Cardiac contractility modulation in patients with heart failure - A review of the literature.

Experimental in vivo and in vitro studies showed that electric currents applied during the absolute refractory period can modulate cardiac contractility. In preclinical studies, cardiac contractility modulation (CCM) was found to improve calcium handling, reverse the foetal myocyte gene programming associated with heart failure (HF), and facilitate reverse remodeling. Randomized control trials and observational studies have provided evidence about the safety and efficacy of CCM in patients with HF. Clinically, CCM therapy is indicated to improve the 6-min hall walk, quality of life, and functional status of HF patients who remain symptomatic despite guideline-directed medical treatment without an indication for cardiac resynchronization therapy (CRT) and have a left ventricular ejection fraction (LVEF) ranging from 25 to 45%. Although there are promising results about the role of CCM in HF patients with preserved LVEF (HFpEF), further studies are needed to elucidate the role of CCM therapy in this population. Late gadolinium enhancement (LGE) assessment before CCM implantation has been proposed for guiding the lead placement. Furthermore, the optimal duration of CCM application needs further investigation. This review aims to present the existing evidence regarding the role of CCM therapy in HF patients and identify gaps and challenges that require further studies.

Radiofrequency versus cryoballoon catheter ablation in patients with persistent atrial fibrillation: A randomized trial.

INTRODUCTION: Patients with persistent atrial fibrillation (AF) represent a challenging population for rhythm control therapies. Catheter ablation (CA) with pulmonary vein isolation (PVI) is an effective treatment option for the reduction of the arrhythmic burden. Data regarding the comparability between radiofrequency (RF) and cryoballoon ablation (CRYO) in persistent AF are limited. METHODS: This is a prospective, randomized, single-center study designed to compare the efficacy in terms of rhythm control between RF and CRYO in persistent AF. Eligible participants were randomized 2:1 in two arms: RF and CRYO. The primary endpoint of the study was arrhythmia relapse in the early postprocedural period (first 3 months) and in the middle term follow-up (3 months to 12 months). Secondary endpoints included procedure duration, fluoroscopy time, and complications. RESULTS: A total of 199 patients participated in the study (133 patients in the RF arm, 66 in the CRYO arm). No statistically significant difference occurred between the two groups regarding the primary endpoint (recurrences ≤3 months: 35.5% RF vs. 37.9% CRYO, p .755, recurrences >3 months: 26.3% RF vs. 27.3% CRYO, p .999). From the secondary endpoints, CRYO was a procedure of significantly shorter duration (75.15 ± 17.21 in CRYO vs. 136.6 ± 43.33 in RF group, p < .05). CONCLUSION: CRYO and RF ablation appear to be equally effective for rhythm control in patients with persistent AF. CRYO ablation is advantageous in terms of procedure duration.

Association between sodium-glucose cotransporter-2 inhibitors and incident atrial fibrillation/atrial flutter in heart failure patients with reduced ejection fraction: a meta-analysis of randomized controlled trials.

Atrial fibrillation (AF) and atrial flutter (AFL) are associated with adverse outcomes in patients with heart failure and reduced ejection fraction (HFrEF). We investigated the effects of sodium-glucose cotransporter-2 inhibitors (SGLT2i) on the incidence of AF and/or AFL in HFrEF patients. PubMed and ClinicalTrials.gov were systematically searched until March 2022 for randomized controlled trials (RCTs) that enrolled patients with HFrEF. A total of six RCTs with 9467 patients were included (N = 4731 in the SGLT2i arms; N = 4736 in the placebo arms). Compared to placebo, SGLT2i treatment was associated with a significant reduction in the risk of AF [relative risk (RR) 0.62, 95% confidence interval CI 0.44-0.86; P = 0.005] and AF/AFL (RR 0.64, 95% CI 0.47-0.87; P = 0.004). Subgroup analysis showed that empagliflozin use resulted in a significant reduction in the risk of AF (RR 0.55, 95% CI 0.34-0.89; P = 0.01) and AF/AFL (RR 0.50, 95% CI 0.32-0.77; P = 0.002). By contrast, dapagliflozin use was not associated with a significant reduction in the risk of AF (RR 0.69, 95% CI 0.43-1.11; P = 0.12) or AF/AFL (RR 0.82, 95% CI 0.53-1.27; P = 0.38). Additionally, a "shorter" duration (< 1.5 years) of treatment with SGLT2i remained associated with a reduction in the risk of AF (< 1.5 years; RR 0.58, 95% CI 0.36-0.91; P = 0.02) and AF/AFL (< 1.5 years; RR 0.52, 95% CI 0.34-0.80; P = 0.003). In conclusion, SGLT2i therapy was associated with a significant reduction in the risk of AF and AF/AFL in patients with HFrEF. These results reinforce the value of using SGLT2i in this setting.

Electrocardiographic changes after balloon pulmonary angioplasty in chronic thromboembolic pulmonary hypertension: Data from the Hellenic Registry.

BACKGROUND: Balloon pulmonary angioplasty (BPA) has provided an effective invasive treatment for inoperable patients with chronic thromboembolic pulmonary hypertension (CTEPH). The hemodynamic improvement achieved by BPA has significantly increased the long-term prognosis of these patients, mostly by reversing the negative remodeling of the right ventricle (RV). MATERIALS AND METHODS: In a cohort of 17 patients with symptomatic CTEPH hemodynamic data were collected before and after the completion of BPA sessions. After the confirmation of statistically significant hemodynamic improvement, we examined the changes in certain prespecified electrocardiographic (ECG) parameters (PR interval duration, QRS duration, QTc interval duration, R wave and S wave amplitude in lead I, R wave and S wave amplitude in precordial leads V1, V5 and V6) before the initiation and one month after the completion of BPA sessions. In addition, ECGs were qualitatively assessed before and after treatment for the presence of ECG abnormalities related to PH, proposed by the guidelines of the European Society of Cardiology (ESC). The term ESC criteria 1-6 was used for their description. RESULTS: Statistically significant correlation (p < 0.05) was found between the reduction in mean pulmonary artery pressure (mPAP) and the decrease of the depth of the S wave in leads I (p 0.0069), V5 (p 0.0003), V6 (p 0.0011) and in the R wave amplitude in leads V5 (p 0.0122) and V6 (p 0.0185). From the ESC criteria, RV strain pattern was the commonest in the initial cohort, with significant improvement after therapies. CONCLUSION: Hemodynamic improvement after BPA therapies is correlated with improved ECG amplitude parameters in leads I, V5 and V6. RV strain pattern is common among untreated patients with significant improvement after therapies.

Atrial cardiomyopathy: Diagnosis, clinical implications and unresolved issues in anticoagulation therapy.

Atrial cardiomyopathy (AC) is an evolving pathophysiological entity that has expanded our understanding regarding the atrium and its role in arrhythmogenesis and cardiac thromboembolism. The pathological myocardium in AC promotes arrhythmogenesis through mechanical dysfunction (hypocontractility, fibrosis), adverse alterations of the endothelium and secretion of prothrombotic factors (IL-6, IL-8, TNF-a). 'Red flags', indicative of AC, can be recognized either non-invasively by electrocardiography, echocardiography and cardiac magnetic resonance imaging or invasively by high-density electroanatomical mapping as low bipolar voltage areas of the affected myocardium. Signs of AC have been strongly associated with an increased risk of ischemic stroke, even embolic strokes of undetermined source, regardless of the coexistence of atrial fibrillation (AF). The underlying existence of AC has been negatively correlated with the success rate of catheter ablation of AF. The clinical value of AC is the provision of a novel pathway regarding the potential mechanisms of cerebrovascular events of cardiac thromboembolic origin. In addition, AC may serve as a risk stratification tool to predict the long-term responders of AF catheter ablation.

Diagnostic and therapeutic dilemmas in a patient with myocarditis, Brugada syndrome and arrhythmic syncope.

We present a case of a previously healthy 23-year-old male who presented with chest pain, palpitations and spontaneous type 1 Brugada electrocardiographic (ECG) pattern. Positive family history for sudden cardiac death (SCD) was remarkable. Initially, clinical symptoms in combination with myocardial enzymes elevation, regional myocardial oedema with late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) and inflammatory lymphocytoid-cell infiltrates in the endomyocardial biopsy (EMB) suggested the diagnosis of a myocarditis-induced Brugada phenocopy (BrP). Under immunosuppressive therapy with methylprednisolone and azathioprine, a complete remission of both symptoms and biomarkers was accomplished. However, the Brugada pattern did not resolve. The eventually spontaneous Brugada pattern type 1 established the diagnosis of Brugada syndrome (BrS). Due to his previous history of syncope, the patient was offered an ICD that he declined. After his discharge he experienced a new episode of arrhythmic syncope. He was readmitted and received an ICD.

Predictors of fatal arrhythmic events in patients with non-compaction cardiomyopathy: a systematic review.

Left ventricular non-compaction cardiomyopathy (LVNC) is a congenital heart disease with autosomal dominant inheritance. This review aims to summarize the existing data about the predictors of fatal arrhythmias in patients with LVNC. Medline and Cochrane library databases were searched from inception to November 2021 for articles on LVNC. The reference lists of the relevant research studies as well as the relevant review studies and meta-analyses were also searched. Clinical symptoms and electrocardiogram findings such as left bundle branch block are significantly associated with ventricular arrhythmias. Other non-invasive tools such as Holter monitoring, echocardiography, and cardiac magnetic resonance (CMR) can provide additional value for risk stratification. CMR-derived left and right ventricular ejection fraction, left ventricular end-diastolic diameter, late gadolinium enhancement, and non-compacted to compacted myocardium ratio are predictive of ventricular arrhythmias. An electrophysiological study can provide additional prognostic data in patients with LVNC who are at moderate risk of ventricular arrhythmias. Risk stratification of LVNC patients with no prior history of a fatal arrhythmic event remains challenging. Symptoms assessment, electrocardiogram, Holter monitoring, and cardiac imaging should be performed on every patient, while an electrophysiological study should be performed for moderate-risk patients. Large cohort studies are needed for the construction of score models for arrhythmic risk stratification purposes.

The role of cardiac magnetic resonance in identifying appropriate candidates for cardiac resynchronization therapy - a systematic review of the literature.

Despite the strict indications for cardiac resynchronization therapy (CRT) implantation, a significant proportion of patients will fail to adequately respond to the treatment. This systematic review aims to present the existing evidence about the role of cardiac magnetic resonance (CMR) in identifying patients who are likely to respond better to the CRT. A systematic search in the MedLine database and Cochrane Library from their inception to August 2021 was performed, without any limitations, by two independent investigators. We considered eligible observational studies or randomized clinical trials (RCTs) that enrolled patients > 18 years old with heart failure (HF) of ischaemic or non-ischaemic aetiology and provided data about the association of baseline CMR variables with clinical or echocardiographic response to CRT for at least 3 months. This systematic review was performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA Statement). Following our search strategy, 47 studies were finally included in our review. CMR appears to have an additive role in identifying the subgroup of patients who will respond better to CRT. Specifically, the presence and the extent of myocardial scar were associated with increased non-response rates, while those with no scar respond better. Furthermore, existing data show that scar location can be associated with CRT response rates. CMR-derived markers of mechanical desynchrony can also be used as predictors of CRT response. CMR data can be used to optimize the position of the left ventricular lead during the CRT implantation procedure. Specifically, positioning the left ventricular lead in a branch of the coronary sinus that feeds an area with transmural scar was associated with poorer response to CRT. CMR can be used as a non-invasive optimization tool to identify patients who are more likely to achieve better clinical and echocardiographic response following CRT implantation.

Mitral Valve Prolapse and Mitral Annular Disjunction Arrhythmic Syndromes: Diagnosis, Risk Stratification and Management.

Although mitral valve prolapse (MVP) is usually considered a benign clinical condition, it has been linked with ventricular arrhythmias and sudden cardiac death in patients with a certain "arrhythmic" phenotype, raising awareness and mandating a specific risk stratification protocol. Mitral annular disjunction (MAD) is considered a "red flag" in malignant MVP syndrome along with bileaflet myxomatous prolapse, female gender, negative or biphasic T waves in the inferior leads, fibrosis in the papillary muscles or inferobasal wall detected by cardiac magnetic resonance imaging and complex arrhythmias of right bundle branch morphology. MAD seems to play a critical role in the chain of morphofunctional abnormalities which lead to increased mechanical stretch and subsequent fibrosis mainly in the papillary muscles, forming the vulnerable anatomic substrate prone to arrhythmogenesis, and associated with long-term severe ventricular arrhythmias. Arrhythmogenesis in MVP/MAD patients is not fully understood but a combination between a substrate and a trigger has been established with premature ventricular contraction triggered ventricular fibrillation being the main mechanism of sudden cardiac death (SCD). Certain characteristics mostly recognized by non-invasive imaging modalities serve as risk factors and can be used to diagnose and identify high risk patients with MAD, while treatment options include catheter ablation, device therapy and surgical intervention. This review focuses on the clinical presentation, the arrhythmogenic substrate, and the incidence of ventricular arrhythmias and SCD in MAD population. The current risk stratification tools in MAD arrhythmogenic entity are discussed.

Right ventricular outflow tract endocardial unipolar substrate mapping: implications in risk stratification of Brugada syndrome.

Brugada syndrome (BrS) is a complex arrhythmogenic disease displaying electrical and micro-structural abnormalities mainly located at the epicardium of the right ventricular outflow tract (RVOT). It is well-known that fibrosis, fatty infiltration, inflammation and reduced gap junction expression have been demonstrated at the epicardial anterior aspect of the RVOT providing the arrhythmogenic substrate for ventricular arrhythmic events in BrS. A number of models have been proposed for the risk stratification of patients with BrS. Endocardial unipolar electroanatomical mapping is an emerging tool that has been reintroduced to identify and quantify epicardial electrical abnormalities. Interestingly, current findings correlate the presence of large-sized endocardial unipolar electroanatomical abnormalities with either ventricular fibrillation inducibility during programmed ventricular stimulation or symptom status. This review aims to present existing data about the role of endocardial unipolar electroanatomical mapping for the identification of RVOT epicardial abnormalities as well as its potential clinical implications in risk stratification of BrS.

Modern mapping and ablation of idiopathic outflow tract ventricular arrhythmias.

Outflow tract (OT) premature ventricular complexes (PVCs) are being recognized as a common and often troubling, clinical electrocardiographic finding. The OT areas consist of the Right Ventricular Outflow Tract (RVOT), the Left Ventricular Outflow Tract (LVOT), the Aortomitral Continuity (AMC), the aortic cusps and the Left Ventricular (LV) summit. By definition, all OT PVCs will exhibit an inferior QRS axis, defined as positive net forces in leads II, III and aVF. Activation mapping using the contemporary 3D mapping systems followed by pace mapping is the cornerstone strategy of every ablation procedure in these patients. In this mini review we discuss in brief all the modern mapping and ablation modalities for successful elimination of OT PVCs, along with the potential advantages and disadvantages of each ablation technique.

Association between sodium-glucose cotransporter-2 inhibitors and risk of sudden cardiac death or ventricular arrhythmias: a meta-analysis of randomized controlled trials.

AIMS: Sudden cardiac death (SCD) and ventricular arrhythmias (VAs) are important causes of mortality in patients with type 2 diabetes mellitus (T2DM), heart failure (HF), or chronic kidney disease (CKD). We evaluated the effect of sodium-glucose cotransporter-2 (SGLT2) inhibitors on SCD and VAs in these patients. METHODS AND RESULTS: We performed a systematic review and meta-analysis of randomized controlled trials (RCTs) that enrolled patients with T2DM and/or HF and/or CKD comparing SGLT2i and placebo or active control. PubMed and ClinicalTrials.gov were systematically searched until November 2020. A total of 19 RCTs with 55 ,590 participants were included. Sudden cardiac death events were reported in 9 RCTs (48 patients receiving SGLT2i and 57 placebo subjects). There was no significant association between SGLT2i therapy and SCD [risk ratio (RR) 0.74, 95% confidence interval (CI) 0.50-1.08; P = 0.12]. Ventricular arrhythmias were reported in 17 RCTs (126 patients receiving SGLT2i and 134 controls). SGLT2i therapy was not associated with a lower risk of VAs (RR 0.84, 95% CI 0.66-1.06; P = 0.14). Besides the subgroup of low-dosage SGLT2i therapy that demonstrated decreased VAs compared to control (RR 0.45, 95% CI 0.25-0.82; P = 0.009), or to placebo (RR 0.46, 95% CI 0.25-0.85; P = 0.01), further subgroup analysis did not demonstrate any significant differences. CONCLUSION: SGLT2i therapy was not associated with an overall lower risk of SCD or VAs in patients with T2DM and/or HF and/or CKD. However, further research is needed since the number of SCD and VA events were relatively few leading to wide confidence intervals, and the point estimates suggested potential benefits.

The prevalence of left and right bundle branch block morphology ventricular tachycardia amongst patients with arrhythmogenic cardiomyopathy and sustained ventricular tachycardia: insights from the European Survey on Arrhythmogenic Cardiomyopathy.

AIMS: In arrhythmogenic cardiomyopathy (ACM), sustained ventricular tachycardia (VT) typically displays a left bundle branch block (LBBB) morphology while a right bundle branch block (RBBB) morphology is rare. The present study assesses the VT morphology in ACM patients with sustained VT and their clinical and genetic characteristics. METHODS AND RESULTS: Twenty-six centres from 11 European countries provided information on 954 ACM patients who had ≥1 episode of sustained VT spontaneously documented during patients' clinical course. Arrhythmogenic cardiomyopathy was defined according to the 2010 Task Force Criteria, and VT morphology according to the QRS pattern in V1. Overall, 882 (92.5%) patients displayed LBBB-VT alone and 72 (7.5%) RBBB-VT [alone in 42 (4.4%) or in combination with LBBB-VT in 30 (3.1%)]. Male sex prevalence was 79.3%, 88.1%, and 56.7% in the LBBB-VT, RBBB-VT, and LBBB + RBBB-VT groups, respectively (P = 0.007). First RBBB-VT occurred 5 years after the first LBBB-VT (46.5 ± 14.4 vs 41.1 ± 15.8 years, P = 0.011). An implanted cardioverter-defibrillator was more frequently implanted in the RBBB-VT (92.9%) and the LBBB + RBBB-VT groups (90%) than in the LBBB-VT group (68.1%) (P < 0.001). Mutations in PKP2 predominated in the LBBB-VT (65.2%) and the LBBB + RBBB-VT (41.7%) groups while DSP mutations predominated in the RBBB-VT group (45.5%). By multivariable analysis, female sex was associated with LBBB + RBBB-VT (P = 0.011) while DSP mutations were associated with RBBB-VT (P < 0.001). After a median follow-up of 103 (51-185) months, death occurred in 106 (11.1%) patients with no intergroup difference (P = 0.176). CONCLUSION: RBBB-VT accounts for a significant proportion of sustained VTs in ACM. Sex and type of pathogenic mutations were associated with VT type, female sex with LBBB + RBBB-VT, and DSP mutation with RBBB-VT.

Predictive risk models for forecasting arrhythmic outcomes in Brugada syndrome: A focused review.

Brugada syndrome (BrS) is a rare disorder characterized by coved or saddle-shaped ST-segment elevation in the right precordial leads on the electrocardiogram. Risk stratification in BrS remains challenging. A number of clinical, electrocardiographic, programmed ventricular stimulation and genetic risk factors have been identified as important predictors of future major arrhythmic events. There is a positive association between the number of risk factors and arrhythmic events. Hence, a multi-parametric approach would provide comprehensive risk assessment and more accurate risk stratification, assisting in therapeutic decisions making, including implantable cardioverter-defibrillator placement or identification of low-risk individuals. However, the extent to which each variable influences the risk and non-linear interactions between the different risk variables make risk stratification challenging. This paper aims to provide a focused review of the multi-parametric risk models for BrS risk stratification published in the literature.

Right ventricular outflow tract electroanatomical abnormalities in asymptomatic and high-risk symptomatic patients with Brugada syndrome: Evidence for a new risk stratification tool?

INTRODUCTION: Microstructural abnormalities at the epicardium of the right ventricular outflow tract (RVOT) may provide the arrhythmia substrate in Brugada syndrome (BrS). Endocardial unipolar electroanatomical mapping allows the identification of epicardial abnormalities. We evaluated the clinical implications of an abnormal endocardial substrate as perceived by high-density electroanatomical mapping (HDEAM) in patients with BrS. METHODS: Fourteen high-risk BrS patients with aborted sudden cardiac death (SCD) (12 males, mean age: 41.9 ± 11.8 years) underwent combined endocardial-epicardial HDEAM of the right ventricle/RVOT, while 40 asymptomatic patients (33 males, mean age: 42 ± 10.7 years) underwent endocardial HDEAM. Based on combined endocardial-epicardial procedures, endocardial HDEAM was considered abnormal in the presence of low voltage areas (LVAs) more than 1 cm2 with bipolar signals less than 1 mV and unipolar signals less than 5.3 mV. Programmed ventricular stimulation (PVS) was performed in all patients. RESULTS: The endocardial unipolar LVAs were colocalized with epicardial bipolar LVAs (p = .0027). Patients with aborted SCD exhibited significantly wider endocardial unipolar (p < .01) and bipolar LVAs (p < .01) compared with asymptomatic individuals. A substrate size of unipolar LVAs more than 14.5 cm2 (area under the curve [AUC]: 0.92, p < .001] and bipolar LVAs more than 3.68 cm2 (AUC: 0.82, p = .001) distinguished symptomatic from asymptomatic patients. Patients with ventricular fibrillation inducibility (23/54) demonstrated broader endocardial unipolar (p < .001) and bipolar LVAs (p < .001) than noninducible patients. The presence of unipolar LVAs more than 13.5 cm2 (AUC: 0.95, p < .001) and bipolar LVAs more than 2.97 cm2 (AUC: 0.78, p < .001) predicted a positive PVS. CONCLUSION: Extensive endocardial electroanatomical abnormalities identify high-risk patients with BrS. Endocardial HDEAM may allow risk stratification of asymptomatic patients referred for PVS.

Safety of smartwatches and their chargers in patients with cardiac implantable electronic devices.

AIMS: Cardiac implantable electronic devices (CIEDs) are susceptible to electromagnetic interference (EMI). Smartwatches and their chargers could be a possible source of EMI. We sought to assess whether the latest generation smartwatches and their chargers interfere with proper CIED function. METHODS AND RESULTS: We included consecutive CIED recipients in two centres. We tested two latest generation smartwatches (Apple Watch and Samsung Galaxy Watch) and their charging cables for potential EMI. The testing was performed under continuous electrocardiogram recording and real-time device telemetry, with nominal and 'worst-case' settings. In vitro magnetic field measurements were performed to assess the emissions from the tested devices, initially in contact with the probe and then at a distance of 10 cm and 20 cm. In total, 171 patients with CIEDs (71.3% pacemakers-28.7% implantable cardioverter-defibrillators) from five manufacturers were enrolled (63.2% males, 74.8 ± 11.4 years), resulting in 684 EMI tests. No EMI was identified in any patient either under nominal or 'worst-case scenario' programming. The peak magnetic flux density emitted by the smartwatches was similar to the background noise level (0.81 µT) even when in contact with the measuring probe. The respective values for the chargers were 4.696 µΤ and 4.299 µΤ for the Samsung and Apple chargers, respectively, which fell at the background noise level when placed at 20 cm and 10 cm, respectively. CONCLUSION: Two latest generation smartwatches and their chargers resulted in no EMI in CIED recipients. The absence of EMI in conjunction with the extremely low intensity of magnetic fields emitted by these devices support the safety of their use by CIED patients.

Use of high-density activation and voltage mapping in combination with entrainment to delineate gap-related atrial tachycardias post atrial fibrillation ablation.

AIMS: An incomplete understanding of the mechanism of atrial tachycardia (AT) is a major determinant of ablation failure. We systematically evaluated the mechanisms of AT using ultra-high-resolution mapping in a large cohort of patients. METHODS AND RESULTS: We included 107 consecutive patients (mean age: 65.7 ± 9.2 years, males: 81 patients) with documented endocardial gap-related AT after left atrial ablation for persistent atrial fibrillation (AF). We analysed the mechanism of 134 AT (94 macro-re-entries and 40 localized re-entries) using high-resolution activation mapping in combination with high-density voltage and entrainment mapping. Voltage in the conducting channels may be extremely low, even <0.1 mV (0.14 ± 0.095 mV, 51 of 134 AT, 41%), and almost always <0.5 mV (0.03-0.5 mV, 133 of 134 AT, 99.3%). The use of multipolar Orion, HDGrid, and Pentaray catheters improved our accuracy in delineating ultra-low-voltage areas critical for maintenance of the circuit of endocardial gap-related AT. Conventional ablation catheters often do not detect any signal (noise level) even using adequate contact force, and only multipolar catheters of small electrodes and shorter interelectrode space can detect clear fractionated low-amplitude and high frequency signals, critical for re-entry maintenance. We performed a diagnosis in 112 out of 134 AT (83.6%) using only activation mapping and in 134 out of 134 AT (100%) using the combination of activation and entrainment mapping. CONCLUSION: High-resolution activation mapping in combination with high-density voltage and entrainment mapping is the ideal strategy to delineate the critical part of the circuit in endocardial gap-related re-entrant AT after AF ablation.

Electrocardiographic and electrophysiological characteristics of idiopathic ventricular arrhythmias with acute successful ablation at the superior portion of the mitral annulus.

BACKGROUND: We sought to identify the electrocardiographic and electrophysiological characteristics of ventricular arrhythmias (VAs), including idiopathic ventricular tachycardia (VT) and premature ventricular contractions (PVCs), with acute successful radiofrequency catheter ablation (RFCA) at the superior portion of the mitral annulus (SP-MA). METHODS AND RESULTS: Among 437 consecutive patients who presented with VAs for RFCA, twenty-six patients with acute successful RFCA at the SP-MA were included in this study. The ratio of the amplitude of the first positive peak (if present) versus the nadir in the unipolar electrogram (EGM) was 0.00-0.03 (0.00) at the acute successful RFCA site. The time interval between the QRS onset and the maximum descending slope (D-Max) in the unipolar EGM (QRS-Uni) was 18.8 ± 13.6 ms. With bipolar mapping, the ventricular QRS (V-QRS) interval was 3.75-17.3 (11) ms, 6 (23.1%) patients showed the earliest V-QRS interval of 0 ms, and the other 20 patients (76.9%) showed a V-QRS interval of 10-54 ms. The RFCA start-to-effect time was 14.1 ± 7.2 s in 23 patients (88.5%). In the remaining 3 patients (11.5%), the mean duration of successful RFCA was not well defined due to the infrequent nature of clinical VAs during RFCA. Early (within 3 days) and late (1-year) recurrence rates were 23.1% (6 patients) and 26.9% (7 patients), respectively. VAs disappeared 3 days later due to delayed RFCA efficacy in 2 patients (7.7%). No complications occurred during the RFCA procedure or the one-year follow-up. CONCLUSIONS: SP-MA VAs are a rare but distinct subgroup of VAs. Bipolar and unipolar EGM features can help to determine the optimal RFCA site, and the QRS-Uni interval may serve as a marker that could be used to guide RFCA.

Ligament of Marshall ablation for persistent atrial fibrillation.

Beyond pulmonary vein isolation, the two main additional strategies: Cox-Maze procedure or targeting of electrical signatures (focal bursts, rotational activities, meandering wavelets), remain controversial. High-density mapping of these arrhythmias has demonstrated firstly that a patchy lesion set is highly proarrhythmogenic, favoring macro-re-entry through conduction slowing and providing pivots for localized re-entry. Secondly, discrete anatomical structures such as the Vein or Ligament of Marshall (VOM/LOM) and the coronary sinus (CS) have epicardial muscular bundles that are more frequently involved in re-entry than previously thought. The Marshall Bundle can be ablated at any point along its course from the mid-to-distal coronary sinus to the left atrial appendage. If necessary, the VOM may be directly ablated using ethanol infusion to eliminate PV contributions and produce conduction block across the mistral isthmus. Ethanol ablation of the VOM, supplemented with RF ablation, may be more effective in producing conduction block at the mitral isthmus than repeat RF ablation alone.

KCNE2 gene mutation and Brugada syndrome.

KCNE2 gene mutations have been associated with atrial fibrillation, long QT syndrome, Brugada syndrome and unexplained sudden cardiac death. Herein, we describe a case of Brugada syndrome carrying an heterozygous variant in the KCNE2 gene [NM_172201.2:c.161 T > C, p.(Met54Thr, M54T)]. Gain of function of the Ito current possibly explains the Brugada ECG phenotype in this case.