Ian Wright

Pulmonary venous isolation by antral ablation with a large cryoballoon for treatment of paroxysmal and persistent atrial fibrillation: medium-term outcomes and non-randomised comparison with pulmonary venous isolation by radiofrequency ablation

Background To prevent atrial fibrillation (AF) recurrence after catheter ablation, pulmonary venous isolation (PVI) at an antral level is more effective than segmental ostial ablation. Cryoablation around the pulmonary venous (PV) ostia for AF therapy is potentially safer compared to radiofrequency ablation (RFA). The aim of this study was to investigate the efficacy of a strategy using a large cryoablation balloon to perform antral cryoablation with ‘touch-up’ ostial cryoablation for PVI in patients with paroxysmal and persistent AF. Methods Paroxysmal and persistent AF patients undergoing their first left atrial ablation were recruited. After cryoballoon therapy, each PV was assessed for isolation and if necessary, treated with focal ostial cryoablation until PVI was achieved. Follow-up with Holter monitoring was performed. Clinical outcomes of the cryoablation protocol were compared, with consecutive patients undergoing PVI by RFA. Results 124 consecutive patients underwent cryoablation. 77% of paroxysmal and 48% of persistent AF subjects were free from AF at 12 months after a single procedure. Over the same time period, 53 consecutive paroxysmal AF subjects underwent PVI with RFA and at 12 months, 72% were free from AF at 12 months (p=NS). There were too few persistent AF subjects (n=8) undergoing solely PVI by RFA as a comparison group. Procedural and fluoroscopic times during cryoablation were significantly shorter than RFA. Conclusions PV isolation can be achieved in less than 2 h by a simple cryoablation protocol with excellent results after a single intervention, particularly for paroxysmal AF.

Improvement in Coronary Blood Flow Velocity with Acute Biventricular Pacing is Predominantly Due to an Increase in a Diastolic Backward-Travelling Decompression (Suction) Wave

Background— Normal coronary blood flow is principally determined by a backward-traveling decompression (suction) wave in diastole. Dyssynchronous chronic heart failure may attenuate suction, because regional relaxation and contraction overlap in timing. We hypothesized that biventricular pacing, by restoring left ventricular (LV) synchronization and improving LV relaxation, might increase this suction wave, improving coronary flow. Method and Results— Ten patients with chronic heart failure (9 males; age 65±12; ejection fraction 26±7%) with left bundle-branch block (LBBB; QRS duration 174±18 ms) were atriobiventricularly paced at 100 bpm. LV pressure was measured and wave intensity calculated from invasive coronary flow velocity and pressure, with native conduction (LBBB) and during biventricular pacing at atrioventricular (AV) delays of 40 ms, 120 ms, and separately preidentified hemodynamically optimal AV delay. In comparison with LBBB, biventricular pacing at separately preidentified hemodynamically optimal AV delay (BiV-Opt) enhanced coronary flow velocity time integral by 15% (7%–25%) (P=0.007), LV dP/dtmax by 15% (10%–21%) (P=0.005), and negdP/dtmax by 17% (9%–22%) (P=0.005). The cumulative intensity of the diastolic backward decompression (suction) wave increased by 26% (18%–54%) (P=0.005). The majority of the increase in coronary flow velocity time integral occurred in diastole (69% [41%–84% ]; P=0.047). The systolic compression waves also increased: forward by 36% (6%–49%) (P=0.022) and backward by 38% (20%–55%) (P=0.022). Biventricular pacing at AV delays of 120 ms generated a smaller LV dP/dtmax (by 12% [5%–23% ], P=0.013) and negdP/dtmax (by 15% [8%–40% ]; P=0.009) increase than BiV-Opt, against LBBB as reference; BiV-Opt and biventricular pacing at AV delays of 120 ms were not significantly different in coronary flow velocity time integral or waves. Biventricular pacing at AV delays of 40 ms was no different from LBBB. Conclusions— When biventricular pacing improves LV contraction and relaxation, it increases coronary blood flow velocity, predominantly by increasing the dominant diastolic backward decompression (suction) wave.

Noninvasive electrocardiographic mapping to guide ablation of outflow tract ventricular arrhythmias

Background Localizing the origin of outflow tract ventricular tachycardias (OTVT) is hindered by lack of accuracy of electrocardiographic (ECG) algorithms and infrequent spontaneous premature ventricular complexes (PVCs) during electrophysiological studies. Objectives To prospectively assess the performance of noninvasive electrocardiographic mapping (ECM) in the pre-/periprocedural localization of OTVT origin to guide ablation and to compare the accuracy of ECM with that of published ECG algorithms. Methods Patients with symptomatic OTVT/PVCs undergoing clinically indicated ablation were recruited. The OTVT/PVC origin was mapped preprocedurally by using ECM, and 3 published ECG algorithms were applied to the 12-lead ECG by 3 blinded electrophysiologists. Ablation was guided by using ECM. The OTVT/PVC origin was defined as the site where ablation caused arrhythmia suppression. Acute success was defined as abolition of ectopy after ablation. Medium-term success was defined as the abolition of symptoms and reduction of PVC to less than 1000 per day documented on Holter monitoring within 6 months. Results In 24 patients (mean age 50 ± 18 years) recruited ECM successfully identified OTVT/PVC origin in 23/24 (96%) (right ventricular outflow tract, 18; left ventricular outflow tract, 6), sublocalizing correctly in 100% of this cohort. Acute ablation success was achieved in 100% of the cases with medium-term success in 22 of 24 patients. PVC burden reduced from 21,837 ± 23,241 to 1143 ± 4039 (P < .0001). ECG algorithms identified the correct chamber of origin in 50%–88% of the patients and sublocalized within the right ventricular outflow tract (septum vs free-wall) in 37%–58%. Conclusions ECM can accurately identify OTVT/PVC origin in the left and the right ventricle pre- and periprocedurally to guide catheter ablation with an accuracy superior to that of published ECG algorithms.

Characterization of the Left Atrial Neural Network and its Impact on Autonomic Modification Procedures

Background—Left atrial (LA) ganglionated plexi (GP) are part of the intrinsic cardiac autonomic nervous system and implicated in the pathogenesis of atrial fibrillation. High frequency stimulation is used to identify GP sites in humans. The effect of ablation on neural pathways connecting GPs in humans is unknown. Methods and Results—Thirty patients undergoing LA ablation with autonomic modification were recruited. In patients with persistent atrial fibrillation, endocardial continuous high frequency stimulation identified GP sites producing AV block. After right lower GP ablation (N=5), 2 of 15 sites remained positive, whereas after ablation of other GPs (N=5), leaving right lower GP intact, all 19 sites remained positive (right lower GP versus other GP, P<0.005), indicating that neural pathways between LAGPs and the AV node are via the right lower GP. In 20 patients with paroxysmal atrial fibrillation, synchronized high frequency stimulation identified sites initiating pulmonary vein (PV) ectopy. After PV isolation (N=8), no sites remained positive. After local GP ablation (N=9), 3 of 14 sites remained positive, suggesting neural connections to the PV were disrupted by both PV isolation and GP ablation. Heart rate variability indices reduced significantly after right upper GP ablation alone, suggesting that neural pathways from the LA to the SA node travel via the right upper GP. Conclusions—We have demonstrated neural pathways connecting LA GPs with the PVs, AV node, and SA node. The effects of high frequency stimulation at GP sites can be prevented by ablating the GP site or the neural pathway. This further delineates the mechanism via which PV isolation prevents atrial fibrillation and highlights important caveats for autonomic modification end points.

Visualizing Localized Reentry With Ultra–High Density Mapping in Iatrogenic Atrial Tachycardia: Beware Pseudo-Reentry

Background— The activation pattern of localized reentry (LR) in atrial tachycardia remains incompletely understood. We used the ultra–high density Rhythmia mapping system to study activation patterns in LR. Methods and Results— LR was suggested by small rotatory activations (carousels) containing the full spectrum of the color-coded map. Twenty-three left-sided atrial tachycardias were mapped in 15 patients (age: 64±11 years). 16 253±9192 points were displayed per map, collected over 26±14 minutes. A total of 50 carousels were identified (median 2; quartiles 1–3 per map), although this represented LR in only n=7 out of 50 (14%): here, rotation occurred around a small area of scar (<0.03 mV; 12±6 mm diameter). In LR, electrograms along the carousel encompassed the full tachycardia cycle length, and surrounding activation moved away from the carousel in all directions. Ablating fractionated electrograms (117±18 ms; 44±13% of tachycardia cycle length) within the carousel interrupted the tachycardia in every LR case. All remaining carousels were pseudo-reentrant (n=43/50 [86%]) occurring in areas of wavefront collision (n=21; median 0.5; quartiles 0–2 per map) or as artifact because of annotation of noise or interpolation in areas of incomplete mapping (n=22; median 1, quartiles 0–2 per map). Pseudo-reentrant carousels were incorrectly ablated in 5 cases having been misinterpreted as LR. Conclusions— The activation pattern of LR is of small stable rotational activations (carousels), and this drove 30% (7/23) of our postablation atrial tachycardias. However, this appearance is most often pseudo-reentrant and must be differentiated by interpretation of electrograms in the candidate circuit and activation in the wider surrounding region.

A narrow complex tachycardia with variable R-R intervals: What is the mechanism?

A 46-year-old man was referred for an invasive electrophysiological study with a view to ablation, for a history of classic sudden onset-offset palpitations. The patients son had recently survived an out-of-hospital cardiac arrest, and was found to have an accessory pathway (details unknown) at another institute, which was ablated. Our patients 12-lead electrocardiogram (ECG) showed sinus rhythm with no evidence of preexcitation. Echocardiography revealed a structurally normal heart. An electrophysiological study was performed with a quadripolar catheter positioned at the high right atrium (HRA), a steerable decapolar catheter in the coronary sinus, and quadripolar catheters along the His bundle and at the right ventricular apex. Baseline atrio-His (AH) and His-ventricular (HV) intervals measured 60 and 40 ms, respectively. Programmed atrial extrastimulus testing revealed decremental AH intervals, before tachycardia was reproducibly induced. Figure 1 shows the tachycardia on a 12-lead ECG. Based on the findings within the figures, what is the mechanism of the tachycardia?

004 Simultaneous invasive pressure and flow measurements during atrioventricular delay improvement reveal a compensatory peripheral vasodilator response which attenuates the initial blood pressure increment: implications for the design of optimisation protocols: Abstract 004 Figure 1

Introduction With synchrony of ventricular contraction already restored by cardiac resynchronisation therapy (CRT), optimisation of atrioventricular (AV) delay relies on improving filling. Although when AV delay is improved blood pressure immediately rises, there is a subsequent partial decline. Is this secondary decline because (1) non-invasive measurements are unreliable, (2) cardiac function increment is short-lived or (3) peripheral vasodilatation occurs? We conducted invasive experiments to distinguish between these hypotheses. Methods Nine patients with heart failure and CRT underwent changes in programmed AV delay from 40 ms to 120 ms. We simultaneously measured beat-by-beat invasive aortic pressure and flow, and non-invasive pressure (Finometer). Triplicate sets of experiments were performed and averaged to minimise the impact of noise. Results There was an immediate increment in invasive blood pressure of +14.7±2.0 mm Hg (p=0.0001), but after ∼10 beats there was a secondary progressive decline to a lower plateau of +8.0±1.8 mm Hg (p=0.004), Abstract 004 figure 1. The initial increment was caused by an immediate rise in flow by +9.1±2.4% (p=0.007) which did not drop later. The secondary decline in pressure was caused by a delayed gradual decline in total peripheral resistance. Finometer-derived non-invasive blood pressure tracked invasive pressure closely (r=0.97).Abstract 004 Figure 1 Conclusion When AV delay is made more favourable, only the instant pressure increment is caused by increase in stroke volume. The secondary pressure decline is caused by systemic vasodilatation. Design of AV optimisation protocols, which face severe challenge of signal vs noise, might benefit from recognition that not all beats are equally informative: the first few after a transition are most signal-rich.