFT was assessed in the same way for the configuration of RV to SVC and active housing twice more, with and without a bystander middle cardiac vein coil electrode in place. The results were middle cardiac vein 7.5 ± 1.7 J, RV and middle cardiac vein 7.3 ± 1.7 J reduced DFT significantly compared to RV 13.8 ± 4.2 J (both P 〈 0.000). There was no significant difference between the middle cardiac vein and the middle cardiac vein and RV (P = 0.67, 95% CI for difference − 0.64–0.96). The DFT of RV to SVC and the active housing was the same with (13.2 ± 4.0) and without (13.7 ± 4.2) the middle cardiac vein bystander coil in place (P = 0.177, 95% CI for difference − 0.33–1.33 J). Shocking to a SVC and active housing cathode, middle cardiac vein, and RV and middle cardiac vein anodes are equally effective in lowering DFT compared to the RV. The middle cardiac vein coil electrode does not exert a passive electrode affect on the RV to the SVC and active housing defibrillation.