Temporal association of ventricular arrhythmias and respiratory events in heart failure patients with central sleep apnoea.

In contrast to obstructive sleep apnoea, the peak of sympathetic tone in central sleep apnoea occurs during the hyperventilation phase. To explore the temporal association of premature ventricular complex (PVC) burden in the context of the apnoea/hypopnoea-hyperpnoea cycle, the duration of apnoea/hypopnoea was defined as 100 %. We assessed the PVC burden throughout the apnoea/hypopnoea-hyperpnoea cycle during the periods of ±150 % in 50 % increments before and after the apnoea/hypopnoea phase. In this subanalysis of 54 SERVE-HF patients, PVC burden was 32 % higher in the late hyperventilation period (50-100 % after apnoea/hypopnoea) compared to the apnoea/hypopnoea phase.

Curvature-mediated source and sink effects on the genesis of premature ventricular complexes in long QT syndrome.

Premature ventricular complexes (PVCs) are spontaneous excitations occurring in the ventricles of the heart that are associated with ventricular arrhythmias and sudden cardiac death. Under long QT conditions, PVCs can be mediated by repolarization gradient (RG) and early afterdepolarizations (EADs), yet the effects of heterogeneities or geometry of the RG or EAD regions on PVC genesis remain incompletely understood. In this study, we use computer simulation to systematically investigate the effects of the curvature of the RG border region on PVC genesis under long QT conditions. We show that PVCs can be either promoted or suppressed by negative or positive RG border curvature depending on the source and sink conditions. When the origin of oscillation is in the source region and the source is too strong, a positive RG border curvature can promote PVCs by causing the source area to oscillate. When the origin of oscillation is in the sink region, a negative RG border curvature can promote PVCs by causing the sink area to oscillate. Furthermore, EAD-mediated PVCs are also promoted by negative border curvature. We also investigate the effects of wavefront curvature and show that PVCs are promoted by convex but suppressed by concave wavefronts; however, the effect of wavefront curvature is much smaller than that of RG border curvature. In conclusion, besides the increase of RG and occurrence of EADs caused by QT prolongation, the geometry of the RG border plays important roles in PVC genesis, which can greatly increase the risk of arrhythmias in cardiac diseases.NEW & NOTEWORTHY The effects of the curvature or geometry of the repolarization gradient region and wavefront curvature on the genesis of premature ventricular complexes are systematically investigated using computer modeling and simulation. Premature ventricular complexes can be promoted by either positive or negative curvature of the gradient region depending on the source and sink conditions. The underlying mechanisms of the curvature effects are revealed, which provides mechanistic insights into arrhythmogenesis in cardiac diseases.

ECGNet: An Efficient Network for Detecting Premature Ventricular Complexes Based on ECG Images.

BACKGROUND: Preoperative prediction of the origin site of premature ventricular complexes (PVCs) is critical for the success of operations. However, current methods are not efficient or accurate enough. In addition, among the proposed strategies, there are few good prediction methods for electrocardiogram (ECG) images combined with deep learning aspects. METHODS: We propose ECGNet, a new neural network for the classification of 12-lead ECG images. In ECGNet, 609 ECG images from 310 patients who had undergone successful surgery in the Division of Cardiology, the First Affiliated Hospital of Soochow University, are utilized to construct the dataset. We adopt dense blocks, special convolution kernels and divergent paths to improve the performance of ECGNet. In addition, a new loss function is designed to address the sample imbalance situation, whose cause is the uneven distribution of cases themselves, which often occurs in the medical field. We also conduct extensive experiments in terms of network prediction accuracy to compare ECGNet with other networks, such as ResNet and DarkNet. RESULTS: Our ECGNet achieves extremely high prediction accuracy (91.74%) and efficiency with very small datasets. Our newly proposed loss function can solve the problem of sample imbalance during the training process. CONCLUSION: The proposed ECGNet can quickly and accurately realize the multiclassification of PVCs after training with little data. Our network has the potential to be helpful to doctors with a preoperative diagnosis of PVCs. We will continue to collect similar cases and perfect our network structure to further improve the accuracy of our network's prediction.

Exercise-Induced Ventricular Ectopy and Cardiovascular Mortality in Asymptomatic Individuals.

BACKGROUND: The prognosis of exercise-induced premature ventricular contractions (PVCs) in asymptomatic individuals is unclear. OBJECTIVES: This study sought to investigate whether high-grade PVCs during stress testing predict mortality in asymptomatic individuals. METHODS: A cohort of 5,486 asymptomatic individuals who took part in the Lipid Research Clinics prospective cohort had baseline interview, physical examination, blood tests, and underwent Bruce protocol treadmill testing. Adjusted Cox survival models evaluated the association of exercise-induced high-grade PVCs (defined as either frequent (>10 per minute), multifocal, R-on-T type, or ≥2 PVCs in a row) with all-cause and cardiovascular mortality. RESULTS: Mean baseline age was 45.4 ± 10.8 years; 42% were women. During a mean follow-up of 20.2 ± 3.9 years, 840 deaths occurred, including 311 cardiovascular deaths. High-grade PVCs occurred during exercise in 1.8% of individuals, during recovery in 2.4%, and during both in 0.8%. After adjusting for age, sex, diabetes, hypertension, lipids, smoking, body mass index, and family history of premature coronary disease, high-grade PVCs during recovery were associated with cardiovascular mortality (hazard ratio [HR]: 1.82; 95% CI: 1.19-2.79; P = 0.006), which remained significant after further adjusting for exercise duration, heart rate recovery, achieving target heart rate, and ST-segment depression (HR: 1.68; 95% CI: 1.09-2.60; P = 0.020). Results were similar by clinical subgroups. High-grade PVCs occurring during the exercise phase were not associated with increased risk. Recovery PVCs did not improve 20-year cardiovascular mortality risk discrimination beyond clinical variables. CONCLUSIONS: High-grade PVCs occurring during recovery were associated with long-term risk of cardiovascular mortality in asymptomatic individuals, whereas PVCs occurring only during exercise were not associated with increased risk.

Discrete sites of frequent premature ventricular complexes cluster within the infarct border zone and coincide with high frequency of delayed afterdepolarizations under adrenergic stimulation.

BACKGROUND: Sympathetic activation in ischemic heart disease can cause lethal arrhythmias. These often are preceded by premature ventricular complexes (PVCs), which at the cellular level could result from delayed afterdepolarizations. OBJECTIVE: The purpose of this study was to identify and map vulnerable areas for arrhythmia initiation after myocardial infarction (MI) and to explore the link between PVCs and cellular events. METHODS: Anterior-septal wall MI was induced by 120 minutes of coronary occlusion followed by reperfusion (27 MI and 16 sham pigs). After 4 weeks, EnSite™ electroanatomic mapping combined with imaging was performed to precisely locate PVC sites of origin and subsequently record monophasic action potentials. Cardiomyocytes were isolated from different regions to study regional cellular remodeling. Isoproterenol was used as a surrogate for adrenergic stimulation both in vivo and in cardiomyocytes. RESULTS: PVCs originated from the MI border zone (BZ) and occurred at discrete areas with clusters of PVCs within the BZ. At these sites, frequent delayed afterdepolarizations and occasional associated spontaneous action potentials translating to a PVC were present. Cardiomyocytes isolated from the MI BZ exhibited more spontaneous action potentials than cardiomyocytes from remote regions. Sensitivity to adrenergic stimulation was increased in MI, in vivo and in cardiomyocytes. In awake, freely moving MI animals, frequent PVCs, ventricular arrhythmia, and sudden cardiac death occurred spontaneously at moderately elevated heart rates. CONCLUSION: Post-MI, arrhythmias initiate from discrete vulnerable areas within the BZ, where delayed afterdepolarizations, related to increased adrenergic response of BZ cardiomyocytes, can generate PVCs.

Reappraisal of electrocardiographic criteria for localization of idiopathic outflow region ventricular arrhythmias.

BACKGROUND: Electrocardiographic (ECG) criteria have been proposed to localize the site of origin of outflow region ventricular arrhythmias (VAs). Many factors influence the QRS morphology of VAs and may limit the accuracy of these criteria. OBJECTIVE: The purpose of this study was to assess the accuracy of ECG criteria that differentiate right from left outflow region VAs and localize VAs within the aortic sinus of Valsalva (ASV). METHODS: One hundred one patients (mean age 52 ± 16 years; 55 [54%] women) undergoing catheter ablation of right ventricular outflow tract (RVOT) or ASV VAs with a left bundle branch block, inferior axis morphology were studied. ECG measurements including V2 transition ratio, transition zone index, R-wave duration index, R/S amplitude index, V2S/V3R index, V1-3 QRS morphology, R-wave amplitude in the inferior leads were tabulated for all VAs. Comparisons were made between the predicted site of origin using these criteria and the successful ablation site. RESULTS: Patients had successful ablation of 71 RVOT and 38 ASV VAs. For the differentiation of RVOT from ASV VAs, the positive predictive values and negative predictive values for all tested ECG criteria ranged from 42% to 75% and from 71% to 82%, respectively, with the V2S/V3R index having the largest area under the curve of 0.852. Morphological QRS criteria in leads V1 through V3 did not localize ASV VAs. The maximum R-wave amplitude in the inferior leads was the sole criterion demonstrating a significant difference between right ASV, right-left ASV commissure, and left ASV sites. CONCLUSION: ECG criteria for differentiating right from left ventricular outflow region VAs and for localizing ASV VAs have a limited accuracy.

Electrocardiographic and electrophysiological characteristics of idiopathic ventricular arrhythmias with acute successful ablation at the superior portion of the mitral annulus.

BACKGROUND: We sought to identify the electrocardiographic and electrophysiological characteristics of ventricular arrhythmias (VAs), including idiopathic ventricular tachycardia (VT) and premature ventricular contractions (PVCs), with acute successful radiofrequency catheter ablation (RFCA) at the superior portion of the mitral annulus (SP-MA). METHODS AND RESULTS: Among 437 consecutive patients who presented with VAs for RFCA, twenty-six patients with acute successful RFCA at the SP-MA were included in this study. The ratio of the amplitude of the first positive peak (if present) versus the nadir in the unipolar electrogram (EGM) was 0.00-0.03 (0.00) at the acute successful RFCA site. The time interval between the QRS onset and the maximum descending slope (D-Max) in the unipolar EGM (QRS-Uni) was 18.8 ± 13.6 ms. With bipolar mapping, the ventricular QRS (V-QRS) interval was 3.75-17.3 (11) ms, 6 (23.1%) patients showed the earliest V-QRS interval of 0 ms, and the other 20 patients (76.9%) showed a V-QRS interval of 10-54 ms. The RFCA start-to-effect time was 14.1 ± 7.2 s in 23 patients (88.5%). In the remaining 3 patients (11.5%), the mean duration of successful RFCA was not well defined due to the infrequent nature of clinical VAs during RFCA. Early (within 3 days) and late (1-year) recurrence rates were 23.1% (6 patients) and 26.9% (7 patients), respectively. VAs disappeared 3 days later due to delayed RFCA efficacy in 2 patients (7.7%). No complications occurred during the RFCA procedure or the one-year follow-up. CONCLUSIONS: SP-MA VAs are a rare but distinct subgroup of VAs. Bipolar and unipolar EGM features can help to determine the optimal RFCA site, and the QRS-Uni interval may serve as a marker that could be used to guide RFCA.

Catheter ablation of premature ventricular complexes associated with left ventricular false tendons.

BACKGROUND: Clinical studies have suggested that there is a significant correlation between left ventricular (LV) false tendon and premature ventricular complexes (PVCs). OBJECTIVE: This study aimed to investigate the electrophysiological characteristics and the outcome of radiofrequency catheter ablation (RFCA) for this category of PVCs. METHODS: From a total of 2284 patients with idiopathic PVCs who underwent catheter ablation at 6 institutions in China, intracardiac echocardiography (ICE) was used during the procedure in 346 cases; 10 patients (2.9%) with PVCs associated with false tendon were retrospectively reviewed and enrolled in the present study. Activation mapping and pace mapping were performed to localize the origin of PVCs. ICE was used in all patients. If the false tendon was directly visualized and identified, we attempted to identify the distinct relationship with the PVC origin. RESULTS: The PVCs were successfully eliminated by ablation in all patients. The target sites were confirmed to be related to false tendon. The origin of PVCs was located at the attachment of the false tendon to the papillary muscle, LV septum, or LV apex. At the target site, high-frequency Purkinje potentials were observed preceding local ventricular activation in 7 patients. CONCLUSION: LV false tendon can be associated with PVCs, which can be cured by RFCA. An ICE-guided electroanatomical approach should be considered to improve the safety and feasibility of this procedure.

High density intramural mapping of post-infarct premature ventricular contractions and ventricular tachycardia.

BACKGROUND: Spontaneous ventricular premature contractions (PVCs) and ventricular tachycardia (VT) in the acute post infarct milieu is assumed to be due to automaticity. However, the mechanism has not been studied with intramural mapping. OBJECTIVE: To study the mechanism of spontaneous PVCs with high density intramural mapping in a canine model, and to test the hypothesis that post-infarct PVCs and VT are due to re-entry rather than automaticity. METHODS: In 15 anesthetized dogs, using 768 intramural unipolar electrograms, simultaneous recordings were made. After 20 min of stabilization, recordings were made during the first 10 min of ischemia, and activation maps of individual beats were constructed. Acute ischemia was produced by clamping the left anterior descending coronary artery proximal to the first diagonal branch. RESULTS: In all experiments ST-T alternans was present. Spontaneous ventricular beats occurred in five of 15 dogs where the earliest ectopic activity was manifested in the endocardium, well within the ischemic zone. From there, activity spread rapidly along the subendocardium, with endo-to epicardial spread along the non-ischemic myocardium. Epicardial breakthrough always occurred at the border of the ischemic myocardium. In three dogs, delayed potentials were observed, which were earliest at the ischemic epicardium and extended transmurally with increasing delay towards the endocardium, where they culminated in a premature beat. A similar sequence was observed in VT that followed. CONCLUSION: Graded responses that occur with each sinus beat intramurally, when able to propagate from epicardium to endocardium are the mechanism of PVCs and VT in post-infarct myocardium.