Longer life expectancy along with advancements in cancer and atrial fibrillation (AF) therapies and treatment strategies have led to an increase in the number of individuals with both diseases. As a result, the complicated management of these patients has become crucial, necessitating individualised treatment that considers the bi-directional relationship between these two diseases. On the one hand, giving appropriate pharmaceutical therapy is exceptionally difficult, considering the recognised thromboembolic risk posed by AF and malignancy, as well as the haemorrhagic risk posed by cancer. The alternative pulmonary vein isolation (PVI) ablation, on the other hand, has been inadequately explored in the cancer patient population; there is yet inadequate data to allow the clinician to unambiguously select patients that can undertake this therapeutic intervention. The goal of this review is to compile the most valuable data and supporting evidence about the characteristics, care, and therapy of cancer patients with AF. Specifically, we will evaluate the pharmaceutical options for a proper anticoagulant therapy, as well as the feasibility and safety of PVI in this population.
Introduction Adults with repaired tetralogy of Fallot (rToF) experience episodes of atrial tachycardia (AT) and radiofrequency catheter ablation (RFCA) is often required but systematic evaluation of the mechanisms and recurrences is lacking. Methods Between January 2013 and October 2021, 20 rToF patients with AT referred for catheter ablation were enrolled. Electrophysiologic study with 3D electroanatomic mapping with multi–electrode mapping catheters was done, with right atrial bipolar voltage and activation mapping of the AT. Three mechanisms were searched: intra–atrial re–entrant tachycardias (IART), focal (FAT), other. Critical isthmus (CI) for IART was identified with activation mapping. FATs were localized according to the earliest uni/bipolar signal. All induced AT were treated. RFCA was aimed at the earliest activation point for FAT and at the critical isthmus for IART, anchoring lesion to fixed obstacles (valve annuli or scar). Written informed consent was provided. Results Among 20 adult (age 46±14 years) and mainly females (n=11, 55%) enrolled pts, 36 AT were documented: 25 (70%) IART, 10 (27%) FAT and only 1 (3%) had a typical atrioventricular nodal reentrant tachycardia. Mean tachycardia cycle length was 307±95 ms. Two ATs were induced in 11 pts, 3 in 4 pts and 4 in 2 during index EPS. Among IART, cavo–tricuspid isthmus (CTI) was the prevalent CI (n=14, 60%), while incisional IART (IARTinc, atriotomy and superior and inferior vena cava orifices, SVC and IVC, respectively) was the second mechanism (n=9, 39%). In two pts, due to non–inducibility, a pre–emptive lesion set comprising in one case CTI and in the second case CTI+SVC–atriotomy–IVC line was performed. Among FAT, in 3 cases the AT was mapped in the coronary sinus, in two at the tricuspid annulus, other at the crista terminalis, right appendage base, posterolateral scar or between atriotomy and SVC. During a median follow–up of 23 months (interquartile range, 6–37) recurrence occurred in 8 pts (25% of pts, 22% of tachycardias). Pts with recurrences were younger (43±7 vs. 48±17 y, p=0.04); no differences were found according to critical isthmus location (4 CTI and 4 IARTinc, 50%, p=ns). Conclusions Among rToF pts with AT, IART is the prevalent mechanism and CTI is the prevalent CI; atriotomy scar, however, is involved in a substantial portion of the critical isthmuses of the IART; FAT location is much more variable. Long–term freedom from AT in this clinical setting is encouraging.
Funding Acknowledgements Type of funding sources: None. Background Differential action potential duration shortening across the right ventricular (RV) myocardial wall is primarily responsible for the Brugada Syndrome (BrS) phenotype [1]. To date, data on electrical substrate characterization in humans with BrS phenotype is limited and risk evaluation is still controversial. Purpose We hypothesized that Uni-JEl mapping could be used as a marker of transmural voltage gradient dispersion resulting. Our aim was to evaluate Uni-JEl mapping in defining arrhythmogenic substrates in patients with BrS phenotype. Methods 12 patients were included in our analysis. 2 normal patients provided control data and 10 asymptomatic subjects with spontaneous type-1 BrS underwent 3D RV mapping (CARTO3 System, Biosense Webster). Among BrS patients we had 3 patients with arrhythmic events (aborted sudden death or appropriate ICD therapies) during follow-up (median 56, interquartile range: 46-74 months) and 7 patients without arrhythmic events. In the former group we had 1 patient with inducibility of VT/VF during EPS (EPS+) and 2 patients non-inducibles during EPS (EPS-), in the latter group we had 3 patients with EPS+ and 4 patients with EPS-. Electrophysiological data and signals were exported and OpenEP [2] was used to convert Carto proprietary data formats into Matlab format (Fig.1). Uni-JEl was calculated for each point map as the unipolar value at J point on surface electrocardiogram. Uni-JEl values were then interpolated in Paraview to create Uni-JEl maps, interpolating data points on the mesh cell (Fig.1). Finally, a region of interest (ROI) was selected and the calculation of mean Uni-JEI (MUni-JEI, as a measure of voltage gradient dispersion), interquartile range and range (intrqUni-JEI and ∆Uni-JEI, as markers of heterogeneity of dispersion) was performed. Results are shown as mean ± standard deviation for the group of BrS patients and the actual values for the two controls. Results BrS patients showed Muni-JEl, intrqUni-JEl and ∆Uni-JEI higher than controls (2.03 mV ± 0.31 mV vs 0,82 mV and 1,1 mV, 1.90 mV ± 0.82 mV vs 1,04 mV and 1,18 mV 6.26 mV ± 1.98 mV vs 3,54 mV and 4,01 mV, respectively). BrS patients with arrhythmic events during the follow-up showed higher intrqUni-JEl and the ∆Uni-JEI respect to BrS with EPS+ and without arrhythmic events during follow-up (2.31 mV ± 0.44 mV vs 0.78 mV ± 0.11 mV and 6.69 mV ± 2.27 mV vs 3.98 mV ± 0.31 mV). Figure 2 shows some examples of calculated Uni-JEl maps for each group under study. Conclusions In this work we introduced a novel workflow for the electrical substrate characterization of subjects with BrS phenotype. The results from our preliminary analysis indicate that a higher transmural voltage gradient dispersion and heterogeneity can be found in type-1 BrS with respect to normal subjects. Voltage gradient dispersion heterogeneity could be used to better recognize high risk BrS patients regardless of VT/VF inducibility during EPS.
Mitral valve prolapse (MVP) is the common valvular heart disease, with a prevalence about 1–3% in the population. MVP is characterized on echocardiography by an abnormal systolic displacement of mitral valve leaflets into left atrium (LA) ≥ 2 mm above the mitral annulus. We described a clinical case of a 15 years–old boy with a first clinical presentation of out–of–hospital cardiac arrest related to ventricular fibrillation (VF) with a successful resuscitation after 2 DC shocks. Retrospectively, an episode of loss of awareness reported as post–minational. No familiar history of sudden cardiac death (SCD) or MVP was noticed. In the emergency room, the patient was hemodynamically unstable and was sedated and intubated. The surface electrocardiogram (ECG) showed sinus rhythm, QRS with fragmentation, and frequent monomorphic isolated premature ventricular contractions (PVCs) with RBBB/LAFB configuration.Frequent monomorphic PVCs with bigeminy was observed during continuous ECG monitoring, so the patient was treated with magnesium sulphate and metoprolol. The patient was subsequently weaned from ventilation support, presenting good gas exchange and without neurological sequalae. The 24h Holter monitoring showed an average of 53 bpm, extremely rare supraventricular extrasystoles, high incidence of monomorphic PVCs (23% of the total beats) with 4 couplets. Transthoracic echocardiography documented normal size and thickness with systolic function (GLS –21%, mild asynchrony of posterior basal segments), bi–leaflet prolapse associated to mild–moderate mitral regurgitation, and mitral annular disjunction (MAD) of 6.2 mm. The late gadolinium enhancement cardiac magnetic resonance showed bi–leaflet prolapse with mild insufficiency and maximum MAD 9 mm, mild LA dilatation, and slightly dilated both ventricles, without regional wall motion abnormalities; no scar or fibrosis at the late gadolinium enhancement was observed. According to guidelines, the patient received a subcutaneous implantable cardiac defibrillator for the secondary prevention of SCD and maintained under betablockers in order to control the arrhythmic burden. The genetic sampling did not show any pathogenetic mutation potentially related to cardiomyopathies or channelopathies. This case show an arrhythmic MVP complex with probably posterior papillary muscle source. The early PVCs with R/T constituted a possible trigger of VF. The betablocker therapy exhibited a full suppression of extrasystolic burden.
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