Publications

AIMS: To test the hypothesis that the dispersive patch (DP) location does not significantly affect the current distribution around the catheter tip during radiofrequency catheter ablation (RFCA) but may affect lesions size through differences in impedance due to factors far from the catheter tip.

METHODS: An in silico model of RFCA in the posterior left atrium and anterior right ventricle was created using anatomic measurements from patient thoracic computed tomography scans and tested the effect of anterior vs. posterior DP locations on baseline impedance, myocardial power delivery, radiofrequency current path, and predicted lesion size.

RESULTS: For posterior left atrium ablation, the baseline impedance, total current delivered, current distribution, and proportion of power delivered to the myocardium were all similar with both anterior and posterior DP locations, resulting in similar RFCA lesion sizes (< 0.2 mm difference). For anterior right ventricular (RV) ablation, an anterior DP location resulted in slightly higher proportion of power delivered to the myocardium and lower baseline impedance leading to slightly larger RFCA lesions (0.6 mm deeper and 0.8 mm wider).

CONCLUSIONS: An anterior vs. posterior DP location will not meaningfully affect RFCA for posterior left atrial ablation, and the slightly larger lesions predicted with anterior DP location for anterior RV ablation are of unclear clinical significance.

To develop a suite of quality indicators (QIs) for the management of patients with ventricular arrhythmias (VA) and the prevention of sudden cardiac death (SCD). The Working Group comprised experts in heart rhythm management including Task Force members of the 2022 European Society of Cardiology (ESC) Clinical Practice Guidelines for the management of patients with VA and the prevention of SCD, members of the European Heart Rhythm Association, international experts, and a patient representative. We followed the ESC methodology for QI development, which involves (i) the identification of the key domains of care for the management of patients with VA and the prevention of SCD by constructing a conceptual framework of care, (ii) the development of candidate QIs by conducting a systematic review of the literature, (iii) the selection of the final set of QIs using a modified-Delphi method, and (iv) the evaluation of the feasibility of the developed QIs. We identified eight domains of care for the management of patients with VA and the prevention of SCD: (i) structural framework, (ii) screening and diagnosis, (iii) risk stratification, (iv) patient education and lifestyle modification, (v) pharmacological treatment, (vi) device therapy, (vii) catheter ablation, and (viii) outcomes, which included 17 main and 4 secondary QIs across these domains. Following a standardized methodology, we developed 21 QIs for the management of patients with VA and the prevention of SCD. The implementation of these QIs will improve the care and outcomes of patients with VA and contribute to the prevention of SCD.

Classically, catheter ablation for scar-related ventricular tachycardia (VT) relied upon activation and entrainment mapping of induced VT. Advances in post-MI therapies have led to VTs that are faster and haemodynamically less stable, because of more heterogeneous myocardial fibrosis patterns. The PAINESD score is one means of identifying patients at highest risk for haemodynamic decompensation during attempted VT induction, who may, therefore, benefit from alternative ablation strategies. One strategy is to use temporary mechanical circulatory support, although this warrants formal assessment of cost-effectiveness. A second strategy is to minimise or avoid VT induction altogether by employing a family of 'substrate'-based approaches aimed at identifying VT isthmuses during sinus or paced rhythm. Substrate mapping techniques are diverse, and focus on the timing, morphology and amplitude of local ventricular electrograms - sometimes aided by advanced non-invasive cardiac imaging modalities. In this review, the evolution of VT ablation over time is discussed, with an emphasis on procedural adaptations to the challenge of haemodynamic instability.

BACKGROUND: Functional substrate mapping during baseline rhythm can identify arrhythmogenic tissue during ventricular tachycardia (VT) ablation. Wall thinning and wall thickness channels (WTCs) derived from computed tomography angiography have been shown to correlate with low voltage and VT isthmuses. The correlation between functional substrate mapping, wall thinning, and WTCs in patients with infarct- or non-infarct-related cardiomyopathies (ICM and NICM, respectively) has not been previously described.

OBJECTIVES: To correlate cardiac CTA-derived myocardial wall thinning with functional VT substrate mapping using isochronal late activation mapping.

METHODS: In 34 patients with ICM or NICM undergoing VT ablation who had a preprocedure computed tomography angiography, myocardial wall thinning was segmented in layers of 1 to 5 mm. Areas of wall thinning and WTCs were then spatially correlated with deceleration zones (DZs) from registered left ventricular endocardial isochronal late activation maps.

RESULTS: In 21 ICM patients and 13 NICM patients, ICM patients had greater surfaces areas of wall thinning (P < 0.001). In ICM patients, 94.1% of primary DZs were located on areas of wall thinning, compared to 20% of DZs in NICM patients overall but 50% if there was any wall thinning present. Fifty-nine percent of DZs in ICM patients and 56% of DZs in NICM patients were located near WTCs. The positive predictive value for WTC in localizing DZs was 22.5% and 37.8% in ICM and NICM patients, respectively.

CONCLUSIONS: Wall thinning is highly sensitive for functional substrate in ICM patients. WTCs had modest sensitivity for functional substrate but low positive predictive value for identifying DZs in ICM and NICM patients. These findings suggest that wall thinning may facilitate more efficient mapping in ICM patients, but WTCs are insufficient to localize wavefront discontinuities.

Cardiac implantable electronic device implantation rates have increased in recent decades. Venous obstruction of the subclavian, brachiocephalic, or superior vena cava veins represents an important complication of implanted leads. These forms of venous obstruction can result in significant symptoms as well as present a barrier to the implantation of additional device leads. The risk factors for the development of these complications remain poorly understood, and diagnosis relies on clinical recognition and cross-sectional imaging. Anticoagulation remains the mainstay of treatment, and thrombus debulking, lead extraction, venoplasty, and stenting are all important therapeutic interventions. This review provides a multidisciplinary-based approach to the evaluation and management of cardiac implantable electronic device lead-associated venous obstruction.

Background: Baseline impedance, radiofrequency current, and impedance drop during radiofrequency catheter ablation are thought to predict effective lesion formation. However, quantifying the contributions of local versus remote impedances provides insights into the limitations of indices using those parameters. Methods: An in silico model of left atrial radiofrequency catheter ablation was used based on human thoracic measurements and solved for (1) initial impedance (Z), (2) percentage of radiofrequency power delivered to the myocardium and blood (3) total radiofrequency current, (4) impedance drop during heating, and (5) lesion size after a 25 W−30 s ablation. Remote impedance was modeled by varying the mixing ratio between skeletal muscle and fat. Local impedance was modeled by varying insertion depth of the electrode (ID). Results: Increasing the remote impedance led to increased baseline impedance, lower system current delivery, and reduced lesion size. For ID = 0.5 mm, Z ranged from 115 to 132 Ω when fat percentage varied from 20 to 80%, resulting in a decrease in the RF current from 472 to 347 mA and a slight decrease in lesion size from 5.6 to 5.1 mm in depth, and from 9.2 to 8.0 mm in maximum width. In contrast, increasing the local impedance led to lower system current but larger lesions. For a 50% fat−muscle mixture, Z ranged from 118 to 138 Ω when ID varied from 0.3 to 1.9 mm, resulting in a decrease in the RF current from 463 to 443 mA and an increase in lesion size, from 5.2 up to 7.5 mm in depth, and from 8.4 up to 11.6 mm in maximum width. In cases of nearly identical Z but different contributions of local and remote impedance, markedly different lesions sizes were observed despite only small differences in RF current. Impedance drop better predicted lesion size (R2 > 0.93) than RF current (R2 < 0.1). Conclusions: Identical baseline impedances and observed RF currents can lead to markedly different lesion sizes with different relative contributions of local and remote impedances to the electrical circuit. These results provide mechanistic insights into the advantage of measuring local impedance and identifies potential limitations of indices incorporating baseline impedance or current to predict lesion quality.

Percutaneous epicardial ventricular tachycardia ablation can decrease implanted cardioverter defibrillator shocks and hospitalizations; proper patient selection and procedural technique are imperative to maximize the benefit-risk ratio. The best candidates for epicardial ventricular tachycardia will depend on history of prior ablation, type of cardiomyopathy, and specific electrocardiogram and cardiac imaging findings. Complications include hemopericardium, hemoperitoneum, coronary vessel injury, and phrenic nerve injury. Modern epicardial mapping techniques provide new understandings of the 3-dimensional nature of reentrant ventricular tachycardia circuits across cardiomyopathy etiologies. Where epicardial access is not feasible, alternative techniques to reach epicardial ventricular tachycardia sources may be necessary.

BACKGROUND: Drugs belonging to diverse therapeutic classes can prolong myocardial refractoriness or slow conduction. These drugs may be effective and well-tolerated, but the risk of sudden cardiac death from torsades de pointes (TdP) remains a major concern. The corrected QT interval has significant limitations when used for risk stratification. Measurement of global electrical heterogeneity (GEH) could help identify the substrate vulnerable to drug-induced ventricular arrhythmias.

OBJECTIVE: The purpose of this study was to improve risk stratification for drug-induced TdP by measuring GEH on the electrocardiogram (ECG).

METHODS: We analyzed ECG data from a case-control study of patients with a history of drug-induced TdP as well as age- and sex-matched controls. Vectorcardiograms were constructed from ECGs. GEH was measured via the spatial ventricular gradient (SVG) vector (magnitude, azimuth, and elevation). Log odds coefficients for TdP were estimated using multivariable logistic regression.

RESULTS: Among 17 cases (47% male; age 58.9 ± 12.5 years) and 17 controls (29% male; age 61.0 ± 12.2 years), 34 ECGs were analyzed. SVG azimuth was significantly different between cases and controls (3.4 vs 22.0 degrees, respectively; P = 0.02). After adjusting for sex and QTc interval, odds of TdP increased by a factor of 3.2 for each 1 SD change in SVG azimuth from the control group mean (95% confidence interval 1.07-9.14; P = .04). QTc was not significant in the multivariable analysis (P = .20).

CONCLUSION: SVG azimuth is correlated with a history of drug-induced TdP independent of QTc. GEH measurement may help identify patients at high risk for drug-induced arrhythmias.

Cardiac sarcoidosis (CS) is a complex disease that can manifest as a diverse array of arrhythmias. CS patients may be at higher risk for sudden cardiac death (SCD), and, in some cases, SCD may be the first presenting symptom of the underlying disease. As such, identification, risk stratification, and management of CS-related arrhythmia are crucial in the care of these patients. Left untreated, CS carries significant arrhythmogenic morbidity and mortality. Cardiac manifestations of CS are a consequence of an inflammatory process resulting in the myocardial deposition of noncaseating granulomas. Endomyocardial biopsy remains the gold standard for diagnosis; however, biopsy yield is limited by the patchy distribution of the granulomas. As such, recent guidelines have improved clinical diagnostic pathways relying on advanced cardiac imaging to help in the diagnosis of CS. To date, corticosteroids are the best studied agent to treat CS but are associated with significant risks and limited benefits. Implantable cardioverter-defibrillators have an important role in SCD risk reduction. Catheter ablation in conjunction with antiarrhythmics seems to reduce ventricular arrhythmia burden. However, the appropriate selection of these patients is crucial as ablation is likely more helpful in the setting of a myocardial scar substrate versus arrhythmia driven by active inflammation. Further studies investigating CS pathophysiology, the pathway to diagnosis, arrhythmogenic manifestations, and SCD risk stratification will be crucial to reduce the high morbidity and mortality of this disease.