PubMed · 5515964
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J C Chignon, R Distel, B Courtois. 1970. [Auricular vectorcardiography].. https://pubmed.ncbi.nlm.nih.gov/5515964/
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Although considerable progress has been made in understanding the process of wavefront propagation and arrhythmogenesis in human atria, technical concerns and issues of patient safety have limited experimental investigations. The present work describes a finite volume-based computer model of human atrial activation and current flow to complement these studies. Unlike previous representations, the model is three-dimensional, incorporating both the left and right atria and the major muscle bundles of the atria, including the crista terminalis, pectinate muscles, limbus of the fossa ovalis, and Bachmann's bundle. The bundles are represented as anisotropic structures with fiber directions aligned with the bundle axes. Conductivities are assigned to the model to give realistic local conduction velocities within the bundles and bulk tissue. Results from simulations demonstrate the role of the bundles in a normal sinus rhythm and also reveal the patterns of activation in the septum, where experimental mapping has been extremely challenging. To validate the model, the simulated normal activation sequence and conduction velocities at various locations are compared with experimental observations and data. The model is also used to investigate paced activation, and a mechanism of the relative lengthening of left versus right stimulation is presented. Owing to both the realistic geometry and the bundle structures, the model can be used for further analysis of the normal activation sequence and to examine abnormal conduction, including flutter. The full text of this article is available at http://www.circresaha.org.
BACKGROUND: Abnormalities of the terminal force of the P wave in Lead V1 (ptf-V1) and dispersion of corrected atrial repolarization (Ta-TcD) are believed to represent interatrial conduction defect. METHODS AND RESULTS: To determine whether atrial conduction disturbance correlates with cardiac allograft rejection, we analyzed 249 twelve-lead-electrocardiograms, echocardiograms, hemodynamic parameters, and endomyocardial biopsys from 137 patients with heart transplantation. Both ptf-V1 and Ta-TcD were significantly increased in patients with severe, moderate, and mild rejection. In 22 patients, significant increases of the ptf-V1 and Ta-TcD were observed before positive histological findings, and significantly correlated with severity of rejection during 5- week to 1-year follow-up. Increase of 0.030 mm x sec in ptf-V1 or 0.040 s1/2 in Ta-TcD indicated cardiac rejection > or =1B with sensitivity of 88 and 83%, specificity of 85 and 77%, respectively. CONCLUSION: These results suggest that the ptf-V1 and Ta-TcD might be an adjunct to detect rejection and reduce the number of surveillance EMB.
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