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AIMS: The left bundle branch block (LBBB) is a strong predictor of response to cardiac resynchronization therapy (CRT). However, a significant number of patients do not respond to the treatment. The study sought to evaluate the impact of the stricter Strauss criteria for left bundle branch block (St-LBBB) on CRT response, hospitalizations, ventricular arrhythmia (VA) events and mortality. METHODS: This study is a retrospective analysis of prospectively collected data on heart failure (HF) patients with LBBB admitted for CRT implantation. Patients were divided into two groups according to the fulfilment or not of St-LBBB criteria. RESULTS: The study included 82 patients with ischaemic (ICM) and non-ischaemic (NICM) cardiomyopathy [46 (56%) with St-LBBB and 36 (44%) with non-St-LBBB]. Patients with St-LBBB showed higher CRT response rates compared with those with non-St-LBBB (P < 0.01), while the group with NICM exhibited the greatest benefit (P < 0.01). St-LBBB CRT responders displayed significantly lower rates of HF hospitalization (P < 0.0001) compared with the non-St-LBBB group. According to Kaplan-Meier time curves, this was primarily evident in patients with NICM (P < 0.0001). CRT responders displayed significantly fewer VA events (P < 0.001) and lower mortality rates (P < 0.0001) than non-responders. Kaplan-Meier estimates demonstrated a significantly lower incidence of VAs in NICM patients with St-LBBB (P = 0.049) compared with ICM patients with St-LBBB (P = 0.25). Lower mortality rates were observed in CRT responders than non-responders (P < 0.0001), with the group of NICM with St-LBBB criteria exhibiting the greatest benefit (P = 0.0238). CONCLUSIONS: Patients with NICM and St-LBBB present the greatest benefit concerning CRT response, HF hospitalizations, VA events and mortality. Although St-LBBB criteria seem to improve patient selection for CRT, more data are needed to elucidate the role of St-LBBB criteria in this setting.

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OBJECTIVE: The electrocardiogram-derived corrected QT (QTc) interval is an indicator of cardiac autonomic activity that has been proposed as a biological measure to investigate the interplay between depression and cardiovascular diseases. This study assesses whether depression is associated with a longer QTc interval across age groups. METHODS: Assessment of depressive symptoms was performed in 1637 participants of the cross-sectional Corinthia study with the Zung Self-Rating Depression Scale in those younger than 65 years (group 1) and with the Geriatric Depression Scale in elderly individuals (≥65 years, group 2). The QT interval was obtained from electrocardiogram recordings and corrected for heart rate (QTc). RESULTS: Individuals in group 1 with depression were predominantly women and had a higher prevalence of coronary artery disease and diabetes mellitus. Group 1 individuals with depression had longer QTc duration (no depression versus depression, 389.3 [27.0] versus 401.1 [32.9] milliseconds; p < .001) and percentage of abnormal QTc (no depression versus depression, 2.0% versus 10.8%; p = .001) compared with those without depression. Elderly individuals (group 2) had similar values of QTc and percentage of abnormal QTc irrespective of depression status. Even after adjustment for known QT-prolonging factors, the presence of depression in younger individuals was associated with an increased QTc by 11.1 milliseconds and with an approximately 10.6-fold higher prevalence of abnormal QTc duration. CONCLUSIONS: Depression was associated with a longer QTc interval especially in individuals younger than 65 years. These findings may indicate an interrelationship between depression and autonomic dysregulation as potential risk factors for cardiovascular disease and sudden cardiac death.

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Brugada syndrome (BrS) is a complex arrhythmogenic disease displaying electrical and micro-structural abnormalities mainly located at the epicardium of the right ventricular outflow tract (RVOT). It is well-known that fibrosis, fatty infiltration, inflammation and reduced gap junction expression have been demonstrated at the epicardial anterior aspect of the RVOT providing the arrhythmogenic substrate for ventricular arrhythmic events in BrS. A number of models have been proposed for the risk stratification of patients with BrS. Endocardial unipolar electroanatomical mapping is an emerging tool that has been reintroduced to identify and quantify epicardial electrical abnormalities. Interestingly, current findings correlate the presence of large-sized endocardial unipolar electroanatomical abnormalities with either ventricular fibrillation inducibility during programmed ventricular stimulation or symptom status. This review aims to present existing data about the role of endocardial unipolar electroanatomical mapping for the identification of RVOT epicardial abnormalities as well as its potential clinical implications in risk stratification of BrS.

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Although mitral valve prolapse (MVP) is usually considered a benign clinical condition, it has been linked with ventricular arrhythmias and sudden cardiac death in patients with a certain "arrhythmic" phenotype, raising awareness and mandating a specific risk stratification protocol. Mitral annular disjunction (MAD) is considered a "red flag" in malignant MVP syndrome along with bileaflet myxomatous prolapse, female gender, negative or biphasic T waves in the inferior leads, fibrosis in the papillary muscles or inferobasal wall detected by cardiac magnetic resonance imaging and complex arrhythmias of right bundle branch morphology. MAD seems to play a critical role in the chain of morphofunctional abnormalities which lead to increased mechanical stretch and subsequent fibrosis mainly in the papillary muscles, forming the vulnerable anatomic substrate prone to arrhythmogenesis, and associated with long-term severe ventricular arrhythmias. Arrhythmogenesis in MVP/MAD patients is not fully understood but a combination between a substrate and a trigger has been established with premature ventricular contraction triggered ventricular fibrillation being the main mechanism of sudden cardiac death (SCD). Certain characteristics mostly recognized by non-invasive imaging modalities serve as risk factors and can be used to diagnose and identify high risk patients with MAD, while treatment options include catheter ablation, device therapy and surgical intervention. This review focuses on the clinical presentation, the arrhythmogenic substrate, and the incidence of ventricular arrhythmias and SCD in MAD population. The current risk stratification tools in MAD arrhythmogenic entity are discussed.

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BACKGROUND: Electrocardiogram (ECG) is considered the initial screening method for the detection of left ventricular hypertrophy (LVH) despite its low sensitivity. However, there are no data on how ECG criteria for LVH perform in patients with concentric (cLVH) and eccentric LVH (eLVH). METHODS: In the setting of the Corinthia cross-sectional study, ECGs were analyzed in 1,570 participants of the study. Seven ECG LVH criteria were calculated (Sokolow-Lyon voltage, index, and product, sex-specific Cornell voltage and product, Lewis voltage, and the Framingham), whereas LVH was defined, based on echocardiographic data, as left ventricular mass indexed for body surface area (BSA) of at least 125 g/m2 in men and at least 110 g/m2 in women. RESULTS: Regarding the frequency encountered for each ECG LVH criterion, there was no difference between eLVH and cLVH. However, when ECG criteria were compared as continuous variables between LVH groups, Cornell voltage and product were higher in cLVH individuals, with a value of Cornell voltage >13.95 mV having 61% sensitivity and 62% specificity to differentiate cLVH from eLVH (p = .05). Even after adjustment for age, sex, body mass index, and hypertension, the occurrence of Cornell voltage or product increased the odds of cLVH by 1.6 times (p = .001). CONCLUSION: Cornell voltage and product criteria disclosed a superior discriminative ability for the detection of LVH via ECG. When further categorizing LVH as concentric and eccentric, Cornell product depicted the higher discriminative ability for cLVH.

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