Cardiac tamponade is a life-threatening condition classically associated with compensatory sinus tachycardia due to impaired diastolic filling and reduced cardiac output; however, paradoxical sinus bradycardia is rare and may delay recognition. We report a case of a 43-year-old woman with obesity status post gastric sleeve, asthma, and hyperlipidemia who presented with two weeks of progressive dyspnea, pleuritic chest pain, and chest tightness following a suspected viral syndrome, with symptoms worsening supine and improving when leaning forward. Initial evaluation demonstrated muffled heart sounds, sinus rhythm with electrical alternans on electrocardiography, cardiomegaly on chest radiography, and a large pericardial effusion on point-of-care ultrasound without initial tamponade physiology. While awaiting further workup, she developed recurrent syncope with profound sinus bradycardia and transient pulselessness requiring vasopressor support. Transthoracic echocardiography revealed right atrial compression and right ventricular diastolic collapse consistent with acute cardiac tamponade. Urgent pericardiocentesis drained 1.3 liters of bloody, turbid fluid with immediate resolution of bradycardia and hemodynamic instability. Pericardial fluid analysis was exudative with inflammatory cells, and there was no evidence of malignancy. The patient was successfully treated with high-dose aspirin and colchicine without recurrence. Notably, the absence of compensatory tachycardia in this case contributed to delayed clinical recognition of tamponade physiology. This case highlights that cardiac tamponade may rarely present with paradoxical sinus bradycardia rather than tachycardia, underscoring the importance of maintaining clinical suspicion and performing prompt echocardiographic assessment, as urgent pericardial drainage can be life-saving even in nonclassical presentations.

Brugada syndrome (BrS) is an inherited cardiac disorder associated with and increased risk of sudden cardiac death. The syndrome is associated with a complex current distribution and repolarization dispersion. The traditional methods for the diagnosis rely on standard electrocardiographic (ECG) assessment of the cardiac dynamics. Recent advancements in magnetocardiography suggest that the magnetic-field based investigation of cardiac electrophysiology could offer novel perspectives for the investigation of current abnormalities in BrS patients which go beyond the conventional ECG capabilities to capture intricate current distributions. In this work, we propose a framework for the magnetic analysis of action potential disturbances in Brugada syndrome. We exploit a 1D reduced-order cable geometry for analyzing the relation between the pathological electrical activity in saddleback and coved type BrS and the corresponding magnetic field. Also, we compute transmural pseudo-magnetocardiograms and demonstrate their capabilities of detecting both types of BrS. Overall, our result highlight the potential of magnetic-field oriented investigation of cardiac disturbances related to BrS.

Left bundle branch area pacing (LBBAP) is now a common implantation strategy for both pacing and resynchronization based device therapies. While LBBAP has been (somewhat paradoxically) demonstrated to be effective in cases of preexisting left bundle branch (LBB) block, and criteria for LBB capture have been established; minimal focus has been towards the intrinsic refractory rate of the LBB. Herein, we demonstrate a case of LBBAP rate exceeding the refractory period of the LBB, resulting in alternating LBBAP capture and non-selective septal pacing. Implicit understanding of this physiology has important sequel for accurate assessment of lead placement during implantation.

Beat-to-beat variability of the QT interval (QTV) is a well-established marker of cardiac health, with increased QTV (>5 ms) often associated with a higher risk of arrhythmias. However, the underlying mechanisms contributing to this phenomenon remain poorly understood. Recently, we showed that cardiac instability is a major cause of QTV. Early afterdepolarizations (EADs) are abnormal electrical oscillations that occur during the plateau phase of the cardiac action potential (AP), often arising when the membrane potential becomes unstable. In this study, we use a physiologically detailed computational model of rabbit ventricular myocytes with stochastic ion channel gating to investigate the relationship between QTV and EAD propensity. We found that increased AP duration (APD) variability, which serves as a surrogate for QTV on the electrocardiogram at the single-cell level, can arise even in the absence of apparent EADs, driven by intrinsic dynamical instability. As the cellular state approaches the threshold for EAD generation, small perturbations in membrane voltage are amplified, leading to increased APD variability. The phase-plane analysis in the voltage-calcium channel inactivation space demonstrates that proximity to the EAD-generating basin of attraction strongly influences repolarization variability, establishing a mechanistic link between QTV and EAD propensity. Furthermore, we observed that QTV increases at longer pacing cycle lengths (PCLs), distinguishing it from alternans-associated APD variability, which increases at shorter PCLs. These findings suggest that increased QTV may serve as an early indicator of arrhythmic risk before the manifestation of EADs, potentially offering a critical window for preventive intervention. Our results provide novel insights into the fundamental mechanisms underlying QTV and its potential role in arrhythmia prediction.

Metabolic syndrome (MetS) has been associated with an increased prevalence of cardiac arrhythmias and sudden cardiac death caused by ventricular fibrillation (VF), but the exact underlying mechanisms are not known. Our aim here was to study the effects that diet-induced MetS produces on ventricular remodelling and its potential electrophysiological arrhythmogenic mechanisms. Thirty-five male NZW rabbits were assigned to a control (n = 16) or MetS group (n = 19), fed for 28 weeks with a high-fat and high-sucrose diet. Echocardiography and electrocardiography were performed before diet and at weeks 14 and 28. Hearts were isolated and perfused in a Langendorff system and epicardial optical mapping was performed using two EMCCD cameras focused on the left (LV) and right (RV) ventricles. mRNA expression levels for ion channel proteins were examined by quantitative RT-PCR. A mixed-model ANOVA and unpaired t test were used for statistical analysis. MetS animals showed LV hypertrophy and electrophysiological abnormalities (increased PQ, QRS, QTc and T wave). In isolated hearts, MetS animals had shorter optical APD90 (action potential duration at 90% repolarization), increased restitution slope and alternans, and faster frequency of activation during VF in the RV, whereas no difference was observed in the LV. The mRNA expression for KvLQT1 and KChIP2 increased in the RV. MetS produced LV hypertrophy, and altered atrioventricular and ventricular conduction and repolarization abnormalities. In isolated hearts, the physiological gradients of refractoriness and frequency of activation during VF were abolished in MetS animals, with fast activation rates in both ventricles, which could be explained, at least in part, by upregulation of KvLQT1 and KChIP2 in the RV. KEY POINTS: Metabolic syndrome (MetS) has been associated with ventricular arrhythmias and sudden cardiac death, but the exact underlying mechanisms are not known. Previous studies have addressed the effects that individual components of MetS exert, individually, upon electrical cardiac remodelling, but the results obtained in some cases prove inconclusive or contradictory. We investigated the effects of diet-induced MetS on ventricular remodelling and its potential electrophysiological arrhythmogenic mechanisms. We found that diet-induced MetS produced altered activation-repolarization abnormalities as well as fast-activation non-stable flattening of the spatial distribution of dominant frequencies driving ventricular fibrillation, which might be explained, at least in part, due to increased expression of potassium channels in the right ventricle.

Dexmedetomidine (DEX) is commonly used in clinical practice because of its sedative, analgesic, antisympathetic, hemodynamic stabilization and antianxiety effects. Previous clinical studies have demonstrated that DEX plays a role in both the prevention and treatment of perioperative arrhythmias. However, the precise mechanisms underlying the effects of DEX remain unclear. Furthermore, few studies have examined the effect of DEX on cardiac electrophysiology. ECG recording was performed in vivo and ex vivo on C57 mice. Simultaneous recording of membrane voltage (Vm) and [Ca2+]i changes was achieved with dual-dye optical mapping, in which voltage- and Ca2+-sensitive dyes are employed. Simultaneous programmed electrical stimulation was used to pacing and induce arrhythmias. Simulating catecholamine-induced arrhythmias with isoprotereno (ISO) and preconditioning with DEX to investigate the antiarrhythmic effects of DEX. Our findings demonstrated that ISO increased the incidence of ventricular tachycardia or ventricular fibrillation in mice during rapid pacing stimulation. DEX preconditioning reduced the incidence of ISO-induced ventricular arrhythmias. Optical mapping with simultaneous recordings of dual dyes (Vm dye and intracellular Ca2+ dye) revealed that DEX pretreatment attenuated the ISO-induced shortening of action potential duration (APD), calcium transient duration (CaTD), and time-to-peak (TTP) of calcium transients, as well as the ISO-induced increase in repolarization heterogeneity. DEX also slowed the conduction velocity. More importantly, DEX preconditioning significantly reduced the calcium transient alternans ratio at 80-ms, 70-ms, and 60-ms pacing cycles. These findings suggest that DEX preconditioning can reduce the incidence of ventricular arrhythmias induced by acute stress simulated by ISO. Prolongation of action potential duration and calcium transient duration and the maintenance of intracellular calcium homeostasis may be the electrophysiological mechanisms involved.

Background and Objectives: Chronic heart failure (CHF) caused by ischemic heart disease (IHD) is the leading cause of death worldwide and presents significant health challenges. Effective management of IHD requires prevention, early detection, and treatment to improve patient outcomes. This study aims to expand the diagnostic utility of various 24 h Holter ECG parameters, such as T-wave alternans (TWA), late ventricular potentials (LVPs), and heart rate variability (HRV) in patients with CHF caused by IHD. Additionally, we seek to explore the association between these parameters and other comorbid conditions affecting the prognosis of CHF patients. Materials and Methods: We conducted a prospective case-control study with 150 patients divided into two subgroups: 100 patients with CHF caused by IHD, and 50 patients in the control group. Data included medical history, physical examination, laboratory tests, echocardiography, and 24 h Holter monitoring. Results: Our comparative analysis demonstrated that both TWA and LVPs were significantly higher in patients with CHF compared to the control group (p < 0.01), indicating increased myocardial electrical vulnerability in CHF patients. Both time and frequency-domain HRV parameters were significantly lower in the CHF group. However, the ratio of NN50 to the total count of NN intervals (PNN50) showed a borderline significance (p = 0.06). While the low-frequency (LF) domain was significantly lower in CHF patients, the high-frequency (HF) domain did not differ significantly between groups. Acceleration and deceleration capacities were also significantly altered in CHF patients. Categorizing CHF patients by left ventricular ejection fraction (LVEF) revealed that the mean of the 5-min normal-to-normal intervals over the complete recording (SDNN Index) was significantly higher in patients with LVEF ≥ 50% compared to those with CHF with reduced EF and CHF with mildly reduced EF (p < 0.001), whereas the other HRV parameters showed no significant differences among the groups. Conclusions: Holter ECG parameters can become a reliable tool in the assessment of patients with CHF. The integration of multiple Holter ECG parameters, such as TWA, LVPs, and HRV, can significantly enhance the diagnostic assessment of CHF caused by IHD. This comprehensive approach allows for a more nuanced understanding of the patient's condition and potential outcomes.