Background Predictors of atrial fibrillation (AF) recurrence after catheter ablation (CA) are not fully defined. We hypothesized that 2D left atrial (LA) regional strain maps would help identify abnormal atrial substrate that increases susceptibility to AF recurrence post-CA. Methods and Results Sixty-three patients (63±10 years, 60% male) underwent CA for symptomatic paroxysmal (75%) or persistent (25%) AF. Baseline LA mechanical function determined using speckle tracking echocardiography was compared between those with AF recurrence (AFR) and no recurrence post-CA. Bi-dimensional global and regional maps of LA wall velocity, strain, and strain rate (SR) were obtained during end ejection and early diastole. After 18±12 months of follow-up, 34 patients were free of AFR post-CA. There were no differences in clinical characteristics, LA and LV volumes, and Doppler estimates of LV diastolic function and filling pressures at baseline between patients with recurrent AF and those that maintained sinus rhythm. However, the LA emptying fraction (55±17% vs. 64±14%, p=0.04), global and regional systolic and diastolic strains, SR, and velocities were reduced in patients with recurrent AF. There was marked attenuation of peak LA lateral wall longitudinal strain (LS; 11±7% vs. 20±14%, p=0.007) and SR (0.9±0.4 vs. 1.3±0.6 s−1, p=0.01). Multivariate analysis revealed lateral wall LS (odds ratio=1.15, 95% CI=1.02–1.28, p=0.01) as an independent predictor of AFR. Conclusions Regional LA lateral wall LS is a pre-procedural determinant of AFR in patients undergoing CA, independent of LA enlargement. Characterization of atrial myocardial tissue properties by speckle tracking echo may aid the appropriate selection of adjunctive strategies and prognostication of patients undergoing CA.

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• Abstract: Mutations in the free radical-scavenging enzyme copper/zinc superoxide dismutase (Cu/Zn-SOD) are associated with neuronal death in humans and mice. Here, we examine the effects of human wild-type (WT SOD) and mutant (Gly 93 -÷ Ala; G93A) Cu/Zn-SOD enzyme on the fate of postnatal midbrain neurons. Oneweek-old cultures from transgenic mice expressing WT SOD enzyme had significantly more midbrain neurons and fewer necrotic and apoptotic neurons than nontransgenic cultures. In contrast, 1-week-old cultures from transgenic G93A mice expressing mutant SOD enzyme had significantly fewer midbrain neurons and more necrotic and apoptotic neurons than nontransgenic cultures. To subject postnatal midbrain neurons to oxidative stress, cultures were incubated with L-DOPA. L-DOPA at 200 pM caused~-..50% loss of tyrosine hydroxylase (TH) -positive neurons in nontransgenic cultures and even greater loss in transgenic G93A cultures; no alterations were noted in GABA neuron numbers. In contrast, 200 pM L-DOPA did not cause any significant reductions in TH-positive or GABA neuron numbers in transgenic WT SOD cultures. L-DOPA at 50 pM had opposite effects, in that it significantly increased TH-positive, but not GABA neuron numbers in transgenic WT SOD and G93A and in nontransgenic cultures. These results indicate that increased amounts of WT SOD enzyme promote cell survival and protect against L-DOPA-induced dopaminergic neurotoxicity, whereas increased amounts of mutated Cu/Zn-SOD enzyme have inverse effects. As the spontaneous loss and L-DOPA-induced loss of postnatal dopaminergic midbrain neurons appear to be mediated by free radicals, our study supports the view that mutated Cu/Zn-SOD enzyme kills cells by oxidative stress.

Background-Predictors of atrial fibrillation (AF) recurrence after catheter ablation (CA) are not fully defined. We hypothesized that 2D left atrial (LA) regional strain maps would help identify abnormal atrial substrate that increases susceptibility to AF recurrence post-CA. Methods and Results-Sixty-three patients (63±10 years, 60% male) underwent CA for symptomatic paroxysmal (75%) or persistent (25%) AF. Baseline LA mechanical function determined using speckle tracking echocardiography was compared between those with AF recurrence (AFR) and no recurrence post-CA. Bi-dimensional global and regional maps of LA wall velocity, strain, and strain rate (SR) were obtained during end ejection and early diastole. After 18±12 months of follow-up, 34 patients were free of AFR post-CA. There were no differences in clinical characteristics, LA and LV volumes, and Doppler estimates of LV diastolic function and filling pressures at baseline between patients with recurrent AF and those that maintained sinus rhythm. However, the LA emptying fraction (55±17% vs. 64±14%, p=0.04), global and regional systolic and diastolic strains, SR, and velocities were reduced in patients with recurrent AF. There was marked attenuation of peak LA lateral wall longitudinal strain (LS; 11±7% vs. 20±14%, p=0.007) and SR (0.9±0.4 vs. 1.3±0.6 s −1 , p=0.01). Multivariate analysis revealed lateral wall LS (odds ratio=1.15, 95% CI=1.02-1.28, p=0.01) as an independent predictor of AFR. Conclusions-Regional LA lateral wall LS is a pre-procedural determinant of AFR in patients undergoing CA, independent of LA enlargement. Characterization of atrial myocardial tissue properties by speckle tracking echo may aid the appropriate selection of adjunctive strategies and prognostication of patients undergoing CA.

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