Activation Delay (activation + delay)

Distribution by Scientific Domains


Selected Abstracts


Activation Delay and VT Parameters in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy: Toward Improvement of Diagnostic ECG Criteria

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2008
MONIEK G.P.J. COX M.D.
Introduction: Desmosomal changes, electrical uncoupling, and surviving myocardial bundles embedded in fibrofatty tissue are hallmarks of activation delay in arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). Currently, generally accepted task force criteria (TFC) are used for clinical diagnosis. We propose additional criteria based on activation delay and ventricular tachycardia (VT) to improve identification of affected individuals. Methods and Results: Activation delay and VT-related 12-lead electrocardiographic (ECG) criteria were studied, while off drugs, in 42 patients with proven ARVD/C according to TFC, and 27 controls with idiopathic VT from the RV outflow tract. Two of three measured TFC could only be identified in a small minority of ARVD/C patients. Additional ECG criteria proposed in this study included (a) prolonged terminal activation duration, an indicator of activation delay; (b) VT with LBBB morphology and superior axis; and (c) multiple different VT morphologies. These criteria were met in 30 (71%), 28 (67%), and 37 (88%) ARVD/C patients, respectively, and in one control patient (P < 0.001). Electrophysiologic studies contributed importantly to yield different VT morphologies. Pathogenic plakophilin-2 mutations were identified in 25 (60%) of ARVD/C patients and in none of the controls. In ARVD/C patients, parameters measured were not significantly different between mutation carriers and noncarriers, except for negative T waves in V1,3, occurring more frequently in patients with mutation. Conclusions: The proposed additional criteria are specific for ARVD/C and more sensitive than the current TFC. Therefore, adding the newly proposed criteria to current TFC could improve ARVD/C diagnosis, independent of DNA analysis. [source]


VACCINATION, WITHIN-HOST DYNAMICS, AND VIRULENCE EVOLUTION

EVOLUTION, Issue 1 2006
Jean-Baptiste André
Abstract We explore the potential consequences of vaccination on parasite epidemiology and evolution. Our model combines a microscopic (within-host dynamics) and a macroscopic (epidemiological dynamics) description of the interaction between the parasite and its host. This approach allows relevant epidemiological traits such as parasite transmission, parasite virulence, and host recovery to emerge from a mechanistic model of acute infection describing the interaction between the parasite and the host immune system. We model the effect of a vaccine as an activator of immunity enhancing the replication rate of lymphocytes, their initial density at infection's initiation, their efficacy to kill the parasite, or their activation delay after infection. We analyze the evolution of the replication rate of parasites and show that vaccination may promote the evolution of faster replicating and, consequently, more virulent strains. We also show that intermediate vaccination coverage may lead to the coexistence of two different parasite strategies (a low-virulence strain adapted to naive hosts, and a high-virulence strain, more generalist, adapted to both naive and vaccinated hosts). We discuss the consequences of various vaccination strategies under different epidemiological situations using several distinct measures to evaluate the cost induced by the parasite on individuals and entire host populations. [source]


Activation Delay and VT Parameters in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy: Toward Improvement of Diagnostic ECG Criteria

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2008
MONIEK G.P.J. COX M.D.
Introduction: Desmosomal changes, electrical uncoupling, and surviving myocardial bundles embedded in fibrofatty tissue are hallmarks of activation delay in arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). Currently, generally accepted task force criteria (TFC) are used for clinical diagnosis. We propose additional criteria based on activation delay and ventricular tachycardia (VT) to improve identification of affected individuals. Methods and Results: Activation delay and VT-related 12-lead electrocardiographic (ECG) criteria were studied, while off drugs, in 42 patients with proven ARVD/C according to TFC, and 27 controls with idiopathic VT from the RV outflow tract. Two of three measured TFC could only be identified in a small minority of ARVD/C patients. Additional ECG criteria proposed in this study included (a) prolonged terminal activation duration, an indicator of activation delay; (b) VT with LBBB morphology and superior axis; and (c) multiple different VT morphologies. These criteria were met in 30 (71%), 28 (67%), and 37 (88%) ARVD/C patients, respectively, and in one control patient (P < 0.001). Electrophysiologic studies contributed importantly to yield different VT morphologies. Pathogenic plakophilin-2 mutations were identified in 25 (60%) of ARVD/C patients and in none of the controls. In ARVD/C patients, parameters measured were not significantly different between mutation carriers and noncarriers, except for negative T waves in V1,3, occurring more frequently in patients with mutation. Conclusions: The proposed additional criteria are specific for ARVD/C and more sensitive than the current TFC. Therefore, adding the newly proposed criteria to current TFC could improve ARVD/C diagnosis, independent of DNA analysis. [source]


Significant Left Atrial Appendage Activation Delay Complicating Aggressive Septal Ablation during Catheter Ablation of Persistent Atrial Fibrillation

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2010
CHEN-XI JIANG M.D.
Background:,This study aims to describe significant left atrial appendage activation following ablation of persistent atrial fibrillation, and explore its relationship with aggressive septal ablation. Methods and Results:,Significant left atrial appendage activation delay was found in 23 out of 201 patients undergoing persistent atrial fibrillation ablation. Of them, 14 were found in their index procedures, of whom septal line ablation was performed in nine (odds ratio 15.2, 95% confidence interval 4.6,50.8, P < 0.001). Another nine were found during their redo procedures (including two with biatrial activation dissociation), all of whom received extensive left septal complex fractionated electrograms ablation in their prior procedures (P = 0.002). Electrocardiograph showed split P wave with the latter component merged into the QRS wave. Activation mapping demonstrated the earliest breakthrough of the left atrium changed to coronary sinus in 18 (85.7%) patients. After 1 month, the mitral A wave velocity was 18.2 ± 17.0 cm/s, and decreased significantly as compared with preablation (20.2 ± 19.1 vs 58.2 ± 17.9 cm/s, P = 0.037) in patients undergoing redo procedures. Fourteen (60.9%) remained arrhythmia-free during follow-up for 10.6 ± 6.2 months. Conclusion:,Septal line ablation and extensive septal complex fractionated electrograms ablation are correlated with significant left atrial activation delay or even biatrial activation dissociation, and should be performed with prudent consideration. (PACE 2010; 33:652,660) [source]