scholarly journals Spatiotemporal Patterns of Early Afterdepolarizations Underlying Abnormal T-Wave Morphologies in a Tissue Model of the Purkinje-Ventricular System

2021 ◽  
Author(s):  
Mengya Yuan ◽  
Pan Li
Keyword(s):  
Ventricular Arrhythmias ◽  
Temporal Dynamics ◽  
Spatial Dynamics ◽  
Tissue Level ◽  
Cellular Level ◽  
Ventricular System ◽  
Early Afterdepolarizations ◽  
Tissue Model ◽  
T Wave ◽  
T Waves

Abstract Background Sudden cardiac death (SCD) is a leading cause of death worldwide, and the majority of SCDs are caused by acute ventricular arrhythmias (VAs). Early afterdepolarizations (EADs) are an important trigger of VA under pathological conditions, e.g., inherited or acquired long QT syndrome (LQTS). However, it remains unclear how EAD events at the cellular level are spatially organized at the tissue level to induce and maintain ventricular arrhythmias and whether the spatial-temporal patterns of EADs at the tissue level are associated with abnormal T-wave morphologies that are often observed in LQTS, such as broad-based, notched or bifid; late appearance; and pointed T-waves. Result Here, a tissue model of the Purkinje-ventricular system (PVS) was developed to quantitatively investigate the complex spatial-temporal dynamics of EADs during T-wave abnormalities, and we found that (1) while major inhibition of ICaL can substantially reduce the excitability of the PVS leading to conduction failures, moderate ICaL inhibition can promote occurrences of AP alternans at short cycle lengths (CLs), and EAD events preferentially occur with a major reduction of IKr (> 50%) at long CLs; (2) with a minor reduction of ICaL, spatially synchronized steady-state EAD events with inverted and biphasic T-waves can be “weakened” into beat-to-beat concurrences of spatially synchronized EADs and T-wave alternans, and as pacing CLs increase, beat-to-beat concurrences of localized EADs with late-appearing and pointed T-wave morphologies can be observed; (3) under certain conditions, localized EAD events in the midmyocardium may trigger slow uni-directional electric propagation with inverted (antegrade) or upright (retrograde) broad-based T-waves; (4) spatially discordant EADs were typically characterized by desynchronized spontaneous onsets of EAD events between two groups of PVS tissues with biphasic T-wave morphologies, and they can evolve into spatially discordant oscillating EAD patterns with sustained or self-terminated alternating EAD and electrocardiogram (ECG) patterns. Conclusion Our results provide new insights into the spatiotemporal aspects of the onset and development of EADs and suggest possible mechanistic links between the complex spatial dynamics of EADs and T-wave morphologies.

scholarly journals Electrophysiological Mechanisms Underlying T-Wave Alternans and Their Role in Arrhythmogenesis

2021 ◽  
Vol 12 ◽  
Author(s):  
Tingting You ◽  
Cunjin Luo ◽  
Kevin Zhang ◽  
Henggui Zhang
Keyword(s):  
Heart Rate ◽  
Tissue Level ◽  
Cellular Level ◽  
Simulation Studies ◽  
Future Perspectives ◽  
Non Invasive ◽  
T Wave ◽  
Dispersion Of Repolarization ◽  
St Segment ◽  
T Wave Alternans

T-wave alternans (TWA) reflects every-other-beat alterations in the morphology of the electrocardiogram ST segment or T wave in the setting of a constant heart rate, hence, in the absence of heart rate variability. It is believed to be associated with the dispersion of repolarization and has been used as a non-invasive marker for predicting the risk of malignant cardiac arrhythmias and sudden cardiac death as numerous studies have shown. This review aims to provide up-to-date review on both experimental and simulation studies in elucidating possible mechanisms underlying the genesis of TWA at the cellular level, as well as the genesis of spatially concordant/discordant alternans at the tissue level, and their transition to cardiac arrhythmia. Recent progress and future perspectives in antiarrhythmic therapies associated with TWA are also discussed.

RESEARCH THE VALUE OF THE COMBINATION OF T WAVE ALTERNANS AND NT-PROBNT IN PREDICTING SUDDEN CARDIAC DEATH

2012 ◽  
pp. 74-83
Author(s):  
Anh Tien Hoang ◽  
Nhat Quang Nguyen
Keyword(s):  
Myocardial Infarction ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Healthy Person ◽  
Treadmill Test ◽  
T Wave ◽  
T Wave Alternans

Background: Decades of research now link TWA with inducible and spontaneous clinical ventricular arrhythmias. This bench-to-bedside foundation makes TWA, NT-ProBNP a very plausible index of susceptibility to ventricular arrythmia, and motivates the need to define optimal combination of TWA and NT-ProBNP in predicting ventricular arrythmia in myocardial infarction patients. We research this study with 2 targets: 1. To evaluate the role of TWA in predicting sudden cardiac death in myocardial infarction patients. 2. To evaluate the role of NT-ProBNP in predicting sudden cardiac death in myocardial infarction patients 3. Evaluate the role of the combined NT-ProBNP and TWA in predicting sudden cardiac death in myocardial infarction patients. Methods: Prospective study with follow up the mortality in 2 years: 71 chronic myocardial infarction patients admitted to hospital from 5/2009 to 5/20011 and 50 healthy person was done treadmill test to caculate TWA; ECG, echocardiography, NT-ProBNP. Results: Cut-off point of NT-ProBNP in predicting sudden cardiac death is 3168 pg/ml; AUC = 0,86 (95% CI: 0,72 - 0,91); Cut-off point of TWA in predicting sudden cardiac death is 107 µV; AUC = 0,81 (95% CI: 0,69 - 0,87); NT-ProBNP can predict sudden cardiac death with OR= 7,26 (p<0,01); TWA can predict sudden cardiac death with OR= 8,45 (p<0,01). The combined NT-ProBNP and TWA in predicting ventricular arrythmia in heart failure patients: OR= 17,91 (p<0,001). Conclusions: The combined NT-ProBNP and TWA have the best predict value of sudden cardiac death in myocardial infarction patients, compare to NT-ProBNP or TWA alone

Spatial-temporal transmission dynamics and control of infectious diseases: Ebola virus disease (EVD) as a case study

2018 ◽  
Author(s):  
Cécile Viboud ◽  
Hélène Broutin ◽  
Gerardo Chowell
Keyword(s):  
Infectious Diseases ◽  
Disease Transmission ◽  
Ebola Virus ◽  
Temporal Dynamics ◽  
Virus Disease ◽  
Spatial Dynamics ◽  
Childhood Diseases ◽  
Middle Income ◽  
Theoretical Concepts ◽  
Dynamics And Control

Disentangling the spatial-temporal dynamics of infectious disease transmission is important to address issues of disease persistence, epidemic growth and optimal control. In this chapter, we review key concepts relating to the spatial-temporal dynamics of infectious diseases in meta-populations, whereby geographically separate subpopulations are connected by migration or mobility rates. We review the dynamics of colonization, persistence and extinction of emerging and recurrent pathogens in meta-populations; the role of demographic and environmental factors; and geographic heterogeneity in epidemic growth rate. We illustrate theoretical concepts by reviewing the spatial dynamics of childhood diseases and other acute infections in low- and middle-income countries, and provide a detailed description of the spatial-temporal dynamics of the 2014–16 Ebola epidemic in West Africa. We further discuss how increased availability of empirical data and recent methodological developments provide a deeper mechanistic understanding of transmission processes in space and time, and make recommendations for future work.

scholarly journals Is ventricular arrhythmias the end for all conditions ?

2021 ◽  
Author(s):  
Ahmet Goktug Ertem ◽  
Mehmet Akif Erdol ◽  
Koray Demirtas ◽  
Sefa Unal ◽  
Mustafa Karanfil ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Risk Factor ◽  
Antiretroviral Therapy ◽  
Ventricular Arrhythmias ◽  
Combination Antiretroviral Therapy ◽  
T Wave ◽  
Medical Status ◽  
Immunodeficiency Virus ◽  
Duration Of Disease ◽  
Severity Of The Disease

Dear Editor, We read the article entitled “Abnormal Dispersion of Ventricular Repolarization as a Risk Factor in Patients with Human Immunodeficiency Virus: Tp-e Interval, Tp-e/QTc Ratio” by Unal Evren et al. with interest[1]. The authors evaluated the changes in Tp-e interval, Tp-e/QT and Tp-e/corrected QT (QTc) ratios, and traditional electrocardiographic features of electrical dispersion in adults infected with Human Immunodeficiency Virus (HIV) and their study revealed that the cTp-e interval, Tp-e/QT and Tp-e/QTc ratios were prolonged and correlated to the severity of the disease in HIV-infected patients. Previous studies have revealed that the Tp–e interval, the Tpeak-Tend interval (Tpe), the interval from the T-wave peak to the end of the T wave, has been related to arrhythmogenesis, is specified as an index of totaldispersion of repolarization[2]. Prolonged Tp–e interval is predictable for ventricular arrhythmias and mortality [3]. Unal et al. showed that HIV-infected patients receiving combination antiretroviral therapy (cART) were associated withlonger Tp–e interval and Tp–e/QTc ratio and correlated positively with the duration of disease and the electrophysiologicalabnormalities, and negatively with CD4 count[4]. There were no informations about medical status of patients with HIV, duration of the disease and why hsCRP is higher in patients’ group. The patients were in active phases of infection. We think that these are important datas for results of the study. We thank the authors for adding this article to the literature

scholarly journals Hierarchical modeling of mechano-chemical dynamics of epithelial sheets across cells and tissue

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoshifumi Asakura ◽  
Yohei Kondo ◽  
Kazuhiro Aoki ◽  
Honda Naoki
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Continuum Model ◽  
Tissue Level ◽  
Chemical Signals ◽  
Cellular Level ◽  
Mathematical Framework ◽  
Collective Cell Migration ◽  
The Continuum ◽  
Cell Cell

AbstractCollective cell migration is a fundamental process in embryonic development and tissue homeostasis. This is a macroscopic population-level phenomenon that emerges across hierarchy from microscopic cell-cell interactions; however, the underlying mechanism remains unclear. Here, we addressed this issue by focusing on epithelial collective cell migration, driven by the mechanical force regulated by chemical signals of traveling ERK activation waves, observed in wound healing. We propose a hierarchical mathematical framework for understanding how cells are orchestrated through mechanochemical cell-cell interaction. In this framework, we mathematically transformed a particle-based model at the cellular level into a continuum model at the tissue level. The continuum model described relationships between cell migration and mechanochemical variables, namely, ERK activity gradients, cell density, and velocity field, which could be compared with live-cell imaging data. Through numerical simulations, the continuum model recapitulated the ERK wave-induced collective cell migration in wound healing. We also numerically confirmed a consistency between these two models. Thus, our hierarchical approach offers a new theoretical platform to reveal a causality between macroscopic tissue-level and microscopic cellular-level phenomena. Furthermore, our model is also capable of deriving a theoretical insight on both of mechanical and chemical signals, in the causality of tissue and cellular dynamics.

Abstract 3265: A Comparison of Echocardiographic and Electrocardiographic Characteristics of Patients with Apical Hypertrophic Cardiomyopathy

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Josepha Binder ◽  
Brandon R Grossardt ◽  
Christine Attenhofer Jost ◽  
Kyle W Klarich ◽  
Michael J Ackerman ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Right Atrial ◽  
Apical Hypertrophic Cardiomyopathy ◽  
T Wave ◽  
Atrial Enlargement ◽  
Lv Ejection Fraction ◽  
The Relationship ◽  
T Waves

Background: Apical hypertrophic cardiomyopathy (apical HCM) is a less common subtype of HCM characterized by a focal thickening in the left ventricular apex. “Classic” ECG features have been described, however, apical HCM can persist for many years without detection. We investigated the relationship between ECG findings and echocardiographic morphometry in a large referral series of patients with apical HCM. Methods: We enumerated all patients diagnosed with apical HCM prior to Sept. 30, 2006 using the Mayo Clinic HCM database. We compared echocardiographic measures separately for patients with positive status for two ECG indices of left ventricular hypertrophy (LVH); the Sokolow-Lyon index and the Romhilt-Estes (RE) point-score. We also compared echocardiographic measurements in patients with and without negative T-waves in the precordial leads. Results: Apical HCM was detected in 177 patients (111 men and 68 women). Only 51% had positive Sokolow criteria and 51% had positive RE criteria. The agreement between Sokolow and RE status was high (agreement = 75.0%; kappa = 0.50; 95% CI = 0.38 – 0.62). In particular, Sokolow positive patients had increased LV ejection fraction (P = 0.02), and decreased LV end-systolic diameter (P = 0.03) compared with Sokolow negative patients. The prevalence of right atrial enlargement (47 vs. 28%; P = 0.02) and intracavity obstruction (22 vs. 8%; P = 0.01) were more common in Sokolow positive patients. Positive RE criteria was associated with a greater thickness of the basal septal and basal posterior walls (P = 0.001 and 0.02, respectively), and with a higher frequency of intracavity obstruction (21 vs. 9%; P = 0.04). Most patients (89%) exhibited at least one negative T-wave in the precordial leads; however, only 10% of patients had a negative T-wave of greater than 1.0 mV. We found that patients with an inverted T-wave larger than 0.4 mV (median) had a significantly increased LV ejection fraction (P = 0.03) compared with patients who had smaller or no negative T-waves. Conclusions: Among patients with apical HCM, nearly half do not have ECG evidence of LVH based on classic criteria and most do not have marked T-wave inversions. However, the majority did have at least a mild expression of negative T-waves.

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