Incidence Of Conduction Block Research Articles

Anthracycline-induced arrhythmias in breast cancer therapy: A meta-analysis of single-arm trials.

As of 2020, breast cancer has emerged as the predominant cause of cancer incidence globally. Anthracycline-based chemotherapy serves as a crucial element in the treatment regimen for breast cancer. However, these anthracycline-based drugs are associated with cardiac toxicity. This study represents the first clinical quantitative analysis aimed at accurately determining the incidences of arrhythmia and abnormal electrocardiogram (ECG) changes, thereby providing valuable data to bolster clinical drug usage and monitoring. A systematic search was conducted across multiple databases including CNKI, VIP, Wanfang, PubMed, Embase, Web of Science, and the Cochrane Library. The incidence of combined arrhythmias in breast cancer patients and the associated heterogeneity were calculated using either a random effect model or a fixed effect model. Statistical analysis was performed using STATA16. The study encompassed a total of 37 articles, which included 5705 breast cancer patients undergoing anthracycline treatment. Among these patients, 2257 developed arrhythmias. The meta-analysis revealed that the incidence of anthracycline-associated arrhythmias and abnormal ECG changes in breast cancer patients was 0.41 (0.37, 0.44). Subgroup analysis indicated that the incidence of ST-T segment change was 0.19 (0.15, 0.23), the incidence of conduction block was 0.04 (0.02, 0.05), the incidence of premature beats was 0.09 (0.07, 0.11), and the incidence of atrial fibrillation was 0.04 (0.00, 0.12). Additional results are presented in Table 3. This pioneering study accurately assesses the incidence of arrhythmias in breast cancer patients treated with anthracyclines. The findings provide clinicians with valuable insights into understanding and managing the cardiac toxicity associated with such treatment. Moreover, this study lays the foundation for future research exploring the mechanisms underlying these arrhythmias and potential preventative strategies.

Predictors of permanent pacemaker implantation in aortic valve diseases after TAVI with vitaFlow liberty system.

Permanent pacemaker implantation (PPI) is a known complication in patients with aortic stenosis following transcatheter aortic valve implantation (TAVI). However, there is limited research on TAVI for pure aortic regurgitation (PAR), and more investigation is needed to determine the occurrence of postoperative cardiac conduction block and the need for PPI in this population. Therefore, this retrospective analysis aimed to evaluate the incidence of cardiac conduction block and the necessity of PPI after TAVI in patients with different types of aortic valve disease, including pure aortic stenosis (PAS), aortic stenosis with regurgitation (ASR), and PAR. Clinical data of 100 patients who TAVI were analyzed retrospectively. The incidence of conduction block was assessed, and clinical factors were examined to predict the necessity of PPI. Cardiac conduction block was found to be a common complication following TAVI, particularly in patients with PAR. PAR was identified as an independent risk factor for requiring PPI. Additionally, first-degree atrioventricular block emerged as a sensitive predictor for PPI in patients with PAR. These findings provide valuable insights into the safety and effectiveness of TAVI, which can help enhance patient management and reduce complications.

Third-Degree Atrioventricular Block in Clinically “Silent” Acute Myocardial Infarction

<p><em>Third-degree atrioventricular (AV) block also termed complete heart block is present when there is complete absence of conduction between atria and ventricles. In adults the most common causes are acute myocardial infarction and age-related degeneration of conduction system. Incidence of conduction block is reported to be 25-30 % in the setting of acute myocardial infarction (AMI) and is 2 to 3 times as commonly associated with inferior than anterior infarction. Proper diagnosis involves noninvasive diagnostic tests (12 lead electrocardiogram (ECG), Holter ECG, or stress/exercise ECG).</em></p><p><strong><em>Keywords: third-degree AV block, complete av block, acute myocardial infarction</em></strong></p>

The need for standardization of time- and frequency-domain analysis of body surface electrocardiograms for assessment of the atrial fibrillation substrate

This editorial refers to ‘Measures of spatiotemporal organization differentiate persistent from long-standing atrial fibrillation’ by L. Uldry et al ., on page 1125 Despite some progress in the earlier decades, the current therapy of atrial fibrillation (AF) is still far from being satisfactory. Antiarrhythmic drugs can restore sinus rhythm only during the first few days after onset of the arrhythmia, are unable to effectively prevent recurrence of AF, and their use carries substantial risk of pro-arrhythmia. Catheter or surgical ablation therapy is effective in patients with paroxysmal AF, but its efficacy to cure persistent AF is still under debate. Moreover, AF ablation is afflicted with a number of potentially serious side effects. Preclinical as well as clinical investigations demonstrate that rhythm control therapy is more successful in individuals with low degree of structural remodelling in the atria. Structural heart diseases and AF itself cause cellular hypertrophy, interstitial fibrosis, inflammatory changes, and amyloidosis, which, in turn, lead to progressive electrical uncoupling between muscle bundles and conduction disturbances. Recent direct contact mapping studies in patients with AF have provided evidence that these alterations result in an increased incidence of conduction block and a higher number and smaller size of separate fibrillation waves.1 This enhancement in the complexity of the substrate for AF is regarded as the key mechanism underlying increasing stability of the arrhythmia in structurally remodelled atria.2 Thus, non-invasive tools for the assessment of AF complexity might be of value for better identification of patients in whom sinus rhythm can be restored and successfully maintained. Quantification of the AF substrate by advanced analysis of surface ECGs appears to be a logical step towards non-invasive quantification of the individual degree of electropathological alterations in the atria. The study by Uldry et al 3 . published in this issue of the Journal …

Conduction block in micropatterned cardiomyocyte cultures replicating the structure of ventricular cross-sections

Structural and functional heterogeneities in cardiac tissue have been implicated in conduction block and arrhythmogenesis. However, the propensity of specific sites within the heart to initiate conduction block has not been systematically explored. We utilized cardiomyocyte cultures replicating the realistic, magnetic resonance imaging-measured tissue boundaries and fibre directions of ventricular cross-sections to investigate their roles in the development of conduction block. The Sprague-Dawley neonatal rat cardiomyocytes were micropatterned to obtain cultures with realistic ventricular tissue boundaries and either random or realistic fibre directions. Rapid pacing was applied at multiple sites, with action potential propagation optically mapped. Excitation either failed at the stimulus site or conduction block developed remotely, often initiating reentry. The incidence of conduction block in isotropic monolayers (0% of cultures) increased with the inclusion of realistic tissue boundaries (17%) and further with realistic fibre directions (34%). Conduction block incidence was stimulus site-dependent and highest (77%) with rapid pacing from the right ventricular (RV) free wall. Furthermore, conduction block occurred exclusively at the insertion of the RV free wall into the septum, where structure-mediated current source-load mismatches acutely reduced wavefront and waveback velocity. Tissue boundaries and sharp gradients in fibre direction uniquely determined the evolution, shape, and position of conduction block lines. Our study suggests that specific micro- and macrostructural features of the ventricle determine the incidence and spatiotemporal characteristics of conduction block, independent of spatial heterogeneities in ion channel expression.

Physiological characteristics and cardiac electrophysiology manifested in Minnesota coding of the "desert people" in Taklimakan Desert: study of 224 cases

To study the physiological characteristics and cardiac electrophysiology of the "desert people" in Taklimakan Desert, an isolated population of Uygurs. Two hundred and twenty-four out of the 1030 "desert people", 133 males aged 37.8 +/- 17.5 (15-99) and 91 females aged 34.1 +/- 12.1 (27-85), underwent measurement of height, body weight, waist circumference, and blood pressure. Twelve-lead resting electrocardiogram was obtained and Minnesota coding was conducted. 150 Kariya Uygurs, 76 males aged 50.7 +/- 15.6 (27-85) and 75 females aged 46.6 +/- 11.7 (24-69) were used as controls. The abnormal Minnesota coding rate in the "desert people" as a whole was 46.0%, significantly higher than that of the controls (35.1%, P < 0.05). In the "desert people", the abnormal Minnesota coding rate was 54.9% in the males, significantly higher than that in the females (33.0%, P < 0.05). In the control group, the abnormal coding rate was 28.0% in the females and 42.1% in the males. The ECG high left R amplitude rate (code 3-1, 3-3) of the "desert people" as a whole was 32.6%, significantly higher than that of the controls (12.6%, P < 0.001). Within the "desert people" group, the ECG high left R amplitude rate of the females was 19.8%, significantly lower than that of the males (41.2%, P < 0.005). Within the control group, the ECG high left R amplitude rate of the females was 10.7%, not significantly different from that of the males (14.5%, P > 0.5). The hypertension rate of the "desert people" was 7.6%, significantly lower than that of the controls (36.4%, P < 0.005). The hypertension rate of the "desert people" coded as with left high R amplitude was 12.2%, significantly lower than that of the controls coded as with left high R amplitude (41.6%, P < 0.005). The overweight and obesity rate of the "desert people" was 9.6%, significantly lower than that of the controls (23%, P < 0.005). The arrhythmia (8-1 - 8-8) rate of the "desert people" was 8.92%, not significantly different from that of the controls (6.62%, P > 0.05). The incidence of conduction block (7-1 - 7-8) of the "desert people" was 3.12%, not significantly different from that of the controls (2.64%, P > 0.05). The higher incidence of ECG high left R amplitudes and low prevalence of hypertension in the "desert people" suggest that the high left R amplitude in "Desert people" may be related to their thin chest wall, low BMI, and physiological left ventricular hypertrophy. The "desert people" have more physical work, and less stress and pollution. They have low incidence of congenital heart disease, rheumatic heart disease and hypertension. All these may be associated with a low incidence of arrhythmia.

479 Role of Bachmann's bundle during chronic atrial fibrillation in patients with mitral valve disease

Introduction Animal studies have shown that bachmann's bundle (BB) is essential for development of mukiple reentrant circuits perpetuating atrial fibrillation (AF). Mapping of BB in humans has sofar not been performed. In this study, high density epicardial mapping of BB was performed to study conduction characteristics of fibrillation waves across BB during chronic AF in humans. Methods Epicardial mapping studies of BB were performed in pts (n=10, age 58-4-3 yrs) with chronic AF during cardiac surgery for mitral valve disease with a template containing 60 unipolar electrodes (interelectrode distance 1.5 mm). Ten seconds of AF were recorded from the middle (MBB), right (RBB) and left site of BB (LBB). Isochronal maps were off-line constructed. For each mapping site, AF cycle length (ACFL), conduction velocity (CV) and the incidence of conduction block (CV< 7.5 cm/s) was determined. Fibrillation potentials were classified according to the degree of fractionation. Results 3988-4-2039 fibrillation potentials and 197-4-56 fibrillation maps/pt were analysed. In most pts, mukiple waves separated by arcs of conduction block were observed. In 3 pts, only single waves propagating at high CV were present. There were no preferential conduction directions. Electrophysiological variables are summarized in Table 1. CV was slower and conduction block occurred more frequently at MBB compared to RBB and LBB (CV: MBB:29+18cm/s vs RBB:46+30cm/s, LLB: 52+20cm/s, p<0.02, conduction block: MBB:20+10% vs RBB:5+3%, LLB:7+2%, p<0.01).

Mechanisms for the maintenance of ventricular fibrillation: The nonuniform dispersion of refractoriness, restitution properties, or anatomic heterogeneities?

Mechanisms for the Maintenance of Ventricular Fibrillation. Introduction: The relative importance of nonuniform dispersion of refractoriness, steep restitution slopes, and anatomic heterogeneities in causing conduction block during ventricular fibrillation (VF) remains unknown. Methods and Results: In six open-chest pigs, ventricular refractoriness and restitution curves were estimated from activation recovery intervals (ARIs) calculated from 504 (21 x 24) unipolar electrode recordings 2 mm apart in a plaque sutured to the left ventricular (LV) free wall. A steady-state restitution protocol was performed twice at each of two pacing sites: the LV base and near the left anterior descending artery. VF was electrically induced four times and the incidence of conduction block at each electrode during the first 20 seconds was determined by an automated algorithm. The gradient of the ARI was calculated at each electrode to estimate the spatial dispersion of refractoriness. An exponential curve was fit to the restitution plots of ARIs versus the corresponding diastolic intervals (DIs) for all pacing cycle lengths at each electrode. The locations of epicardial blood vessels were noted after the study. Spatial patterns of conduction block were significantly correlated between the four VF episodes in the same animal (r = 0.66 ′ 0.07, P 2 msec/mm were present between many clusters and ∼90% of restitution slopes were >1. Instead, conduction block frequently appeared to cluster along epicardial vessels. Conclusion: Neither the dispersion of refractoriness nor action potential duration restitution determined during rapid pacing by itself is the major determinant of the location of conduction block during early VF in normal pigs. It may be that these factors interact synergistically with each other as well as with other factors, including anatomic heterogeneities such as those caused by blood vessels, which may be particularly important for the formation of conduction block and maintenance of VF.

Mechanisms for the Maintenance of Ventricular Fibrillation: The Nonuniform Dispersion of Refractoriness, Restitution Properties, or Anatomic Heterogeneities?

The relative importance of nonuniform dispersion of refractoriness, steep restitution slopes, and anatomic heterogeneities in causing conduction block during ventricular fibrillation (VF) remains unknown. In six open-chest pigs, ventricular refractoriness and restitution curves were estimated from activation recovery intervals (ARIs) calculated from 504 (21 x 24) unipolar electrode recordings 2 mm apart in a plaque sutured to the left ventricular (LV) free wall. A steady-state restitution protocol was performed twice at each of two pacing sites: the LV base and near the left anterior descending artery. VF was electrically induced four times and the incidence of conduction block at each electrode during the first 20 seconds was determined by an automated algorithm. The gradient of the ARI was calculated at each electrode to estimate the spatial dispersion of refractoriness. An exponential curve was fit to the restitution plots of ARIs versus the corresponding diastolic intervals (DIs) for all pacing cycle lengths at each electrode. The locations of epicardial blood vessels were noted after the study. Spatial patterns of conduction block were significantly correlated between the four VF episodes in the same animal (r = 0.66 +/- 0.07, P < 0.05). At the shortest pacing cycle length, the spatial distribution of ARIs, ARI gradients, and restitution slopes was not random but formed clusters of similar values. However, none of these variables was significantly correlated with the incidence of conduction block, even though ARI gradients >2 msec/mm were present between many clusters and approximately 90% of restitution slopes were >1. Instead, conduction block frequently appeared to cluster along epicardial vessels. Neither the dispersion of refractoriness nor action potential duration restitution determined during rapid pacing by itself is the major determinant of the location of conduction block during early VF in normal pigs. It may be that these factors interact synergistically with each other as well as with other factors, including anatomic heterogeneities such as those caused by blood vessels, which may be particularly important for the formation of conduction block and maintenance of VF.

Pulmonary Vein Electrogram Characteristics in Patients with Focal Sources of Paroxysmal Atrial Fibrillation

The major source of ectopic beats initiating paroxysmal atrial fibrillation (AF) is from pulmonary veins (PVs). However, the electrogram characteristics of PVs are not well defined. Group I consisted of 129 patients with paroxysmal AF. Group II consisted of 10 patients with a concealed left-sided free-wall accessory pathway. All group I patients had spontaneous AF initiated by ectopic beats, including 169 ectopic foci originating from the PVs. We analyzed PV electrograms from the 169 ectopic foci during sinus beats and ectopic beats. During AF initiation, most (70%) ectopic beats showed PV spike potential followed by atrial potential; 16% of ectopic beats showed PV fragmented potential followed by atrial potential; and 14% showed fusion potentials. The coupling interval between the sinus beat and the ectopic beat was significantly shorter in the inferior PVs than in the superior PVs (171 +/- 48 msec vs 222 +/- 63 msec, P = 0.001) and was significantly shorter in the distal foci than in the ostial foci of PVs (206 +/- 52 msec vs 230 +/- 56 msec, P = 0.01). The incidence of conduction block in the PVs during AF initiation was significantly higher in the inferior PVs than in the superior PVs (12/24 vs 37/145, P = 0.03) and was significantly higher in the distal foci than in the ostial foci of PVs (43/121 vs 6/48, P = 0.04). The maximal amplitude of PV potential was significantly larger in the left PVs than in the right PVs, and the maximal duration of PV potential was significantly longer in the superior PVs than in the inferior PVs during sinus beats in both group I and II patients. PV electrogram characteristics were different among the four PVs. Detailed mapping and careful interpretation are the most important steps in ablation of paroxysmal AF originating from PVs.

Effects of ischemic preconditioning on ventricular arrhythmias during ischemia and reperfusion using a retrograde blood flow model in dogs.

We examined the effects of ischemic preconditioning on ventricular arrhythmias during ischemia and reperfusion from the electrophysiologic point of view by using the retrograde blood flow (RBF) model, which causes severe ischemia. A total of 51 anesthetized dogs were divided into 3 groups. Group 1 (10-min simple occlusion) consisted of 15 dogs; group 2 (10-min RBF) consisted of 20 dogs; and group 3 (10-min RBF with preconditioning) consisted of 16 dogs. Preconditioning consisted of 5 cycles of 2 min of ischemia (RBF) and 5 min of reperfusion. In the subepicardium, myocardial blood flow (MBF) in group 2 was significantly lower than in group 1 or group 3 [group 2 (4.7 +/- 2.3 ml/min per 100 g) vs group 1 (35.0 +/- 5.8) or group 3 (22.0 +/- 4.6); p < 0.01 and p < 0.05 respectively]. However, there were no differences in MBF in the subendocardium between the 3 groups. The incidence of conduction block in the subepicardium was significantly higher in group 2 than in group 1 or group 3 [group 2 (85%) vs group 1 (33%), p < 0.01; vs group 3 (38%), p < 0.01]. There were no differences in the incidence of conduction block in the subendocardium between the 3 groups. During 10-min ischemia, the incidences of ventricular fibrillation (VF) were 7% in group 1, 35% in group 2, and 6% in group 3 (group 2 vs group 1, p < 0.05; and group 2 vs group 3, p < 0.05). During 10-min reperfusion, the incidences of VF were 29% in group 1, 77% in group 2, and 33% in group 3 (group 2 vs group 1, p < 0.05; and group 2 vs group 3, p < 0.05). Ventricular arrhythmias were reduced during both 10-min ischemia and 10-min reperfusion as a result of the improvement in the conduction components by ischemic preconditioning which increased MBF in the subepicardium.

Differential Nerve Block

Clinically, differential block is manifested by the loss of small fiber mediated sensation (e.g., temperature) two or more dermatomes beyond the sensory limit for large fiber mediated sensations. These observations support the belief that sensitivity to local anesthetics is inversely proportional to axon diameter. This study reports the first measurements of differential sensitivity to lidocaine in individual myelinated and unmyelinated mammalian dorsal root axons. Lumbar dorsal roots and vagus nerves were isolated from anesthetized adult rats and maintained in vitro in a perfusion/recording chamber at 37 +/- 0.3 degrees C. Using single fiber techniques, evoked action potentials in individual myelinated and unmyelinated axons were digitized and recorded for subsequent analysis. Axons were exposed to lidocaine at 150, 260, or 520 microM. Sensitivity to local anesthetic was assessed by measuring the incidence of conduction block and the magnitude of conduction velocity slowing under steady-state conditions. Data were obtained from 77 dorsal root axons and 41 vagal axons. The estimated steady-state EC50 lidocaine concentration for myelinated dorsal root axons (232 microM) was comparable to that for unmyelinated axons (228 microM). Similarly, the incidence of conduction block was not significantly different among dorsal root axon groups. However, unmyelinated dorsal root axons were significantly less sensitive to the conduction velocity slowing effect of lidocaine than their myelinated counterparts (P < 0.01). The incidence of conduction block in short (mean length 13.5 mm) dorsal root axons was not significantly different from that in long (mean length 22.4 mm) axons. Compared with dorsal root axons, the estimated EC50s for vagal myelinated and unmyelinated axons (345 and 285 microM, respectively), while lower were not significantly different. However, the incidence of conduction block at 260 microM lidocaine was significantly lower (16.7% vs. 56.7%; P < 0.05) in vagal myelinated axons. Although no difference in sensitivity to the conduction blocking effects of lidocaine could be demonstrated among dorsal root axons, myelinated axons were more sensitive to the conduction velocity slowing effects of lidocaine. This differential effect cannot explain clinical observations of differential nerve block. Differential sensory block with lidocaine may depend on factors (e.g., physiologic function) related only indirectly to individual axon conduction velocity (diameter).

Lack of Size-Related Differential Sensitivity to Equilibrium Conduction Block among Mammalian Myelinated Axons Exposed to Lidocaine

This study sought to evaluate the sensitivity of individual, relatively thick myelinated axons of mammalian nerve to equilibrium conduction block by lidocaine, and to compare this to the incidence of conduction block previously measured in individual thinner myelinated axons. The incidence of conduction block by lidocaine 0.3 and 0.6 mM (8.1-16.2 mg/dl) was determined on 35 individual axons in dissected filaments of rabbit recurrent laryngeal nerve (RLN) in which the control conduction velocity ranged from 28 to 77 m/sec. Thirty-four axons (97%) remained excitable in lidocaine 0.3 mM; 2 axons (6%) remained excitable in lidocaine 0.6 mM. These proportions did not differ significantly (P greater than 0.2) from those in thinner axons of vagus, either in comparisons with previous data from extracellular recordings or with new data from filament recordings. The results imply that differential blocks observed under clinical conditions probably depend on factors other than a size-related difference in the minimal equilibrium blocking concentration among myelinated axons. Equilibrium depression of the amplitude of RLN compound action potentials by lidocaine 0.3 and 0.6 mM was disproportionately great relative to the incidence of equilibrium conduction block in individual axons, confirming that depression of the compound action potential is not a reliable measure of nerve conduction block.

Differential effect of nerve fiber structure on block by local anesthetic.

The incidence of conduction block by lidocaine 0.3 mmol/l (8.1 mg/dl) in several successive lengths of individual afferent axons of rabbit was compared. The conduction velocity of the axons was either "slow," "intermediate" (1.3-4 m/s), or "fast." The "intermediate" group showed a higher incidence of proximal acceleration of conduction (P less than 0.001) and a greater incidence of block (P less than 0.001) than the "slow" and "fast" fiber groups. The results were interpreted as indicating that the fibers of the "intermediate" group had an unmyelinated peripheral and a myelinated proximal length, with a junctional heminodal region that was the seat of the high sensitivity to block. The potential clinical significance of the observation is discussed in terms of the known distribution of heminodes in the peripheral nervous system.

Failure of Standard Cardioplegic Techniques to Protect the Conducting System

To determine the site of persistent electrical activity during cardioplegic arrest, microelectrodes that were also capable of recording temperature were placed along the conducting system in dogs undergoing one hour of cardioplegic arrest. Electrical activity was highest in the atrioventricular (AV) junction area (AV node and proximal bundle of His), and the temperature in this area could not be lowered to the level of the temperature in the left ventricular apex by routine cardioplegic technique. Neither changing K + concentration (16 to 20 mEq/L) nor adding procaine hydrochloride abolished the activity of the conducting system during cardioplegia, and only 2 of 15 dogs were in sinus rhythm 30 minutes after reperfusion. When the conducting system temperatures were lowered to less than 15°C by right AV lavage with iced saline solution, electrical activity was abolished during arrest and all 4 of 4 animals were in sinus rhythm 30 minutes after reperfusion. This study localizes the site of persistent conducting system activity during cardioplegic arrest, confirms it can be abolished with local cooling, and establishes the relationship between conducting system activity during cardioplegia and the incidence of conduction block and junctional rhythm following reperfusion.