Radiofrequency ablation lesions in low-, intermediate-, and normal-voltage myocardium: an in vivo study in a porcine heart model.

AIMS: Contact force (CF) between radiofrequency (RF) ablation catheter and myocardium and ablation index (AI) correlates with RF lesion depth and width in normal-voltage (>1.5 mV) myocardium (NVM). We investigate the impact of CF on RF lesion depth and width in low (<0.5 mV) (LVM) and intermediate-voltage (0.5-1.5 mV) myocardium (IVM) following myocardial infarction. Correlation between RF lesion depth and width evaluated by native contrast magnetic resonance imaging (ncMRI) and gross anatomical evaluation was investigated. METHODS AND RESULTS: Twelve weeks after myocardial infarction, 10 pigs underwent electroanatomical mapping and endocardial RF ablations were deployed in NVM, IVM, and LVM myocardium. In vivo ncMRI was performed before the heart was excised and subjected to gross anatomical evaluation. Ninety (82%) RF lesions were evaluated. Radiofrequency lesion depth and width were smaller in IVM and LVM compared with NVM (P < 0.001). Radiofrequency lesion depth and width correlated with CF, AI, and impedance drop in NVM (CF and AI P < 0.001) and IVM (CF and AI depths P < 0.001; CF and AI widths P < 0.05). Native contrast magnetic resonance imaging evaluated RF lesion depth and width correlated with gross anatomical depth and width (NVM and IVM P < 0.001; LVM P < 0.05). CONCLUSIONS: Radiofrequency lesions deployed by similar duration, power and CF are smaller in IVM and LVM than in NVM. Radiofrequency lesion depth and width correlated with CF, AI, and impedance drop in NVM and IVM but not in LVM. Native contrast magnetic resonance imaging may be useful to assess RF lesion depth and width in NVM, IVM, and LVM.

Voltage and pace-capture mapping of linear ablation lesions overestimates chronic ablation gap size.

Aims: Conducting gaps in lesion sets are a major reason for failure of ablation procedures. Voltage mapping and pace-capture have been proposed for intra-procedural identification of gaps. We aimed to compare gap size measured acutely and chronically post-ablation to macroscopic gap size in a porcine model. Methods and results: Intercaval linear ablation was performed in eight Göttingen minipigs with a deliberate gap of ∼5 mm left in the ablation line. Gap size was measured by interpolating ablation contact force values between ablation tags and thresholding at a low force cut-off of 5 g. Bipolar voltage mapping and pace-capture mapping along the length of the line were performed immediately, and at 2 months, post-ablation. Animals were euthanized and gap sizes were measured macroscopically. Voltage thresholds to define scar were determined by receiver operating characteristic analysis as <0.56 mV (acutely) and <0.62 mV (chronically). Taking the macroscopic gap size as gold standard, error in gap measurements were determined for voltage, pace-capture, and ablation contact force maps. All modalities overestimated chronic gap size, by 1.4 ± 2.0 mm (ablation contact force map), 5.1 ± 3.4 mm (pace-capture), and 9.5 ± 3.8 mm (voltage mapping). Error on ablation contact force map gap measurements were significantly less than for voltage mapping (P = 0.003, Tukey's multiple comparisons test). Chronically, voltage mapping and pace-capture mapping overestimated macroscopic gap size by 11.9 ± 3.7 and 9.8 ± 3.5 mm, respectively. Conclusion: Bipolar voltage and pace-capture mapping overestimate the size of chronic gap formation in linear ablation lesions. The most accurate estimation of chronic gap size was achieved by analysis of catheter-myocardium contact force during ablation.

Identifying drug-induced repolarization abnormalities from distinct ECG patterns in congenital long QT syndrome: a study of sotalol effects on T-wave morphology.

BACKGROUND: The electrocardiographic QT interval is used to identify drugs with potential harmful effects on cardiac repolarization in drug trials, but the variability of the measurement can mask drug-induced ECG changes. The use of complementary electrocardiographic indices of abnormal repolarization is therefore warranted. Most drugs associated with risk are inhibitors of the rapidly activating delayed rectifier potassium current (I(Kr)). This current is also inhibited in the congenital type 2 form of the long QT syndrome (LQT2). It is therefore possible that electrocardiographic LQT2 patterns might be used to identify abnormal repolarization patterns induced by drugs. OBJECTIVE: To develop distinct T-wave morphology parameters typical of LQT2 and investigate their use as a composite measure for identification of d,l-sotalol (sotalol)-induced changes in T-wave morphology. METHODS: Three independent study groups were included: a group of 917 healthy subjects and a group of 30 LQT2 carriers were used for the development of T-wave morphology measures. The computerized measure for T-wave morphology (morphology combination score, MCS) was based on asymmetry, flatness and notching, which are typical ECG patterns in LQT2. Blinded to labels, the new morphology measures were tested in a third group of 39 healthy subjects receiving sotalol. Over 3 days the sotalol group received 0, 160 and 320 mg doses, respectively, and a 12-lead Holter ECG was recorded for 22.5 hours each day. Drug-induced prolongation of the heart rate corrected QT interval (QTcF) was compared with changes in the computerized measure for T-wave morphology. Effect sizes for QTcF and MCS were calculated at the time of maximum plasma concentrations and for maximum change from baseline. Accuracy for separating baseline from sotalol recordings was evaluated by area under the receiver operating characteristic curves (AUCs) using all recordings from the time immediately post-dose to maximum change. RESULTS: MCS separated baseline recordings from sotalol treatment with higher accuracy than QTcF for the 160 mg dose: (AUC) 84% versus 72% and for the 320 mg dose: (AUC) 94% versus 87%, p < 0.001. At maximum serum-plasma concentrations and at maximum individual change from baseline, the effect sizes for QTcF were less than half the effect sizes for MCS, p < 0.001. Effect sizes at peak changes of the mean were up to 3-fold higher for MCS compared with QTcF, p < 0.001. In subjects receiving sotalol, T-wave morphology reached similarity to LQT2, whereas QTcF did not. CONCLUSION: Distinct ECG patterns in LQT2 carriers effectively quantified repolarization changes induced by sotalol. Further studies are needed to validate whether this measure has general validity for the identification of drug-induced disturbed repolarization.

The superior transseptal surgical approach to mitral valve creates slow conduction.

BACKGROUND: Atrial tachycardia is very frequent after mitral valve surgery using the superior transseptal approach. METHODS: Sixteen patients operated on for mitral valve disease (superior transseptal approach = Group A, n = 9, and left atrial approach = Group B, n = 7) underwent radiofrequency catheter ablation of atrial tachycardia guided by electroanatomic mapping. Twenty-six consecutive patients without previous cardiac surgery with typical atrial flutter served as controls (Group C). RESULTS: Atrial tachycardia occurred earlier after the operation in Group A than in Group B (median 97 vs 2,159 days, P = 0.003). Typical atrial flutter was the most frequent circuit in all groups (Group A-7 patients, Group B-5 patients, Group C-26 patients). Three patients in Group A developed right atrial incisional tachycardia. Ten of 14 tachycardia circuits (typical atrial flutter, n = 7, incisional tachycardia, n = 3) in Group A depended on the corridor between the right atrial part of the atriotomy and the tricuspid annulus. Slow conduction during typical atrial flutter was detected in this corridor in Group A, but not in the corresponding region in Groups B and C (P < 0.001). The cycle length of typical atrial flutter was longer in Groups A and B than in Group C (mean 283 ms and 282 ms vs 233 ms, P = 0.003). Patients in Group B with typical atrial flutter had larger right atria than patients in Group A or Group C (mean 156 mL vs 96 mL and 113 mL, P = 0.033). CONCLUSIONS: The superior transseptal incision may predispose to atrial tachycardia by creating slow conduction between the atriotomy and the tricuspid annulus.

Ablation of atrial tachycardia after surgery for congenital and acquired heart disease using an electroanatomic mapping system: Which circuits to expect in which substrate?

OBJECTIVES: The purpose of this study was to compare atrial tachycardia circuits after a range of cardiac operations. BACKGROUND: Knowledge of circuits occurring in a given postsurgical substrate should help to ablate these challenging tachycardias and develop potential preventive strategies. METHODS: We analyzed tachycardia circuits in 83 consecutive patients (60 males; median age 47 years, range 9-73) after atrial incisions undergoing ablation of atrial tachycardias. A combined strategy of electroanatomic (CARTO) and entrainment mapping was used. Fifty-two patients (63%) underwent operation for congenital and 31 (37%) for acquired heart disease. Patients were divided into subgroups based on the intervention performed in the atria: right lateral atriotomy (39 patients), left atrial (11) and superior transseptal (10) approach to the mitral valve, biatrial heart transplantation (8), Mustard (8) and Fontan (4) procedure, and other interventions (3). RESULTS: Most of the 119 tachycardias mapped were isthmus-dependent atrial flutter (66) and incisional tachycardia (30). Isthmus-dependent atrial flutter was the most frequent arrhythmia in all subgroups except for Fontan patients, in whom incisional tachycardia was most frequent. The distribution of tachycardia circuits did not differ significantly among groups. CONCLUSIONS: The observed circuits did not differ among the postsurgical substrates. Isthmus-dependent atrial flutter should be the first circuit considered in patients after atrial incisions.