By Topic

A theoretical analysis of acute ischemia and infarction using ECG reconstruction on a 2-D model of myocardium

Sign In

Cookies must be enabled to login.After enabling cookies , please use refresh or reload or ctrl+f5 on the browser for the login options.

Formats Non-Member Member
$31 $13
Learn how you can qualify for the best price for this item!
Become an IEEE Member or Subscribe to
IEEE Xplore for exclusive pricing!
close button

puzzle piece

IEEE membership options for an individual and IEEE Xplore subscriptions for an organization offer the most affordable access to essential journal articles, conference papers, standards, eBooks, and eLearning courses.

Learn more about:

IEEE membership

IEEE Xplore subscriptions

3 Author(s)
Cimponeriu, A. ; Sch. of Med., Patras Univ., Greece ; Starmer, C.Frank ; Bezerianos, A.

The authors developed a two-dimensional ventricular tissue model in order to probe the determinants of electrocardiographic (ECG) morphology during acute and chronic ischemia. Hyperkalemia was simulated by step changes in [K +] out, while acidosis was induced by reducing Na + and Ca 2+ conductances. Hypoxia was introduced by its effect on potassium activity. During the initial moments of ischemia, ECG changes were characterized by increases in QRS amplitude and ST segment shortening, followed in the advanced phase by ST baseline elevation, T conformation changes, widening of the QRS and significant decreases in QRS amplitude in spite of an enlarged Q. During each phase, potential proarrhythmic mechanisms were investigated. The presence of unexcitable regions of simulated myocardial infarction led to polymorphic ECG. The authors also observed a nonuniform deflection of the ST segment from beat to beat. They used similar protocols to explore the responses of infarcted myocardium after impairment resolving. They found that despite irreversible uncoupling of the necrotic region, the restored normal ionic concentrations produced an isopotential ST segment and monomorphic ECG complexes, while an enlarged Q wave was still visible. In summary, these numerical experiments indicate the possibility to track in the ECG pathologic changes following the altered electrophysiology of the ischemic heart.

Published in:

Biomedical Engineering, IEEE Transactions on  (Volume:48 ,  Issue: 1 )