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Up to one-third of patients who undergo cardiac resynchronization therapy do not obtain clinical benefit. A systematic approach can identify treatable causes in many nonresponding patients. We present a case of nonresponse to cardiac resynchronization therapy that resolved by ablation of the atrioventricular node in a patient with complete atrioventricular block. (Level of Difficulty: Advanced.), Graphical abstract

Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Instituto de Salud Carlos III BACKGROUND Cardiac regenerative therapy is a promising treatment for patients with myocardial infarction (MI) and heart failure. Nevertheless, previous ex-vivo studies have raised concern on the potential increased risk of arrhythmic events following certain cell therapies. Adipose graft transposition procedure (AGTP) is a cardiac reparative therapy consisting in transposing a vascularized adipose flap from the autologous pericardium and placing it over the epicardial scar area and has demonstrated to reduce infarct size and improve the left ventricular ejection fraction in preclinical and human studies. PURPOSE To assess the effect of the AGTP on the post-MI scar composition and image-based ventricular tachycardia (VT) corridors detection by means of late gadolinium enhanced cardiac magnetic resonance (LGE-CMR). METHODS A left circumflex artery (first marginal branch) MI was induced in 9 Landrace X Large White Pigs by delivering 1-3 coils. Two weeks post-MI, all subjects underwent a 3 Tesla LGE-CMR and randomized to the AGTP or sham group. LGE-CMR was repeated 30 days post-treatment (6 weeks post-MI). The arrhythmogenic substrate was characterized with an advanced image post-processing tool (ADAS 3D) and included quantification of dense scar and border zone (BZ) mass and detection of ventricular tachycardia (VT) corridors (including corridor scar mass). RESULTS The overall scar mass did not differ between scans in the overall population (7.6 ± 3.5 g vs 7.5 ± 2.2 g in the baseline and post-treatment scans, respectively; p = 0.9). Compared to the sham subjects, those receiving AGTP showed an absolute reduction of the total (-3.2 ± 1.4 g vs. +2.4 ± 1.7 g, p = 0.04) and dense scar (-0.9 ± 0.4 g vs. +0.7 ± 0.5 g, p = 0.03). BZ mass tended to decrease in the AGTP group (-2.2 vs 1.63 g; p = 0.06). The AGTP group showed a trend to reduce the number of VT corridors (-1 ± 0.7 vs. +0.4 ± 0.2, p = 0.078) and corridor scar mass (-0.3 ± 0.26 g vs. +0.1 ± 0.1 g, p = 0.11) (figure). CONCLUSIONS Cardiac reparative therapy of MI with AGTP reduced dense scar mass, compared to the increase observed in the sham group. The trend to reduce the BZ mass and the number/mass of VT corridors suggests a beneficial effect on the arrhythmic remodeling of the post-MI scar. Abstract Figure. Reduction in corridor"s number

Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Insituto de Salud Carlos III BACKGROUND Cardiac regenerative therapy is a promising treatment for patients with ischemic heart disease, but there are some concerns on the potential increased risk of arrhythmic events following specific cell therapies. Adipose graft transposition procedure (AGTP) is a cardiac reparative therapy consisting in transposing a vascularized adipose flap from the autologous pericardium and placing it over the epicardial scar area and has demonstrated to reduce infarct size and improve the left ventricular ejection fraction in preclinical and human studies. Specific electrophysiological properties of the scar, (i.e. slow conduction velocity (CV)) have been identified as key features of ventricular tachycardia (VT) isthmuses. PURPOSE To assess the effect of the AGTP on VT inducibility and the electrophysiological properties of the post-MI scar with ultra-high density (UHD) mapping. METHODS A left circumflex artery (first marginal branch) MI was induced in 10 Landrace X Large White pigs by delivering 1-3 coils. Two weeks post-MI, all subjects underwent baseline left ventricular endocardial UHD mapping during right ventricular pacing with 64-electrode basket mapping catheter, as well as electrophysiological study (EPS) to test for VT inducibility. Following the mapping, subjects were allocated 1:1 to AGTP or sham group. UHD mapping and EPS were repeated 30 days post-treatment (6 weeks after MI). Voltage and activation maps were analyzed off-line with self-customized Paraview-based software. Voltage cut-offs of 1.5 and 0.5mV (bipolar) defined normal tissue, border zone (BZ) and dense scar, respectively, and 6.7mV for unipolar. Conduction velocity (CV) was determined for every pair of contiguous points and areas of similar CV were quantified for every 0.2m/s steps (for up to 4 m/s). RESULTS There were no differences between groups with regard of dense scar, BZ an low unipolar voltage areas. The AGTP group had a significant reduction of the size of slow CV ( CONCLUSIONS Cardiac reparative therapy with AGTP of post-MI scar reduced the size of slow conduction areas and could provide a protective effect against arrhythmic events in ischemic heart disease. Abstract Figure.

Funding Acknowledgements Type of funding sources: None. BACKGROUND Left atrial fibrosis is a marker of atrial disease and it has an important role in the pathophysiology of atrial fibrillation (AF). Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) is an emerging tool to detect left atrial fibrosis. However, data on the correlation between LGE-CMR detected fibrosis and low voltage areas to define fibrotic tissue is scarce. PURPOSE To assess the correlation and degree of concordance between LGE-CMR and high-density bipolar voltage mapping for the identification of left atrial abnormal tissue. METHODS Seven patients scheduled for AF ablation (including first and redo procedures) underwent a preprocedural 1.5 Tesla LGE-CMR including left atrial 3D inversion-recovery steady-state free precession sequence (ECG and respiratory triggering) 20 minutes after the injection of 0.2 mmol/kg of gadobutrol. A high-density electroanatomical voltage mapping was acquired with a 16-electrode grid configuration mapping catheter during sinus rhythm. LGE-CMR studies were analyzed off-line with an advanced image post-processing tool (ADAS 3D). Atrial wall intensity was normalized to blood pool, obtaining an image intensity ratio (IIR) value for each CMR point of the 3D model. High-density bipolar voltage maps and LGE-CMR 3D left atrial reconstruction were merged (figure, panel A). Voltage points were projected to the LGE-CMR left atrial 3D model, allowing point-by-point correlation analysis between voltage (log transformed due to non-normal distribution) with IIR. Left atrial fibrosis area and percentage were quantified using the standard cut-off values (bipolar voltage 1.2). We assessed the degree of concordance for normal and abnormal (fibrosis) tissue classification between the two techniques using different cut-off values (< 0.5mV and 0.9, >1, >1.1 and >1.2 for IIR). RESULTS The average fibrosis area detected with LGE-CMR was lower than that detected with high-density bipolar voltage, using standard cut-off values (18.6 ± 5.7 cm2 vs. 40.6 ± 12.5 cm2, p = 0.13 respectively). There was a poor global point-by-point correlation between log-transformed voltage and IIR was r=-0.093, p 1, with an agreement percentage of 54.6%. CONCLUSIONS Left atrial tissue characterization between LGE-CMR and high-density bipolar voltage mapping showed significant but poor point-by-point correlation. Although the highest concordance was obtained using standard cutoff values, the Kappa index was best when applying non-standard cutoffs (1mV for bipolar voltage and >1 for IIR). Abstract Figure.

Myocardial infarction (MI) is the leading cause of mortality worldwide. Despite the use of evidence-based treatments, including coronary revascularization and cardiovascular drugs, a significant proportion of patients develop pathological left-ventricular remodeling and progressive heart failure following MI. Therefore, new therapeutic options, such as cellular and gene therapies, among others, have been developed to repair and regenerate injured myocardium. In this context, animal models of MI are crucial in exploring the safety and efficacy of these experimental therapies before clinical translation. Large animal models such as swine are preferred over smaller ones due to the high similarity of swine and human hearts in terms of coronary artery anatomy, cardiac kinetics, and the post-MI healing process. Here, we aimed to describe an MI model in pig by permanent coil deployment. Briefly, it comprises a percutaneous selective coronary artery cannulation through retrograde femoral access. Following coronary angiography, the coil is deployed at the target branch under fluoroscopic guidance. Finally, complete occlusion is confirmed by repeated coronary angiography. This approach is feasible, highly reproducible, and emulates the pathogenesis of human non-revascularized MI, avoiding the traditional open-chest surgery and the subsequent postoperative inflammation. Depending on the time of follow-up, the technique is suitable for acute, sub-acute, or chronic MI models.

Evidence regarding any association of HDL-particle (HDL-P) derangements and HDL-cholesterol content with cardiovascular (CV) death in chronic heart failure (HF) is lacking. To investigate the prognostic value of HDL-P size (HDL-Sz) and the number of cholesterol molecules per HDL-P for CV death in HF patients. Outpatient chronic HF patients were enrolled. Baseline HDL-P number, subfractions and HDL-Sz were measured using 1H-NMR spectroscopy. The HDL-C/P ratio was calculated as HDL-cholesterol over HDL-P. Endpoint was CV death, with non-CV death as the competing event. 422 patients were included and followed-up during a median of 4.1 (0–8) years. CV death occurred in 120 (30.5%) patients. Mean HDL-Sz was higher in CV dead as compared with survivors (8.39 nm vs. 8.31 nm, p

A 52-year-old man was admitted due to out-hospital cardiac arrest. Recurrent ventricular fibrillation (VF) occurred under therapeutic hypothermia thereafter. Previously inadverted full pre-excitation was documented exclusively and immediately prior to 4 out of the 5 VF relapses. Coronary vasospasm and early repolarization were also documented. An electrophysiological study demonstrated poor anterograde conduction over a left-sided accessory pathway. We theorize that maximum pre-excitation favored in-hospital VF by augmenting the repolarization vulnerability induced by therapeutic hypothermia, with coronary vasospasm accounting as the probable cause of out-hospital VF. A plausible VF mechanism in WPW syndrome unrelated to pre-excited atrial fibrillation is discussed.

Background: Persistent symptoms after the acute SARS-CoV-2 infection are referred to as post-COVID-19 syndrome(PCS). Fatigue, palpitations and exercise intolerance are common complains among PCS patients in whom unexplained sinus tachycardia is a frequent observation. Objective: To evaluate the prevalence and the pathophysiological mechanisms of IST in a consecutive and prospective population of patients with PCS. Methods: Consecutive patients with persistent symptoms 3 months after an acute COVID-19 were prospectively evaluated at a multi-disciplinary PCS unit. All patients were screened for IST and those with confirmed criteria underwent comprehensive CV examination: ECO, 24h Holter (assessment of the cardiac autonomic function), QoL Questionnaire (MLHFQ), six-min walking test (6MWT) and blood sample with inflammation and myocardial biomarkers. Two control patients, matched by age and gender, were assigned to each case: one with previous SARS-CoV-2 infection without PCS (group 2,recovered asymptomatic) and one without prior COVID (group 3,uninfected). Results: IST were met in 43/200 PCS patients (21%) being more common in young (mean age 39y) woman (91%) without clinical history and with mild COVID (not requiring hospital admission during the acute phase). Mean HR 96±3 (supine) and 112±17 (upright position), with 8 patients fulfilling diagnostic of POTS. No underlying structural heart disease, proinflammatory state, myocyte injury or hypoxia were identified 6MWT showed a significantly diminished exercise capacity(59% of the estimated distance). An impaired QoL was also identified. Regarding the 24h Holter, all HRV parameters were significantly deteriorated in IST patients compared with control groups (significantly decrease in time and frequency domain parameters). The most reduced components were those related with the cardiovagal tone: PNN50 4±4 in group 1 (vs 11±9 in group 2 and 18±9 in group 3;p

Obese patients with chronic Heart Failure (HF) have better outcome than their lean counterparts, although little is known about the pathophysiology of this obesity paradox. Our aim was to evaluate the hypothesis that patients with chronic HF and obesity (defined as body mass index (BMI)≥30kg/m(2)), may have an attenuated neurohormonal activation in comparison with non-obese patients.The present study is the post-hoc analysis of a cohort of 742 chronic HF patients from a single-center study evaluating sympathetic activation by measuring baseline levels of norepinephrine (NE). Obesity was present in 33% of patients. Higher BMI and obesity were significantly associated with lower NE levels in multivariable linear regression models adjusted for covariates (p0.001). Addition to NE in multivariate Cox proportional hazard models attenuated the prognostic impact of BMI in terms of outcomes. Finally, when we explored the prognosis impact of raised NE levels (70th percentile) carrying out a separate analysis in obese and non-obese patients we found that in both groups NE remained a significant independent predictor of poorer outcomes, despite the lower NE levels in patients with chronic HF and obesity: all-cause mortality hazard ratio=2.37 (95% confidence interval, 1.14-4.94) and hazard ratio=1.59 (95% confidence interval, 1.05-2.4) in obese and non-obese respectively; and cardiovascular mortality hazard ratio=3.08 (95% confidence interval, 1.05-9.01) in obese patients and hazard ratio=2.08 (95% confidence interval, 1.42-3.05) in non-obese patients.Patients with chronic HF and obesity have significantly lower sympathetic activation. This finding may partially explain the obesity paradox described in chronic HF patients.