<abstract>
<sec><title>Background</title><p>The utility of T wave alternans (TWA) in identifying arrhythmia risk has been demonstrated. During myocardial ischemia (MI), TWA could be induced by cellular alternans. However, the relationship between cellular alternans patterns and TWA patterns in MI has not been investigated thoroughly.</p>
</sec>
<sec><title>Methods</title><p>We set MI conditions to simulate alternans. Either prolonging Ca<sup>2+</sup> release or increasing spark-induced sparks (secondary sparks) can give rise to different patterns of APD alternans and TWA. In addition, different ischemic zones and reduced conduction velocity are also considered in one dimensional simulation.</p>
</sec>
<sec><title>Results</title><p>Delay of Ca<sup>2+</sup> release can produce discordant Ca<sup>2+</sup>-driven alternans in single cell simulation. Increasing secondary sparks leads to concordant alternans. Correspondingly, morphology and magnitude of TWA vary in two different cellular alternans. Epi ischemia results in alternans concentrating in the first half of T wave. Endo and transmural ischemia lead to fluctuations in the second half of T wave. In addition, slowing conduction velocity has no effect on TWA magnitude.</p>
</sec>
<sec><title>Conclusion</title><p>Specific ionic channel dysfunction and ischemic zones affect TWA patterns.</p>
</sec>
</abstract>
Investigating two kinds of cellular alternans and corresponding TWA induced by impaired calcium cycling in myocardial ischemia