Stability of rotors and focal sources for human atrial fibrillation: focal impulse and rotor mapping (FIRM) of AF sources and fibrillatory conduction.

INTRODUCTION: Several groups report electrical rotors or focal sources that sustain atrial fibrillation (AF) after it has been triggered. However, it is difficult to separate stable from unstable activity in prior studies that examined only seconds of AF. We applied phase-based focal impulse and rotor mapping (FIRM) to study the dynamics of rotors/sources in human AF over prolonged periods of time. METHODS: We prospectively mapped AF in 260 patients (169 persistent, 61 ± 12 years) at 6 centers in the FIRM registry, using baskets with 64 contact electrodes per atrium. AF was phase mapped (RhythmView, Topera, Menlo Park, CA, USA). AF propagation movies were interpreted by each operator to assess the source stability/dynamics over tens of minutes before ablation. RESULTS: Sources were identified in 258 of 260 of patients (99%), for 2.8 ± 1.4 sources/patient (1.8 ± 1.1 in left, 1.1 ± 0.8 in right atria). While AF sources precessed in stable regions, emanating activity including spiral waves varied from collision/fusion (fibrillatory conduction). Each source lay in stable atrial regions for 4,196 ± 6,360 cycles, with no differences between paroxysmal versus persistent AF (4,290 ± 5,847 vs. 4,150 ± 6,604; P = 0.78), or right versus left atrial sources (P = 0.26). CONCLUSIONS: Rotors and focal sources for human AF mapped by FIRM over prolonged time periods precess ("wobble") but remain within stable regions for thousands of cycles. Conversely, emanating activity such as spiral waves disorganize and collide with the fibrillatory milieu, explaining difficulties in using activation mapping or signal processing analyses at fixed electrodes to detect AF rotors. These results provide a rationale for targeted ablation at AF sources rather than fibrillatory spiral waves.

The incidence, diagnosis, and management of pulmonary vein stenosis as a complication of atrial fibrillation ablation.

PURPOSE: Pulmonary vein isolation (PVI) during ablation of atrial fibrillation (AF) is associated with pulmonary vein stenosis (PVS). Although the reported incidence of PVS has fallen in recent years, the precise rate of PVS is unknown. Coherent guidelines for screening and treatment of PVS are not established. We reviewed literature to investigate the incidence, diagnosis, and management of PVS as a complication of PVI. METHODS: We reviewed 41 manuscripts that described a total of 4,615 subjects (median, 84 subjects/study). RESULTS: The incidence of PVS after PVI reported in literature from 1999 to 2004 ranges from 0 to 44% (mean, 6.3%; median, 5.4%), whereas studies after 2004 report an incidence of 0-19% (mean, 2%; median, 3.1%; p < 0.001). PVS symptoms typically occur with reduction of lung perfusion by 20-25%. Variable criteria exist for diagnosis of PVS by magnetic resonance imaging, computed tomography, and perfusion imaging. The restenosis rate for treatment with balloon angioplasty ranges from 30 to 87% (mean, 60%; median, 47%), compared with immediate stenting that ranges from 14 to 57% (mean, 34%; median, 33%). CONCLUSIONS: Recent peer-reviewed articles suggest that PVI carries a 3-8% risk of developing PVS, but they likely underestimate the incidence of PVS, as specific screening and diagnostic guidelines are not established. Imaging modalities should be used to screen patients after ablation of AF since early recognition of PVS improves treatment outcomes. Treatment with angioplasty and stent placement can improve symptoms and lung perfusion but the benefit of treatment with immediate stent placement remains controversial. It is critical to maintain a high clinical index of suspicion for PVS in at-risk individuals to ensure timely detection and treatment.

Three-dimensional echocardiographic assessment of patent foramen ovale in platypnea-orthodeoxia.

Platypnea-orthodeoxia is an uncommon syndrome characterized by positional dyspnea and hypoxia when upright that improves with lying down. We present a 75-year-old man with platypnea-orthodeoxia in the setting of a patent foramen ovale (PFO) and a 2.1 cm highly mobile atrial septal aneurysm with 2 cm bowing. Prior reports have established the use of three-dimensional echocardiography to facilitate percutaneous closure of PFO and atrial septal defect, but its use in patients with platypnea-orthodeoxia is unclear. We document three-dimensional echocardiographic images that accurately estimated PFO defect size and confirmed placement of the occluder device.

Atrial conduction slows immediately before the onset of human atrial fibrillation: a bi-atrial contact mapping study of transitions to atrial fibrillation.

OBJECTIVES: The aim of this study was to determine whether onset sites of human atrial fibrillation (AF) exhibit conduction slowing, reduced amplitude, and/or prolonged duration of signals (i.e., fractionation) immediately before AF onset. BACKGROUND: Few studies have identified functional determinants of AF initiation. Because conduction slowing is required for reentry, we hypothesized that AF from pulmonary vein triggers might initiate at sites exhibiting rate-dependent slowing in conduction velocity (CV restitution) or local slowing evidenced by signal fractionation. METHODS: In 28 patients with AF (left atrial size 43 ± 5 mm; n = 13 persistent) and 3 control subjects (no AF) at electrophysiological study, we measured bi-atrial conduction time (CT) electrogram fractionation at 64 or 128 electrodes with baskets in left (n = 17) or both (n = 14) atria during superior pulmonary vein pacing at cycle lengths (CL) accelerating from 500 ms (120 beats/min) to AF onset. RESULTS: Atrial fibrillation initiated in 19 of 28 AF patients and no control subjects. During rate acceleration, conduction slowed in 23 of 28 AF patients (vs. no control subjects, p = 0.01) at the site of AF initiation (15 of 19) or latest activated site (20 of 28). The CT lengthened from 79 ± 23 ms to 107 ± 39 ms (p < 0.001) on acceleration, in a spectrum from persistent AF (greatest slowing) to control subjects (least slowing; p < 0.05). Three patterns of CV restitution were observed: 1) broad (gradual CT prolongation, 37% patients); 2) steep (abrupt prolongation, at CL 266 ± 62 ms, 42%); and 3) flat (no prolongation, 21% AF patients, all control subjects). The AF initiation was more prevalent in patients with CV restitution (17 of 23 vs. 2 of 8; p = 0.03) and immediately followed abrupt re-orientation of the activation vector in patients with broad but not steep CV restitution (p < 0.01). Patients with broad CV restitution had larger atria (p = 0.03) and were more likely to have persistent AF (p = 0.04). Notably, neither amplitude nor duration (fractionation) of the atrial signal at the AF initiation site were rate-dependent (both p = NS). CONCLUSIONS: Acceleration-dependent slowing of atrial conduction (CV restitution) precedes AF initiation, whereas absence of CV restitution identifies inability to induce AF. Conduction restitution, but not fractionated electrograms, may thus track the functional milieu enabling AF initiation and has implications for guiding AF ablation and pharmacological therapy.

Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm.

Recent surveys and reports suggest that many athletes and bodybuilders abuse anabolic-androgenic steroids (AAS). However, scientific data on the cardiac and metabolic complications of AAS abuse are divergent and often conflicting. A total of 49 studies describing 1,467 athletes were reviewed to investigate the cardiovascular effects of the abuse of AAS. Although studies were typically small and retrospective, some associated AAS abuse with unfavorable effects. Otherwise healthy young athletes abusing AAS may show elevated levels of low-density lipoprotein and low levels of high-density lipoprotein. Although data are conflicting, AAS have also been linked with elevated systolic and diastolic blood pressure and with left ventricular hypertrophy that may persist after AAS cessation. Finally, in small case studies, AAS abuse has been linked with acute myocardial infarction and fatal ventricular arrhythmias. In conclusion, recognition of these adverse effects may improve the education of athletes and increase vigilance when evaluating young athletes with cardiovascular abnormalities.