The traditional electrocardiographic diagnosis of left ventricular hypertrophy (LVH) rests on the Voltage Paradigm, which assumes a linear relationship between QRS amplitude and left ventricular mass. High-resolution cardiac imaging has exposed fundamental anomalies in this framework: most patients with anatomic LVH have normal QRS amplitudes, while many with high amplitudes have normal mass. These discrepancies arise from non-spatial determinants-conduction velocity, fibrosis, cell-to-cell coupling and thoracic conductivity-that the linear model cannot accommodate. We propose replacing the term 'ECG-LVH' with Left Ventricular Electrical Remodeling (LVER), a framework endorsed by the International Society of Electrocardiology and the International Society for Holter and Noninvasive Electrocardiology encompassing four phenotypes: high QRS amplitude, conduction delay, low QRS amplitudes and QRS fragmentation. Each phenotype reflects a specific electrophysiological substrate carrying prognostic information independent of mass. LVER reframes the clinical task as electrical risk phenotyping.

A 70-year-old man with a history of prior ablation for atrial fibrillation presented with atrial tachycardia (AT). Electrophysiological studies revealed roof-dependent and localized-reentrant ATs. During each AT, widespread breakthrough activation was observed just anterior to the low-voltage area on the anterior wall, suggesting that Bachmann's bundle served as an epicardial bypass within the tachycardia circuits. This case highlights the potential role of Bachmann's bundle in the development of ATs in the remodeled left atrium.

BackgroundAmyloid deposition is a key pathologic hallmark of Alzheimer's disease (AD). Since cardiac amyloidosis also involves abnormal amyloid accumulation, shared proteinopathy mechanisms may underlie both conditions.ObjectiveWe investigated whether brain amyloidosis on PET imaging is associated with electrocardiogram (EKG) findings of cardiac involvement by AD pathology.MethodsWe included 191 participants (mean age 66 ± 13.0 years) in our analysis, who underwent amyloid PET imaging and EKG within one year. EKG abnormalities (including low QRS voltage, poor R-wave progression (PRWP), bundle branch block, and sinus bradycardia) were assessed for associations with brain amyloid deposition, quantified in Centiloids, and cognitive function. A subset (n = 164) also underwent [18]F-MK6240 tau PET, and the relationship between these EKG abnormalities and tau deposition was also assessed.ResultsPRWP was associated with greater brain amyloid deposition (coefficient = 45 ± 12.15, p < 0.001) and worse cognition on the Clinical Dementia Rating scale (coefficient = 0.22 ± 0.098, p = 0.027). There was a trend for higher likelihood of cortical tau deposition with PRWP (odds ratio = 3.66, p = 0.05). Sinus bradycardia was associated with higher likelihood of cortical tau deposition (odds ratio = 2.81, p = 0.009). Other EKG abnormalities were not significantly associated with brain amyloid/tau deposition or cognition.ConclusionsPRWP and sinus bradycardia were found to be associated with AD pathology in the brain. These findings warrant further investigation into how cardiac electrophysiologic abnormalities may reflect a possible link between brain and cardiac pathologies or AD-associated cardiac dysfunction.

A 76-year-old outpatient with light-chain monoclonal gammopathy of undetermined significance presented for evaluation of new-onset, nonspecific symptoms. Paraproteinemia remained stable for over 25 years without prior signs of organ manifestation. Physical examination was unremarkable. To complete routine diagnostics, a 12-lead electrocardiogram was performed, demonstrating features suggestive of amyloidosis, including low QRS voltages and an unexplained anterior pseudoinfarction pattern. It contributed to initiating further evaluation, leading to the diagnosis of light-chain cardiac amyloidosis. TAKE-HOME MESSAGE: This case highlights the potential of electrocardiography as an easily accessible tool for increasing suspicion of cardiac complications in long-standing monoclonal gammopathy of undetermined significance, even in clinically inconclusive cases.

Brugada syndrome (BrS) is a rare but potentially life-threatening condition that may lead to sudden cardiac death. Among the causes, dysfunctions of ion channels involved in the cardiac action potential (specifically in SCN5A and SCN10A genes) are particularly significant. Among diagnosed Brugada patients, fever-induced episodes occur in 20-30% of cases. Fever worsens sodium channel dysfunction, as elevated temperature further reduces their conductance. First clinical manifestation of BrS occurs usually during a febrile episode, especially in young people. We performed a multiparametric examination in addition to genetic analysis. We treated a 19-year-old man presenting with subfebrility. During the patient's subfebrile episodes, 12-lead ECG recordings revealed ST-segment elevations in leads V1-V3. Notably, the patient remained asymptomatic. Targeted genetic testing of SCN5A did not reveal any disease-causing variants as an underlying cause of the syndrome, but the temperature-inducing effect was demonstrated. The occurrence of the Brugada type 1 pattern has also been observed at subfebrile episodes, although significantly rarely. This case demonstrates that in susceptible patients, even a relatively mild elevation in body temperature can trigger ion channel dysfunctions. Timely diagnosis and follow-up are important in preserving quality of life and preventing fatal outcomes.