Supernormal phenomena are uncommon findings in routine electrocardiographic evaluation, and both their electrophysiological substrate and their clinical significance remain controversial. We present two cases with electrocardiographic tracings consistent with supernormal excitability in a patient with a dysfunctional epicardial pacemaker, and supernormal conduction in another patient with complete atrioventricular block. In addition to their unexpected nature, both phenomena share a common electrophysiological substrate, which is thought to be mediated, at least in part, by the availability of functional Na + channels during the terminal portion of phase 3 of repolarization, known as the supernormal phase.
BACKGROUND:Inferior ST-segment elevation (STE) may accompany anterior myocardial infarction (MI) and is traditionally attributed to wraparound left anterior descending (LAD) anatomy with inferior-wall injury. Whether the spatial orientation of the resulting electrical field also contribute remains uncertain. We investigated the anatomical and cardiac magnetic resonance (CMR)-defined myocardial substrate of concomitant inferior STE. METHODS:This exploratory pilot analysis included patients with first anterior STEMI who underwent successful primary percutaneous coronary intervention and CMR within 1 week. Patients were classified by the presence of STE in all three inferior leads. LAD anatomy was categorized into four types according to distal extent, and CMR was used to assess regional edema, late gadolinium enhancement (LGE), and infarct size. RESULTS:Sixty-eight patients were included; seven (10.3%) had inferior STE. Basal/mid anterior edema was less frequent in patients with inferior STE (57.1% vs 90.2%; odds ratio, 0.15; 95% confidence interval, 0.03-0.81; P = 0.044). No patient with inferior STE had basal/mid inferior edema and LGE, whereas apical inferior involvement was common. LADs reaching or extending beyond the apex (types III-IV) were more frequent with inferior STE (85.7% vs 42.4%; P = 0.045), whereas type IV anatomy specifically supplying the basal/mid inferior wall was not (28.6% vs 20.3%; P = 0.634). CONCLUSIONS:In this small exploratory cohort, inferior STE accompanying anterior MI was associated with a regional injury pattern characterized by less basal/mid anterior involvement and without detectable basal/mid inferior extension. These findings are compatible with a contribution of spatial injury distribution to inferior‑lead STE but larger prospective studies are needed.
A 63-year-old woman with sick sinus syndrome and recurrent syncope underwent left bundle branch area pacing lead implantation using a continuous pacing and recording technique. Multicomponent local ventricular electrograms were observed during left ventricular septal pacing, nonselective left bundle branch pacing, and selective left bundle branch pacing, challenging the specificity of discrete electrograms for selective capture. Potential mechanisms included overlapping potentials from distinct septal sources and far-field contributions. These findings suggested that selective left bundle branch capture should be confirmed through comprehensive unipolar threshold testing and systematic analysis of output-dependent electrophysiological transitions rather than electrogram morphology alone.
BACKGROUND:Electrocardiographic (ECG) abnormalities are a hallmark of transthyretin amyloid cardiomyopathy (ATTR-CM), yet longitudinal ECG changes under disease-modifying therapy remain poorly characterized. METHODS:In this retrospective multicenter study, 140 patients with confirmed ATTR-CM receiving tafamidis underwent serial 12‑lead ECG assessment at baseline and after one year. ECG parameters were analyzed in relation to biomarker-based disease stage, clinical progression, and all-cause mortality. Longitudinal ECG changes were evaluated using Wilcoxon signed rank and McNemar tests. Survival analyses were conducted using Kaplan-Meier estimates and univariable Cox regression. RESULTS:At baseline, PR interval, QRS duration, and QTc were significantly associated with advanced disease stage, whereas QRS voltage and heart rate were not. During follow-up, patients showed clinical progression with worsening functional status despite stable biomarker-based disease stage. Serial ECG assessment demonstrated ongoing electrical remodeling with significant QRS prolongation (109 vs. 114 ms, p < 0.001), increasing conduction disturbances, and a doubling of pacemaker stimulation. These changes occurred independently of disease stage and were confirmed in patients without pacemaker-stimulated rhythm. Longitudinal changes in QRS voltage were inconsistent and depended on the analytic approach. Baseline QRS duration ≥120 ms and markedly prolonged PR interval (>220 ms) were associated with adverse outcome, whereas longitudinal ECG changes were not independently associated with mortality. CONCLUSIONS:In ATTR-CM, baseline conduction abnormalities - but not longitudinal ECG changes - were associated with adverse outcomes. Despite tafamidis therapy, ECG abnormalities continued to progress, predominantly reflecting ongoing conduction system involvement independent of biomarker-based disease stage, suggesting that serial ECG assessment may complement disease monitoring rather than risk stratification.
Left-sided concealed accessory pathways (LCAPs) are a common cause of paroxysmal supraventricular tachycardia (PSVT) treated with radiofrequency ablation (RFA); however, the inferoposterior myocardial bundle, myocardial sleeve connections between the left atrium and coronary sinus (LA-CS), and the creation of mitral isthmus block (MIB) can complicate the procedure by inducing complex electrophysiological changes. We report a case of a 29-year-old male with an LCAP who developed a functional MIB during RFA, which was characterized by dual-component potentials within the LA-CS myocardial sleeves and dynamic shifts in the retrograde atrial activation sequence. Initial ablation via a retrograde aortic approach at the 3 o'clock position on the mitral annulus modified the activation pattern without eliminating the pathway. Subsequent transseptal remapping localized the effective target at the 1 o'clock position, where ablation successfully produced ventriculoatrial dissociation. The patient had no PSVT recurrence at one-year follow-up. These findings are consistent with the presence of multiple LA-CS electrical connections and clarify how a functional MIB can modulate atrial activation by altering breakthrough sites. Recognizing these electrophysiological patterns and promptly considering a functional MIB in cases of unexpected activation changes are essential for optimizing outcomes in complex LCAP ablations.
BACKGROUND:Standard 12‑lead electrocardiograms (ECGs) use a 0.05 Hz high-pass filter, while continuous bedside monitoring systems commonly employ higher filter settings (≥0.5 Hz) to reduce baseline wander. Building upon foundational studies of filter-induced artifact, we aimed to apply modern parametric modeling to quantify the magnitude, anatomical distribution, and clinical determinants of this phenomenon. METHODS:We conducted a repeated-measures analysis of 150 patients referred for electrophysiology study. Standard 12‑lead ECGs were analyzed using four high-pass filter settings: 0.05 Hz, 0.1 Hz, 0.5 Hz, and 1.0 Hz. Linear mixed-effects models assessed the effects of filter frequency and baseline QRS morphology on ST-segment deviation. Logistic regression was used to determine the odds of clinically significant false-positive ST elevation (≥1.0 mm). RESULTS:Increasing high-pass filter frequency produced significant, frequency-dependent ST-segment elevation, with a pronounced "ceiling effect" occurring at the standard telemetry default of 0.5 Hz. The artifact was anatomically selective, predominantly affecting the right precordial leads (maximum increase at 1.0 Hz: V1 + 0.51 mm, V2 + 0.80 mm; both p < 0.001), while limb leads were minimally affected (Lead I + 0.09 mm, Lead II +0.19 mm). An R/S ratio < 1 in the right precordial leads significantly amplified artifact magnitude at 1.0 Hz. Use of a 1.0 Hz filter independently increased the odds of false-positive ST elevation ≥1.0 mm nearly ten-fold in V1 (OR: 9.14, 95% CI: 4.16-20.11; p < 0.0001) and five-fold in V2 (OR 4.96, 95% CI 2.87-8.58; p < 0.001). CONCLUSIONS:High-pass filter settings ≥0.5 Hz induce substantial, anatomically selective ST-segment elevation, highlighting the need for caution when interpreting ST segments on bedside monitoring systems.
BACKGROUND:Rapid and accurate exclusion of acute coronary syndrome (ACS) in patients presenting with chest pain remains a major clinical challenge. Deep learning models applied to the 12‑lead electrocardiogram (ECG) may improve diagnostic efficiency, yet multicenter validation data remain limited. METHODS:We conducted a prospective, multicenter diagnostic accuracy study enrolling 6743 consecutive adults presenting to five emergency departments with suspected ACS between January 2020 and December 2023. Patients with ST-elevation myocardial infarction were excluded. A deep learning ECG (DL-ECG) model based on a residual convolutional neural network was developed using nested five-fold stratified cross-validation. Model performance was compared against emergency physician clinical assessment (Standard Care) and the HEART score using the 30-day adjudicated ACS diagnosis as the reference standard. RESULTS:Among 6743 patients (mean age 61.9 years; 59.8% male), 1099 (16.3%) received an ACS diagnosis within 30 days. The DL-ECG model achieved an area under the receiver operating characteristic curve (AUC) of 0.954 (95% CI, 0.948-0.960), significantly exceeding Standard Care (0.921; P < 0.001) and the HEART score (0.876; P < 0.001). At matched sensitivity of 97.5%, the DL-ECG model demonstrated superior specificity (0.746 vs. 0.568 and 0.354) and negative predictive value (0.994 vs. 0.992 and 0.987). Performance was consistent across demographic subgroups and study centers. CONCLUSIONS:A deep learning model analyzing the standard 12‑lead ECG significantly outperformed both clinical assessment and the HEART score for ruling out ACS. If validated prospectively, this approach could facilitate earlier discharge of low-risk patients.
BACKGROUND:Left bundle branch area pacing (LBBAP) may restore a more physiological pattern of ventricular activation in patients with conduction delay; however, QRS narrowing alone may incompletely characterize electrical resynchronization. Ultra-high-frequency ECG (UHF-ECG) provides quantitative markers of ventricular activation timing and dyssynchrony. OBJECTIVE:To quantify paired OFF-to-ON changes in conventional ECG and UHF-ECG metrics during LBBAP in patients with baseline wide QRS and to assess the relationship between paced R-wave peak time (RWPT) and residual UHF-ECG dyssynchrony. METHODS:In this prospective single-center paired study, 21 patients with bradycardia and baseline wide QRS underwent standard ECG and UHF-ECG assessment during intrinsic rhythm (pacing OFF) and during LBBAP (pacing ON). Endpoints included QRS duration, signed VED16, absolute VED16 (|VED16|), mean ventricular delay (meanVD), and a clinically interpretable distance-to-normal metric defined as dist = max(|VED16|-20, 0). Paired changes were summarized as medians with bootstrap 95% confidence intervals and tested using the Wilcoxon signed-rank test. Associations between paced RWPT and residual dyssynchrony during pacing were evaluated using Pearson and Spearman correlation coefficients. RESULTS:LBBAP significantly narrowed QRS duration from 136.8 [130.2-153.6] ms during intrinsic rhythm to 116.0 [107.8-125.6] ms during pacing (median Δ -21.0 ms; 95% CI -33.9 to -18.6; p < 0.001). Signed VED16 did not change significantly (median Δ 0.4 ms; p = 1.000), consistent with the mixed conduction-phenotype composition of the cohort. In contrast, severity-oriented UHF-ECG endpoints improved: |VED16| decreased numerically (median Δ -5.2 ms; p = 0.070), whereas dist decreased significantly (median Δ -0.7 ms; 95% CI -14.4 to 0.0; p = 0.015). The proportion of patients within the normal dyssynchrony band (|VED16| ≤ 20 ms) increased from 7/21 (33.3%) to 12/21 (57.1%). Median paced RWPT was 66.6 [58.6-74.6] ms, and shorter RWPT correlated with lower residual |VED16| during pacing (Pearson r = -0.45, p = 0.038). CONCLUSIONS:In patients with baseline wide QRS, LBBAP produces marked QRS narrowing, whereas UHF-ECG provides complementary quantification of residual electrical dyssynchrony. Severity-oriented UHF-ECG endpoints, particularly a distance-to-normal metric, may offer an interpretable mechanistic framework beyond conventional ECG alone. Shorter paced RWPT was associated with lower residual dyssynchrony during pacing, supporting physiological coherence between procedural and high-resolution electrocardiographic markers.
BACKGROUND:The V2 - V1 Precordial Bipolar Lead (PBL) selectively evaluates the right-to-left retrosternal axis and has shown diagnostic value beyond the standard 12‑lead electrocardiogram. However, its use has been limited by the need for raw electrocardiographic data and post-processing software. This study evaluated whether a simple physical reconfiguration of limb electrodes could reproduce the digitally derived V2 - V1 morphology with sufficient accuracy for clinical application. METHODS:Thirty-seven subjects underwent two sequential 10-s 12‑lead recordings using a Cardiovit FT-1 electrocardiograph sampled at 1000 Hz. In the standard recording, the digital PBL was calculated as V2 - V1. In the second recording, the right-arm and left-arm electrodes were repositioned to the V1 and V2 sites so that Lead I directly recorded the retrosternal dipole. Signals were filtered, synchronized, and analyzed using median beats. Morphological agreement was assessed with Pearson correlation on Z-normalized signals, while absolute agreement was evaluated using Lin's concordance correlation coefficient (CCC), intraclass correlation coefficient (ICC (Lewis, 1931; Nehb, 1938 [1,2])), root mean square error (RMSE), and Bland-Altman analysis. RESULTS:Mean Pearson correlation between digital and physical PBL was 0.955 (SD 0.043), with segment-specific correlations of 0.953 (SD 0.054) for QRS and 0.967 (SD 0.052) for ST-T. Lin's CCC and ICC(2,1) were both 0.871 (SD 0.110), and RMSE was 0.091 (SD 0.049) mV. Bland-Altman analysis showed minimal bias (-0.008 mV). CONCLUSIONS:Physical acquisition of the V2 - V1 PBL achieved high agreement with the digitally derived signal, supporting a simplified analog method for broader clinical implementation.
An apparently irregular rhythm was observed on bedside monitoring in a 32-week preterm infant receiving high-flow nasal cannula support during kangaroo care. The single‑lead ECG tracing demonstrated alternating QRS morphologies, initially raising concern for neonatal arrhythmia. Closer inspection revealed two independent rhythms with different cycle lengths, one representing incomplete monitor detection of the infant's underlying sinus rhythm and the other representing a second rhythm with distinct morphology. After repositioning the infant and adjusting the respiratory interface, the abnormal complexes disappeared and the heart rate increased. The tracing illustrates an important pitfall in neonatal ECG interpretation, where maternal cardiac signals may be detected by neonatal monitoring electrodes during skin-to-skin contact, mimicking arrhythmia.
BACKGROUND:Posterior/inferolateral myocardial ischemia is frequently underrecognized on standard 12‑lead electrocardiography (ECG). Synthesized posterior leads derived from the standard 12‑lead ECG have been proposed as an alternative to directly measured posterior leads; however, their accuracy under controlled ischemic conditions has not been fully validated. METHODS:We prospectively enrolled 26 consecutive patients undergoing percutaneous coronary intervention (PCI) in whom simultaneously recorded measured and synthesized posterior lead ECGs (V7-V9) were obtained during balloon-induced myocardial ischemia. ST-segment deviation was measured at the ST junction (STJ), 40 ms (ST1), and 80 ms (ST2) thereafter. Agreement between measured and synthesized posterior leads was assessed using Pearson correlation and Bland-Altman analyses. As an exploratory patient-level analysis, diagnostic performance was compared with reciprocal anterior ST-segment depression (V1-V4). RESULTS:Strong correlations were observed between measured and synthesized posterior lead ST-segment deviations (V7: r = 0.89; V8: r = 0.86; V9: r = 0.83; all P < 0.001). Bland-Altman analysis demonstrated minimal systematic bias (within ±0.004 mV) and narrow limits of agreement. Synthesized posterior leads showed higher diagnostic performance than reciprocal anterior ST-segment depression (AUC 0.917 vs. 0.708), although the difference was not statistically significant (DeLong test, P = 0.197). Using a 0.05 mV threshold, synthesized posterior leads demonstrated 83.3% sensitivity, 100% specificity, and 96.2% overall accuracy. CONCLUSIONS:Synthesized posterior leads closely reproduced measured posterior lead ST-segment deviations during percutaneous coronary intervention (PCI)-induced myocardial ischemia, supporting the technical validity of posterior lead reconstruction. Larger prospective studies are warranted to determine whether synthesized posterior leads provide incremental diagnostic value beyond careful interpretation of the standard 12‑lead ECG.
Background The corrected QT interval (QTc) is obtained through automated ECG computations or manual physician measurements. We hypothesized that differences exist in children between the measured and automated QTc intervals within and between Healthy and hypertrophic cardiomyopathy (HCM) subjects with greater differences for HCM due to structural abnormalities. Methods QT measurements - Bazett correction- automated (aQTc) and measured (mQTc), were extracted from the GE MUSE database for 385 Healthy pediatric (single ECG) and 208 HCM subjects (2 ECGs), stratified by age < 12 and ≥ 12 yrs., sex, race, and ethnicity. QTc means (SD), automated and measured differences, and the difference of the differences of aQTc and mQTc were analyzed overall and by subgroups. All ECGs were read by one pediatric cardiologist with a second cardiologist reading a random subset of HCM ECGs to evaluate intraclass correlations and agreement. Results The mQTc intervals were shorter than aQTc intervals within Healthy (p < 0.001) and within first HCM ECGs (p < 0.001) with both aQTc and mQTc shorter in Healthy than HCM (p < 0.001). The difference in these differences was significant overall using HCM ECG 1 but not HCM ECG 2. Healthy subject aQTc and mQTc intervals differed by age, sex, and race (p < 0.002). HCM ECG 1 aQTc- mQTc intervals differed for age < 12 yrs., as well as by sex and race. HCM ECG 2 intervals differed only for age < 12 yrs. Conclusions Compared to measured values, automated QTc values were significantly longer in both Healthy and HCM subjects. Automated measurements may overestimate the QTc.
A 60-year-old gentleman with severe left ventricular systolic dysfunction, multivessel coronary artery disease, and chronic kidney disease presented with New York Heart Association (NYHA) class III breathlessness without any history of syncope or presyncope. The electrocardiogram (ECG) showed sinus rhythm with alternating bundle branch block and a variable PR interval. This was most likely due to consistent conduction delay through the left anterior and posterior fascicles, with intermittent conduction delay or block in the right bundle branch. The patient subsequently underwent dual chamber permanent pacemaker implantation, with the ventricular lead placed at left bundle branch area.
P-wave indices derived from the surface electrocardiogram are increasingly used as markers of atrial cardiomyopathy and predictors of atrial fibrillation and stroke. Their widespread adoption has been driven by automated ECG analysis, enabling large-scale studies and integration into clinical workflows. However, this expansion has occurred without sufficient scrutiny of the methodological assumptions underlying automated measurement and interpretation. In this review, the current approaches to P-wave analysis are reviewed with focus on the most common P-wave indices used in large-scale studies, the issues associated with the use of fully automatic ECG processing, inconsistent definitions, the use of fixed thresholds, and analytical treatment of inherently non-linear variables as continuous measures. These limitations hamper the validity and reproducibility of findings and may hinder their clinical translation, thus highlighting the need for a shift toward physiologically informed, integrative approaches that move beyond rigid thresholds and isolated indices.
Background Permanent pacemakers and cardiac implantable electronic devices have become integral to contemporary cardiology practice. Despite advances in remote monitoring and intracardiac electrograms, the surface electrocardiogram remains the critical bedside tool for assessing device function, particularly during symptomatic presentations or emergencies. However, modern pacing modalities—including cardiac resynchronization therapy and conduction system pacing—have substantially increased ECG complexity, creating interpretive challenges for clinicians and trainees. Objective This review, the first in a two-part series, aims to provide a systematic framework for pacemaker ECG interpretation that remains applicable across device platforms, vendors, and evolving pacing practices. Summary We propose a three-step approach integrating timing assessment, morphological pattern recognition, and malfunction detection. First, we explain the fundamental timing logic of pacemakers—escape, inhibition, and triggering—and how these principles manifest on the surface ECG across single-chamber and dual-chamber modes. Second, we describe the characteristic QRS morphologies associated with different pacing sites, including conventional right ventricular pacing, biventricular pacing, His-bundle pacing, and left bundle branch area pacing. Third, we outline the ECG recognition of basic malfunctions: failure to pace, failure to capture, undersensing, and oversensing. Conclusions Modern paced ECG interpretation requires understanding timing logic as the foundation for recognizing normal device behavior and detecting malfunction. This approach helps clinicians distinguish appropriate device function from true malfunction across single-chamber, dual-chamber, CRT, and conduction system pacing.
