Background: Current electrocardiographic algorithms lack sensitivity to diagnose acute myocardial infarction ( AMI ) in the presence of left bundle branch block. Methods and Results: A multicenter retrospective cohort study including consecutive patients with suspected AMI and left bundle branch block, referred for primary percutaneous coronary intervention between 2009 and 2018. Pre‐2015 patients formed the derivation cohort (n=163, 61 with AMI ); patients between 2015 and 2018 formed the validation cohort (n=107, 40 with AMI ). A control group of patients without suspected AMI was also studied (n=214). Different electrocardiographic criteria were tested. A total of 484 patients were studied. A new electrocardiographic algorithm ( BARCELONA algorithm) was derived and validated. The algorithm is positive in the presence of ST deviation ≥1 mm (0.1 mV) concordant with QRS polarity, in any lead, or ST deviation ≥1 mm (0.1 mV) discordant with the QRS , in leads with max (R|S) voltage (the voltage of the largest deflection of the QRS , ie, R or S wave) ≤6 mm (0.6 mV). In both the derivation and the validation cohort, the BARCELONA algorithm achieved the highest sensitivity (93%–95%), negative predictive value (96%–97%), efficiency (91%–94%) and area under the receiver operating characteristic curve (0.92–0.93), significantly higher than previous electrocardiographic rules ( P <0.01); the specificity was good in both groups (89%–94%) as well as the control group (90%). Conclusions: In patients with left bundle branch block referred for primary percutaneous coronary intervention , the BARCELONA algorithm was specific and highly sensitive for the diagnosis of AMI , leading to a diagnostic accuracy comparable to that obtained by ECG in patients without left bundle branch block.

Background and Aims: The prediction of the first major arrhythmic event (MAE) is still an unmet need in the recently defined scenario of non-dilated left ventricular cardiomyopathy (NDLVC). Methods: A cohort of 337 patients with NDLVC and no history of MAE was retrospectively identified at two large centres. Patient-tailored diagnostic workup included cardiac magnetic resonance (CMR), endomyocardial biopsy, and genetic testing. The primary endpoint was the occurrence of the first MAE, including sustained ventricular tachycardia (VT), ventricular fibrillation, or appropriate implantable cardioverter-defibrillator therapy, by 60-month follow-up. A pool of 216 NDLVC patients from 11 European centres served as a validation cohort. Results: In the study cohort (mean age 37 ± 15 years, 62% male), the mean left ventricular ejection fraction (LVEF) was 52 ± 8%, and 79% of patients had late gadolinium enhancement (LGE) at baseline CMR. By 60-month follow-up, 51 patients (15%) experienced a MAE. The primary endpoint was predicted by male sex [hazard ratio (HR) 2.4, 95% confidence interval (CI) 1.3–4.4, P = .007], baseline non-sustained VT (HR 3.1, 95% CI 1.7–5.6, P < .001), LVEF < 45% (HR 5.5, 95% CI 2.7–11.0, P < .001), septal (HR 2.0, 95% CI 1.0–4.0, P = .046) and ring-like pattern of LGE (HR 1.3, 95% CI .6–2.6, P = .54), pathogenic/likely pathogenic variants in guideline-defined high-risk genes (HR 4.6, 95% CI 2.3–9.1, P < .001), and biopsy/CMR-proven myocardial inflammation (HR 15.7, 95% CI 6.1–40.3, P < .001). The results were confirmed in the validation cohort (Uno’s C-index 0.81, 95% CI .75–.88). A novel risk score was subsequently derived. Conclusions: In NDLVC, male sex, non-sustained VT, LVEF < 45%, septal and ring-like LGE, high-risk genotypes, and myocardial inflammation predicted the first episode of MAE by 60 months.

To evaluate whether cardiac magnetic resonance (CMR)-based parametric mapping and strain analysis can improve the risk-stratification for ventricular arrhythmias (VA) and sudden death (SD) in non-ischaemic cardiomyopathy (NICM). Secondary analysis of a prospective single-centre-registry (NCT02326324), including 703 consecutive NICM patients, 618 with extracellular volume (ECV) available. The combined primary endpoint included appropriate implantable cardioverter defibrillator therapies, sustained ventricular tachycardia, resuscitated cardiac arrest and SD. During a median follow-up of 21 months, 14 patients (2%) experienced the primary endpoint. Native T1 was not associated with the primary endpoint. Left ventricular global longitudinal strain lost its significant association after adjustment for left ventricular ejection fraction (LVEF). Among patients with ECV available, 11 (2%) reached the primary endpoint. Mean ECV was significantly associated with the primary endpoint and the best cut-off was 30%. ECV ≥ 30% was the strongest independent predictor of the primary endpoint (hazard ratio 14.1, P = 0.01) after adjustment for late gadolinium enhancement (LGE) and LVEF. ECV ≥ 30% discriminated the arrhythmic risk among LGE+ cases and among those with LVEF ≤ 35%. A simple clinical risk-stratification model, based on LGE, LVEF ≤ 35% and ECV ≥ 30%, achieved an excellent predictive ability (Harrell’s C 0.82) and reclassified the risk of 32% of the study population as compared to LVEF ≤ 35% alone. Comprehensive CMR evaluation in NICM showed that ECV was the only parameter with an independent and strong predictive value for VA/SD, on top of LGE and LVEF. A risk-stratification model based on LGE, LVEF ≤ 35% and ECV ≥ 30% achieved an excellent predictive ability for VA/SD. UHSM CMR study (NCT02326324) https://clinicaltrials.gov/ct2/show/NCT02326324.

Background and Aims: Conduction system pacing has emerged as an alternative to biventricular pacing (BiVP) for cardiac resynchronization therapy (CRT). The left-bundle CRT trial evaluated whether left-bundle branch area pacing (LBBAP) is non-inferior to BiVP in patients eligible for CRT. Methods: The left-bundle CRT trial was a multi-centre, randomized, investigator-initiated, and non-inferiority study. Patients with guideline-based CRT indications and left-bundle branch block per Strauss criteria were randomized to BiVP-CRT or LBBAP-CRT. The primary endpoint was the proportion of patients with a positive CRT response at 6-months, defined as either an improved clinical composite score (CCS) or a ≥15% reduction in left ventricular end-systolic volume. The non-inferiority margin was the lower bound of the 95% confidence interval (CI) and was set at 10%. Patients were followed for 12-months; secondary endpoints included echocardiographic, clinical, and quality-of-life outcomes. Results: The baseline characteristics of the 176 patients randomized to BiVP-CRT (n=84) or LBBAP-CRT (n=92) were similar, except for a wider intrinsic QRS in the LBBAP group: median 172 ms [IQR 158–184] vs. 165 ms [152–180]; P=0.04. Crossovers occurred in 26 patients (14.9%). In the intention-to-treat analysis, the primary endpoint was achieved in 94.6% of BiVP-CRT and 89.7% of LBBAP-CRT patients (RR 0.95; 95% CI 0.88–1.02), not meeting non-inferiority. CCS improved in 77% and 68% of patients randomized to BiVP-CRT and LBBAP-CRT, respectively and 85% and 79% had a ≥15% reduction in left ventricular end-systolic volume. Rates of adverse events and heart failure hospitalization were similar between groups. Conclusions: In CRT candidates with typical LBBB, LBBAP-CRT was not shown to be non-inferior to BiVP-CRT. Both strategies yielded high response rates and similar clinical outcomes.