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Myocardial ischemia is the response of the heart to reduced coronary blood flow, leading to changes in ST segment potentials. ST segment depression is regarded as an indicator of nontransmural myocardial ischemia; however, not all nontransmural ischemia results in ST depression. This apparent discrepancy may be the result of many complex factors in cardiac response mechanisms to reduced blood flow. As a result, sophisticated computer models have emerged that have provided key insights into this complex phenomenon and the circumstances surrounding ST depression. Though these models have been able to produce ST depressions, many have neglected the effect of intracavitary blood volume, associated with different phases of the cardiac cycle. To explore the influence of the cardiac blood volume variability on epicardial potentials during nontransmural ischemia, we incorporated a thin, subendocardial ischemic zone geometry into an anatomically realistic, image-based ventricular model, and generated a finite element, static bidomain solution to determine the resulting epicardial surface potentials. It was first determined that, under baseline conditions (i.e., expanded left ventricular volumes corresponding to diastole), a predictable ST depression developed over the ischemic region. Left ventricular volume was then incrementally reduced, while maintaining the size and general shape of the is-chemic region, in order to reflect the systolic phase of the cardiac cycle. As blood volume geometries decreased, epicardial ST depression overlying the ischemic region first increased in surface area as blood volume was reduced and before dramatically reducing near 30% blood volume reduction — accentuating the role and importance of blood volume variation in computational models ofischemia.

The Role of Reduced Left Ventricular, Systolic Blood Volumes in ST Segment Potentials Overlying Diseased Tissue of the Ischemic Heart