The effect of catheter ablation for ventricular arrhythmias originating from the left ventricular papillary muscles on mitral valve function.

BACKGROUND: Ablation of ventricular arrhythmias (VA) originating from the left ventricular (LV) papillary muscles (PM) has the potential to damage the mitral valve apparatus resulting in mitral regurgitation (MR). This study sought to evaluate the effect of radiofrequency (RF) ablation of a PM on MR severity. METHODS: Patients with pre- and postablation transthoracic echocardiograms who underwent PM ablation for treatment of VA were retrospectively identified and compared to similar patients who underwent VA ablation at non-PM sites. MR severity was evaluated pre- and postablation in both groups and graded as none/trace (Grade 0); mild/mild-to-moderate (Grade 1); moderate (Grade 2); moderate-to-severe/severe (Grade 3). RESULTS: A total of 45 and 49 patients were included in the PM and non-PM groups, respectively. There were no significant baseline demographic differences. The PM group had longer RF ablation times (22.3 vs. 13.3 min, p < .01) compared to the non-PM group. Most patients had low-grade MR in both groups at baseline. Change in pre- versus postablation MR within the PM group was not statistically significant by Wilcoxon rank-sum test (Figure 2, p = .46). MR severity following ablation was also evaluated using logistic regression models. The odds ratio for worsening MR in the PM group compared to non-PM was 0.19 (95% confidence interval: 0.008-4.18, p = .29) after adjusting for comorbidities, LV ejection fraction, and LV internal end-diastolic diameter. CONCLUSION: RF ablation of VA originating from PM under intracardiac echocardiography guidance did not result in clinically or statistically significant worsening of MR.

Pericardial fat is independently associated with human atrial fibrillation.

OBJECTIVES: The purpose of this study was to investigate the association between atrial fibrillation (AF) and pericardial fat. BACKGROUND: Pericardial fat is visceral adipose tissue that possesses inflammatory properties. Inflammation and obesity are associated with AF, but the relationship between AF and pericardial fat is unknown. METHODS: Pericardial fat volume was measured using computed tomography in 273 patients: 76 patients in sinus rhythm, 126 patients with paroxysmal AF, and 71 patients with persistent AF. RESULTS: Patients with AF had significantly more pericardial fat compared with patients in sinus rhythm (101.6 +/- 44.1 ml vs. 76.1 +/- 36.3 ml, p < 0.001). Pericardial fat volume was significantly larger in paroxysmal AF compared with the sinus rhythm group (93.9 +/- 39.1 ml vs. 76.1 +/- 36.3 ml, p = 0.02). Persistent AF patients had a significantly larger pericardial fat volume compared with paroxysmal AF (115.4 +/- 49.3 ml vs. 93.9 +/- 39.1 ml, p = 0.001). Pericardial fat volume was associated with paroxysmal AF (odds ratio: 1.11; 95% confidence interval: 1.01 to 1.23, p = 0.04) and persistent AF (odds ratio: 1.18, 95% confidence interval: 1.05 to 1.33, p = 0.004), and this association was completely independent of age, hypertension, sex, left atrial enlargement, valvular heart disease, left ventricular ejection fraction, diabetes mellitus, and body mass index. CONCLUSIONS: Pericardial fat volume is highly associated with paroxysmal and persistent AF independent of traditional risk factors including left atrial enlargement. Whether pericardial fat plays a role in the pathogenesis of AF requires future investigation.

Electroanatomic mapping of postpacing intervals clarifies the complete active circuit and variants in atrial flutter.

BACKGROUND: Typical atrial flutter is characterized by cavotricuspid isthmus dependence and activation sequentially around the tricuspid annulus (TA), usually counterclockwise. However, analysis of the upper portion of the annulus by postpacing interval after entrainment sometimes suggests it is outside the circuit. Details on the true active circuit are limited, particularly in the upper portions. OBJECTIVE: The purpose of this study was to define the full active circuit in atrial flutter. METHODS: In 26 patients with isthmus-dependent atrial flutter, we created detailed electroanatomic maps of postpacing intervals throughout the entire right atrium. Postpacing intervals within 20 ms of the flutter cycle length were defined as within the circuit. RESULTS: Creating postpacing interval maps allowed characterization of the full active circuit in all patients, and revealed significant variations despite similar counterclockwise or clockwise patterns with activation mapping. In 8, the active circuit was solely around the TA. In 14, an oblique course between the anterior and posterior borders was found, with the upper circuit off the annulus, posterior to the right atrial appendage base. Of these, 8 coursed anterior to the SVC, 5 behind the SVC and 1 bifurcated the SVC. In 4 others, bifurcation of the upper circuit was seen around the right atrial appendage (n = 3), or around the combined right atrial appendage-superior vena cava (n = 1). CONCLUSION: Despite similar activation around the TA, creating electroanatomic postpacing interval maps distinguishes the active flutter circuit from passively activated myocardium. Significant variability exists in the active circuit, with only a minority around the TA. Most commonly, the circuit courses not around a single barrier but obliquely between anterior and posterior borders.

New approaches to the treatment and prevention of neurally mediated reflex (neurocardiogenic) syncope.

Neurally mediated reflex syncope (sometimes referred to as neurocardiogenic syncope), encompasses a group of disorders of which the best known and most frequently occurring forms are the vasovagal (or common) faint, and carotid sinus syndrome. Postmicturition syncope, defecation syncope, cough syncope, and other situational reflex faints are also included among these conditions. With the exception of carotid sinus syndrome in which cardiac pacing is effective, treatment of most neurally mediated reflex faints is shifting from reliance on various drugs to greater emphasis on education and nonpharmacologic therapy. Initial management should include counseling of patients regarding recognition of early warning symptoms, and avoidance of precipitating factors. Volume expansion with salt tablets or electrolyte-containing beverages and patient education on how to perform isometric arm contractions and/or leg crossing in order to abort impending syncope are also important. Thereafter, tilt-training has demonstrated benefit in several clinical studies. When symptoms remain despite the above-noted interventions, pharmacologic therapy with midodrine or a nonselective b-blocker can be considered. In the case of most neurally mediated reflex faints, permanent cardiac pacing should be reserved only for those older patients with significant bradycardia or asystole at time of syncope when all other interventions have failed.