Felipe Bisbal

Background: Empagliflozin and sacubitril/valsartan are established in heart failure treatment, but their effects after myocardial infarction (MI) are less clear. This study evaluated early empagliflozin initiation, with or without sacubitril/valsartan, on post‐MI inflammation, oxidative stress, metabolism, fibrosis, cardiac function, and ventricular tachycardia (VT) risk in a pig model. Methods: A total of 24 of 30 pigs survived the MI procedure and were subsequently randomized to receive beta‐blocker treatment alone (control‐MI), beta‐blocker+empagliflozin, or beta‐blocker+empagliflozin+sacubitril/valsartan. Immune response, metabolic profile, and cardiac function were monitored. At 30 days after MI, programmed electrical stimulation and high‐density mapping were performed and VT inducibility was assessed. Tissue samples were collected for cardiac inflammation, oxidative stress, and metabolic analyses. Results: Empagliflozin reduced circulating leukocytes at 2 and 15 days after MI ( P =0.010 and P =0.050, respectively) and decreased C‐C chemokine receptor 2+ monocytes at 15 days ( P =0.049). Nitric oxide bioavailability increased in remote myocardium ( P =0.059), along with cardioprotective liver lipids and collagen III in the myocardial scar ( P =0.023). No effect on cardiac function or VT inducibility was observed at 30 days. With empagliflozin+sacubitril/valsartan, scar collagen I decreased ( P =0.082), left ventricular compliance improved ( P =0.029), electrophysiological remodeling improved (reduced border‐zone corridors [ P =0.006] and deceleration zones [ P =0.008]), and VT inducibility decreased ( P =0.025). Conclusions: In this pig model of nonreperfused MI treated with beta‐blocker, early initiation of empagliflozin reduced inflammation, improved nitric oxide bioavailability, increased protective liver lipids, and modified scar composition without affecting cardiac function or VT risk. With empagliflozin+sacubitril/valsartan treatment, scar collagen I and VT inducibility declined and left ventricular remodeling was enhanced.

Aims: Pre-procedural imaging can facilitate scar-related ventricular tachycardia (VT) ablation, although only limited data have been reported. This prospective registry aimed to analyse procedural data and outcomes in a multi-centre setting of a pre-defined VT ablation strategy facilitated by the integration of pre-procedural imaging into the navigation system. Methods and results: Consecutive patients referred for scar-related left-sided VT ablation were prospectively enrolled at five European tertiary hospitals. Pre-procedural cardiac magnetic resonance (CMR)–derived scar maps and/or multi-detector computed tomography (MDCT)–derived wall thinning maps of the left ventricle (LV) were obtained and integrated into the navigation system. An endocardial or endoepicardial approach was chosen based on the scar distribution at pre-procedural imaging. The decision of performing a detailed electro-anatomical map (EAM) of the LV (image-aided) or to using the pre-procedural imaging for guiding the ablation without obtaining an EAM (image-guided) was left to the physician’s discretion. One hundred and seventy-one patients (71% with ischaemic cardiomyopathy) were included. Cardiac magnetic resonance was integrated in 159 (93%), MDCT in 113 (66%), and both in 101 (59%) procedures. Procedure-related complications occurred in 9 (5%) patients. At a mean follow-up of 18 ± 19 months, the overall survival and VT recurrence-free survival were 91 and 74.4%, respectively. There were no significant differences in long-term ablation outcomes based on the type of cardiomyopathy (P = 0.88) or the pre-procedural imaging modality employed (P = 0.33). An image-guided approach appears feasible, safe, and faster, with reduced procedure, radiofrequency, and fluoroscopy times, without compromising efficacy. Conclusion: In a large multi-centre prospective cohort, VT ablation facilitated by pre-procedural imaging is associated with favourable long-term outcomes.

Background: Ethanol infusion into the vein of Marshall (EI‐VOM) is an adjunctive therapy to pulmonary vein isolation (PVI), which improves the efficacy of persistent atrial fibrillation (AF) ablation procedures. It is unknown how EI‐VOM scar formation impacts left atrium (LA) structure and function.Objective: To characterize scar formation after EI‐VOM, and its impact on LA function, by cardiac magnetic resonance (CMR).Methods: Consecutive patients referred for persistent AF ablation, or any repeat procedure, were included. Ablation strategy included PVI, EI‐VOM and linear lesions when deemed necessary. LA was assessed by late gadolinium enhancement (LGE) CMR at baseline and 3‐month follow‐up. CMR was post‐processed off‐line with dedicated software. The LA was regionalized into 17 segments, and global and regional scarring were calculated. Strain parameters were analyzed—including LA reservoir, conduit, and booster strain; LA ejection fraction; and LA passive and active emptying function. Follow‐up LGE‐CMR reconstruction was coregistered with the voltage map, ablation RF points, and fluoroscopy to compare the scar location with the VOM trajectory.Results: This study included 21 patients (65 ± 8 years; 76% men; 57% ablation of persistent AF). After EI‐VOM, 95% of patients presented new low‐voltage areas, all of whom exhibited new LGE‐CMR scarring at follow‐up. Voltage map and LGE‐CMR coregistration showed comparable scar areas (p = 0.287). LGE‐CMR scarring frequently involved the whole VOM trajectory, predominantly affecting the LA ridge, mitral isthmus, and left posterior wall. LA volume was significantly reduced after ablation, without significant changes in LA functional parameters.Conclusion: EI‐VOM causes permanent scarring at 3‐month follow‐up, with no adverse impact on CMR LA functional parameters.

Background: The spontaneous type 1 ECG pattern (ECG-T1) is diagnostic of Brugada syndrome (BrS) and implies an increased arrhythmic risk, while pharmacologically-induced ECG-T1 without other clinical features only makes the diagnosis possible, according to ESC guidelines. Given the dynamic nature of the ECG patterns in BrS, tools to increase the detection of ECG-T1 are needed to improve BrS diagnosis and adequately assess the arrhythmic risk. Purpose: To assess the diagnostic yield of a smartphone-operated, 6-lead device (6L-mobile ECG) in BrS. Methods: Eighteen patients with spontaneous or drug-induced ECG-T1 (Figure 1-a), 18 patients with type 2 ECG pattern (ECG-T2, figure 2-a) and 18 controls were included. A 12-lead ECG and a 6L-mobile ECG were obtained by placing leads V1 and V2 in 2nd, 3rd and 4th intercostal space (ICS). The 6L-mobile ECG was placed with the 2 frontal electrodes in contact with the patients’ chest. Each 12-lead ECG and 6L-mobile ECG recording was classified as ECG-T1, ECG-T2 or non-diagnostic (ND), by considering the lead/ICS with the most evident pattern for analysis. Results: Sixteen 6L-mobile ECG recordings were diagnostic of ECG-T1 (figure 1-b), 18 of ECG-T2 (figure 2-b) and 20 were ND. Unipolar 6-L mobile ECG recordings at any ICS had a 77% sensitivity and 94% specificity for the diagnosis of ECG-T1 (NPV 89%, PPV 88%, p<0.0001). For ECG-T2, the 6L-mobile ECG showed a 89% sensitivity and 94% specificity (NPV 94%; PPV 89%, p<0.0001). Conclusions: The 6-L mobile ECG device showed a high diagnostic yield for type 1 and type 2 ECG patterns and may emerge as a new diagnostic and monitoring tool in BrS.

BACKGROUND: Sacubitril/valsartan (Sac/Val) is superior to angiotensin-converting enzyme inhibitors in reducing the risk of heart failure hospitalization and cardiovascular death, but its mechanistic data on myocardial scar after myocardial infarction (MI) are lacking. The objective of this work was to assess the effects of Sac/Val on inflammation, fibrosis, electrophysiological properties, and ventricular tachycardia inducibility in post-MI scar remodeling in swine. METHODS: After MI, 22 pigs were randomized to receive β-blocker (BB; control, n=8) or BB+Sac/Val (Sac/Val, n=9). The systemic immune response was monitored. Cardiac magnetic resonance data were acquired at 2-day and 29-day post MI to assess ventricular remodeling. Programmed electrical stimulation and high-density mapping were performed at 30-day post MI to assess ventricular tachycardia inducibility. Myocardial samples were collected for histological analysis. RESULTS: Compared with BB, BB+Sac/Val reduced acute circulating leukocytes ( P =0.009) and interleukin-12 levels ( P =0.024) at 2-day post MI, decreased C-C chemokine receptor type 2 expression in monocytes ( P =0.047) at 15-day post MI, and reduced scar mass ( P =0.046) and border zone mass ( P =0.043). It also lowered the number and mass of border zone corridors ( P =0.009 and P =0.026, respectively), scar collagen I content ( P =0.049), and collagen I/III ratio ( P =0.040). Sac/Val reduced ventricular tachycardia inducibility ( P =0.034) and the number of deceleration zones ( P =0.016). CONCLUSIONS: After MI, compared with BB, BB+Sac/Val was associated with reduced acute systemic inflammatory markers, reduced total scar and border zone mass on late gadolinium-enhanced magnetic resonance imaging, and lower ventricular tachycardia inducibility.

The aim of our study was to analyse the response to short-coupled atrial extrastimuli to identify areas of hidden slow conduction (HSC) and their relationship with the atrial fibrillation (AF) phenotype. Twenty consecutive patients with paroxysmal AF and persistent AF (10:10) underwent the first pulmonary vein isolation procedure. Triple short-coupled extrastimuli were delivered in sinus rhythm (SR), and the evoked response was analysed: sites exhibiting double or highly fragmented electrograms (EGM) were defined as positive for HSC (HSC+). The delta of the duration of the bipolar EGM was analysed, and bipolar EGM duration maps were built. High-density maps were acquired using a multipolar catheter during AF, SR, and paced rhythm. Spatial co-localization of HSC+ and complex fractionated atrial EGMs (CFAE) during AF was evaluated. Persistent AF showed a higher number and percentage of HSC+ than paroxysmal AF (13.9% vs. 3.3%, P < 0.001). The delta of EGM duration was 53 ± 22 ms for HSC+ compared with 13 ± 11 (10) ms in sites with negative HSC (HSC−) (P < 0.001). The number and density of HSC+ were lower than CFAE during AF (19 vs. 56 per map, P < 0.001). The reproducibility and distribution of HSC+ in repeated maps were superior to CFAE (P = 0.19 vs. P < 0.001). Sites with negative and positive responses showed a similar bipolar voltage in the preceding sinus beat (1.65 ± 1.34 and 1.48 ± 1.47 mV, P = 0.12). Functional mapping identifies more discrete and reproducible abnormal substrates than mapping during AF. The HSC+ sites in response to triple extrastimuli are more frequent in persistent AF than in paroxysmal AF.

BACKGROUND: In patients with persistent atrial fibrillation (PersAF), catheter ablation aiming for pulmonary vein isolation (PVI) is associated with moderate clinical effectiveness. We investigated the benefit of continuing previously ineffective class 1C or 3 antiarrhythmic drug therapy (ADT) in the setting of a standardized PVI-only ablation strategy. METHODS: In this multicenter, randomized controlled study, patients with PersAF (≥7 days and 30 seconds beyond 3 months. Prospectively defined secondary end points included repeat ablations, unscheduled arrhythmia-related visits, and quality of life among groups. RESULTS: Of 200 PersAF patients, 98 were assigned to ADT OFF and 102 to ADT ON. The longest atrial fibrillation episode qualifying for PersAF was 28 (10–90) versus 30 (11–90) days. Clinical characteristics and procedural characteristics were similar. Recurrence of atrial tachyarrhythmia was comparable in both groups (20% OFF versus 21.2% ON). No differences were observed in repeat ablations and unscheduled arrhythmia-related visits. Marked improvement in quality of life was observed in both groups. CONCLUSIONS: In patients with PersAF, there is no benefit in continuing previously ineffective ADT beyond the blanking period after catheter ablation. The high success rate of PVI-only might be explained by the high rate of durable isolation after optimized PVI and the early stage of PersAF (POWDER-AF2). REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03437356.

Over the last decades, cardiac electronic implantable devices (CEID) have incorporated a myriad of technological capabilities that are not conveniently inferred by using the conventional ICHD and NBG coding systems. We propose a new coding system (i.e., the C‐ARL‐A coding system) aimed at overcoming this important limitation.