Aims: To investigate the distribution of left atrioventricular coupling index (LACI) among patients with heart failure and left ventricular ejection fraction (LVEF) < 50% and to explore its association with the combined endpoint of all-cause death or HF hospitalization at long-term follow-up. Methods and results: Patients with HF and LVEF < 50% undergoing cardiac magnetic resonance were evaluated. Patients with atrial fibrillation or flutter were excluded. Left atrioventricular coupling index was measured as the ratio between the left atrial (LA) and the LV end-diastolic volumes. Patient population was divided according to LACI tertiles and followed up. Total of 478 patients (mean age 62 ± 12 years, 78% male) were included. The median value of LACI was 27.1% (interquartile range 19.9–34.5). Patients within the worst LACI tertile (≥30.9%) showed smaller LV volumes and larger LA volumes as compared with patients in the first or second tertile (LACI 6.2–22.2 and LACI 22.3–30.9, respectively). Left atrioventricular coupling index was significantly associated with the combined endpoint [hazard ratio (HR) 1.87, P = 0.01]. After adjusting for sex, age, ischaemic HF aetiology, LVEF, LA reservoir strain, diabetes mellitus, LV scar, mitral regurgitation, and LVEDVi, LACI remained significantly associated with the combined endpoint (HR 1.77, P = 0.02). Patients with the highest LACI values had worse outcomes compared with patients in first and second tertiles (HR 1.69, P = 0.02 and HR 1.77, P = 0.02, respectively). Conclusion: In patients with HF and LVEF <50%, LACI is independently associated with adverse events. Patients with most impaired left atrioventricular coupling have the worst clinical outcomes.

Aims: Update data regarding the atrial fibrillation (AF)-related mortality trend in Europe remain scant. We assess the age- and sex-specific trends in AF-related mortality in the European states between the years 2008 and 2019. Methods and results: Data on cause-specific deaths and population numbers by sex for European countries were retrieved through the publicly available World Health Organization mortality dataset for the years 2008–2019. Atrial fibrillation-related deaths were ascertained when the International Classification of Diseases, 10th Revision code I48 was listed as the underlying cause of death in the medical death certificate. To calculate annual trends, we assessed the average annual % change (AAPC) with relative 95% confidence intervals (CIs) using Joinpoint regression. During the study period, 773 750 AF-related deaths (202 552 males and 571 198 females) occurred in Europe. The age-adjusted mortality rate (AAMR) linearly increased from 12.3 (95% CI: 11.2–12.9) per 100 000 population in 2008 to 15.3 (95% CI: 14.7–15.7) per 100 000 population in 2019 [AAPC: +2.0% (95% CI: 1.6–3.5), P < 0.001] with a more pronounced increase among men [AAPC: +2.7% (95% CI: 1.9–3.5), P < 0.001] compared with women [AAPC: +1.7% (95% CI: 1.1–2.3), P < 0.001] (P for parallelism 0.01). Higher AAMR increases were observed in some Eastern European countries such as Latvia, Lithuania, and Poland, while the lower increases were mainly clustered in Central Europe. Conclusion: Over the last decade, the age-adjusted AF-related mortality has increased in Europe, especially among males. Disparities still exist between Western and Eastern European countries.

Aims: How the underlying aetiology and pathophysiology of left ventricular (LV) hypertrophy affects left atrial (LA) remodelling and function remains unexplored. The present study aims to investigate the influence of various hypertrophic phenotypes on LA remodelling and function. Methods and results: Patients with LV hypertrophy who underwent cardiac magnetic resonance (CMR) were compared to a control group. CMR data were analysed retrospectively to assess LA strain, volume, sphericity, and left atrioventricular coupling index (LACI). Independent clinical associates of LA strain were assessed using multivariable linear regression analysis. A total of 375 individuals were included: 148 with hypertrophic cardiomyopathy (HCM), 35 with cardiac amyloidosis (CA), 41 with hypertensive (HTN) heart disease, 97 with severe asymptomatic aortic stenosis (AS), and 54 with normal CMR. Indexed LA end-systolic (iLVmax), diastolic volumes, and LA sphericity were the largest in patients with CA (59.1 ± 16.9 mL/m2, 46.8 ± 16.4 mL/m2, and 83.2 ± 2.1%, respectively). Patients with CA presented a higher LACI when compared with other groups (58 ± 2% vs. 42 ± 2% in HCM, 39 ± 2% in HTN heart disease, 37 ± 2% in AS, and 22 ± 1% in normal), while no differences were observed across others. Patients with CA showed the lowest LA reservoir [9.6% (0.6–18.6%)] and booster strain (9.1 ± 5.4%), whereas no differences were observed across other groups. LACI and iLAVmax were independently correlated with LA reservoir (β = 0.15 and β = −39.33, respectively), LA conduit (β = 0.08 and β = −17.08, respectively), and LA booster strains (β = 0.1 and β = −28.69, respectively). LA sphericity was independently correlated with LA reservoir strain (β = −0.51). Finally, LV global longitudinal strain was independently correlated with LA reservoir (β = −0.43), conduit (β = −0.20), and booster strain (β = −0.24). Conclusion: LA characteristics differ among LV hypertrophic phenotypes. LACI and iLAVmax are independently correlated with LA function, while LA sphericity correlates independently with LA reservoir strain.

Background: Physiological pacing has gained significant interest due to its potential to achieve optimal hemodynamic response. This study aimed to assess left ventricular performance in terms of electrical parameters, specifically QRS duration and mechanical performance, evaluated as myocardial work. We compared His Bundle Pacing (HBP) and Left Bundle Branch Area Pacing (LBBAP) to evaluate their effects. Methods: Twenty-four patients with class I or IIa indications for pacing were enrolled in this study, with twelve patients undergoing HBP implantation and another twelve undergoing LBBAP implantation. A comprehensive analysis of myocardial work was conducted. Results: Our findings indicate that there were no major differences in terms of spontaneous and HBP activation in myocardial work, except for global wasted work (217 mmHg% vs. 283 mmHg%; p 0.016) and global work efficiency (87 mmHg% vs. 82 mmHg%; p 0.049). No significant differences were observed in myocardial work between spontaneous activation and LBBAP. Similarly, no significant differences in myocardial work were found between HBP and LBBAP. Conclusions: Both pacing modalities provide physiological ventricular activation without significant differences when compared to each other. Moreover, there were no significant differences in QRS duration between HBP and LBBAP. However, LBBAP demonstrated advantages in terms of feasibility, as it achieved better lead electrical parameters compared to HBP (threshold@0.4 ms 0.6 V vs. 1 V; p = 0.045—sensing 9.4 mV vs. 2.4 mV; p < 0.001). Additionally, LBBAP required less fluoroscopy time (6 min vs. 13 min; p = 0.010) and procedural time (81 min vs. 125 min; p = 0.004) compared to HBP.

Brugada syndrome (BrS) is an inherited disorder with high allelic and genetic heterogeneity clinically characterized by typical coved-type ST segment elevation at the electrocardiogram (ECG), which may occur either spontaneously or after provocative drug testing. BrS is classically described as an arrhythmic condition occurring in a structurally normal heart and is associated with the risk of ventricular fibrillation and sudden cardiac death (SCD). We studied five patients with spontaneous or drug-induced type 1 ECG pattern, variably associated with symptoms and a positive family history through a Next Generation Sequencing panels approach, which includes genes of both channelopathies and cardiomyopathies. We identified variants in MYBPC3 and in MYH7, hypertrophic cardiomyopathy (HCM) genes (MYBPC3: p.Lys1065Glnfs*12 and c.1458-1G > A, MYH7: p.Arg783His, p.Val1213Met, p.Lys744Thr). Our data propose that Brugada type 1 ECG may be an early electrocardiographic marker of a concealed structural heart disease, possibly enlarging the genotypic overlap between Brugada syndrome and cardiomyopathies.

The aim of this review is to identify possible structural abnormalities of BrS and their potential association with symptoms, risk stratification, and prognosis. (1) Background: BrS has always been considered a purely electrical disease and imaging techniques do not currently play a specific role in the diagnosis of this arrhythmic syndrome. Some authors have recently hypothesized the presence of structural and functional abnormalities. Therefore, several studies investigated the presence of pathological features in echocardiography and cardiac magnetic resonance imaging (MRI) in patients with BrS, but results were controversial. (2) Methods: We performed a systematic review of the literature on the spectrum of features detected by echocardiography and cardiac MRI. Articles were searched in Pubmed, Cochrane Library, and Biomed Central. Only papers published in English and in peer-reviewed journals up to November 2021 were selected. After an initial evaluation, 596 records were screened; the literature search identified 19 relevant articles. (3) Results: The imaging findings associated with BrS were as follows: right ventricular dilation, right ventricular wall motion abnormalities, delayed right ventricular contraction, speckle and feature tracking abnormalities, late gadolinium enhancement, and fat infiltration in the right ventricle. Furthermore, these features emerged more frequently in patients carrying the genetic mutation on the sodium voltage-gated channel α-subunit 5 (SCN5A) gene. (4) Conclusions: Specific imaging features detected by echocardiography and cardiac magnetic resonance are associated with BrS. However, this population appears to be heterogeneous and imaging anomalies emerged to be more frequent in patients carrying genetic mutations of SCN5A. Future studies with an evaluation of BrS patients are needed to identify the specific association linking the Brugada pattern, imaging abnormalities and their possible correlation with prognosis.