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  <title><![CDATA[PhD Defense by Mikael Toye  ]]></title>
  <body><![CDATA[<p><strong>School of Physics&nbsp;Thesis Dissertation Defense</strong></p><p>&nbsp;</p><p><strong>Mikael Toye &nbsp;</strong></p><p>Dr. Flavio Fenton, School of Physics, Georgia Institute of Technology (Advisor)</p><p>&nbsp;</p><p><strong>Experimental Determination of Chaos in Cardiac Tissue: Period-3, Intermittency, Unstable Dynamics, and Control</strong></p><p>Date: Monday, April 13, 2026</p><p>Time: 12:00 p.m.</p><p>Location:&nbsp;Howey Physics Building, W401&nbsp;</p><p>&nbsp;</p><p><strong>Committee members</strong>:</p><p>Dr. Predrag Cvitanović, School of Physics, Georgia Institute of Technology</p><p>Dr. Michael Schatz, School of Physics, Georgia Institute of Technology</p><p>Dr. Kurt Wiesenfeld, School of Physics, Georgia Institute of Technology</p><p>Dr. Carolyn Martsberger, Physics, Wofford College</p><p>&nbsp;</p><p><strong>Abstract</strong>:</p><p>The complex voltage dynamics underlying ventricular fibrillation can rapidly lead to death in affected individuals. The mechanisms driving these abnormal cardiac behaviors, often hypothesized to be chaotic, have not been fully explored. This work investigates whether constant rapid pacing induces bifurcation cascades that lead to deterministic chaos in cardiac voltage dynamics. Microelectrode recordings in bullfrog ventricles near the pacing site reveal a progression from alternans to higher-order periodicity, including period-3 behavior and aperiodic dynamics characterized by periodic orbit shadowing and positive Lyapunov exponents. Optical mapping in rapidly paced frog and human ventricles demonstrates that chaotic-like dynamics emerge near structural heterogeneities and spread throughout the tissue. This gives rise to spatiotemporal dynamics across the heart within which discordant alternans can emerge, ultimately leading to ventricular fibrillation. Additionally, S1–S2 experiments show that these arrhythmic voltage dynamics are highly sensitive to initial conditions. Temperature variation and pacing perturbations further systematically modulate the dynamics. Together, these findings suggest that complex cardiac voltage dynamics consistent with deterministic chaos can arise from coupled cellular- and tissue-scale mechanisms, highlighting potential pathways for targeted control.</p><p>&nbsp;</p>]]></body>
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