Evaluation of left atrial remodeling by 2D-speckle-tracking echocardiography versus by high-density voltage mapping in patients with atrial fibrillation.

BACKGROUND: Strain imaging during left atrial (LA) reservoir phase (LASr) is used as a surrogate for LA structural remodeling and fibrosis. Atrial fibrillation (AF) patients with >5% low-voltage zones (LVZs) obtained by 3D-electro-anatomical-mapping have higher recurrence rate post-ablation. We investigated the relationship between LA remodeling using two-dimensional-speckle-tracking echocardiography (2D-STE) and high-density voltage mapping in AF patients. METHODS: A prospective study of 42 consecutive patients undergoing AF ablation. 2D-echo, 2D-STE, and high-density contact LA bipolar voltage maps were constructed before ablation. LVZs were determined with different bipolar amplitudes and their ratio per patient's LA area were investigated for correlation with LASr. We compared 2D-LASr results in patients with LVZs ≥ 5% (LVZs group) versus those with LVZ < 5% (non-LVZs group). RESULTS: Compared with non-LVZs group (n = 15), LVZs group (n = 27) included significantly older patients, more women, more persistent AF, higher CHA2 DS2 -VASc score, higher E/A ratio and higher LA volume index (p < .05). LVZs group had lower %LASr values (12.4 ± 5.9% vs. 21.1 ± 6.3, respectively; p<.001). LVZs% in different amplitudes (<0.1 mV, <0.2 mV, and <0.5 mV) were negatively correlated with %LASr (r = -.63, r = -.68, and r = -.72, respectively; p< .001). Atrial strain thresholds for LVZs ≥ 5% in amplitudes <0.1 mV, <0.2 mV, and <0.5 mV were associated with %LASr 12.98, 16.16 and 19.55, respectively; p< .05). In a multivariate analysis, %LASr was the only independent indicator of LVZs (OR, 0.8; 95% CI, 0.6-0.9; p= .04). CONCLUSIONS: LVZs ≥ 5% has a negative association with atrial %LASr. Thus, a simple 2D-STE measurement of %LASr can be used as a noninvasive method to evaluate significant LA remodeling and fibrosis in AF patients.

Management of Brugada Syndrome: Thirty-Three-Year Experience Using Electrophysiologically Guided Therapy With Class 1A Antiarrhythmic Drugs.

BACKGROUND: Information on long-term clinical outcome of patients with Brugada syndrome treated with electrophysiologically guided class 1A antiarrhythmic drugs (AAD) is limited. METHODS AND RESULTS: An aggressive protocol of programmed ventricular stimulation was performed in 96 patients with Brugada syndrome (88% males; mean age, 39.8±15.9 years). Ten patients were cardiac arrest survivors, 27 had presented with syncope, and 59 were asymptomatic. Ventricular fibrillation was induced in 66 patients, including 100%, 74%, and 61% of patients with cardiac arrest, syncope, and no symptoms, respectively. All but 6 of the 66 patients with inducible ventricular fibrillation underwent electrophysiological testing on quinidine (n=54), disopyramide (n=2), or both (n=4). Fifty-four (90%) patients were electrophysiological responders to >1 AAD with similar efficacy rates (≈90%) in all patients groups. Patients with no inducible ventricular fibrillation at baseline were left on no therapy. After a mean follow-up of 113.3±71.5 months, 92 patients were alive, whereas 4 died from noncardiac causes. No arrhythmic event occurred during class 1A AAD therapy in any of electrophysiological drug responders and in patients with no baseline inducible ventricular fibrillation. Arrhythmic events occurred in only 2 cardiac arrest survivors treated with implantable cardioverter-defibrillator alone but did not recur on quinidine. All cases of recurrent syncope (n=12) were attributed to a vasovagal (n=10) or nonarrhythmic mechanism (n=2). Class 1A AAD therapy resulted in 38% incidence of side effects that resolved after drug discontinuation. CONCLUSIONS: Our data suggest that electrophysiologically guided class 1A AAD treatment has a place in our therapeutic armamentarium for all types of patients with Brugada syndrome.