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Remodeling of Myocardial Passive Electrical Properties: Insights Into the Mechanisms of Malignant Arrhythmias and Sudden Cardiac Death

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Remodeling of Myocardial Passive Electrical Properties: Insights Into the Mechanisms of Malignant Arrhythmias and Sudden Cardiac Death Remodeling of Myocardial Passive Electrical Properties: Insights into the Mechanisms of Malignant Arrhythmias and Sudden Cardiac Death. DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Carlos Luis del Rio, M.S. Graduate Program in Electrical and Computer Science The Ohio State University 2015 Dissertation Committee: Professor Bradley D. Clymer, Ph.D., Advisor Professor George E. Billman, Ph.D., Co-Advisor Professor Furrukh S. Khan, Ph.D. Copyright by Carlos Luis del Rio 2015 Abstract Despite extensive research, sudden cardiac death (SCD) resulting from ischemia-induced malignant arrhythmias, such as ventricular fibrillation (VF), remains a leading cause of death, particularly following myocardial infarction (MI). Furthermore, SCD is generally the first and most common manifestation of the disease, as current risk-stratifying tools are inaccurate and insufficient. Acute/chronic changes in the passive electrical properties governing electrotonic coupling in the myocardium have been proposed as a potential mechanism mediating both the onset and maintenance of arrhythmias, as the loss of homogenizing electrotonic coupling can exacerbate intrinsic pro-arrhythmic electrical heterogeneities within the ventricle, especially during repolarization. However, no study to date has assessed the ability of indices reflective of electrotonic changes to stratify intrinsic arrhythmic susceptibility in vivo. Leveraging a well-established in vivo post-MI canine model of SCD and lethal arrhythmias, this research work investigates the pro-arrhythmic role of changes in the passive electrical properties of the myocardium, as measured by its complex electrical impedance spectrum (MEI). The studies were performed under the general hypothesis that the loss of electrotonic coupling accompanies and facilitates the development of malignant arrhythmias in the setting of ischemia and post-MI ventricular/autonomic remodeling. Specifically, acute/chronic electrotonic changes/heterogeneities in the setting of three well- ii established risk factors for arrhythmias/SCD, namely acute ischemia, myocardial infarction, and/or autonomic imbalances, were evaluated. Furthermore, since the experimental post-MI model used yields two well-defined populations of animals, one prone and the other resistant to ischemia-induced lethal arrhythmias, the prognostic value of electrotonic changes to detect intrinsic arrhythmic susceptibility was also assessed. In short, both infarcted and remote (i.e., non-infarcted) myocardium were shown to undergo chronic electrotonic remodeling following a sustained ischemic insult (coronary artery ligation). Overall, the healing infarction was shown to have lower impedance than remote myocardium, with animals prone to malignant arrhythmias showing a wider electrotonic gradient (i.e., impedance difference) between these two regions. In the electrotonically-remodeled post-MI myocardium, acute β-adrenoceptor activation (either during bouts of exercise or via a direct pharmacological challenge) acutely increased passive (electrotonic) coupling in the remote myocardium, with animals susceptible to SCD showing the greatest electrotonic responsiveness. Meanwhile, electrotonic uncoupling induced by an acute ischemic insult (coronary artery occlusion) to the non- infarcted myocardium of post-MI animals susceptible to malignant arrhythmias, was shown to facilitate/uncover (i.e., predict) pro-arrhythmic ventricular electrical oscillations and repolarizarion abnormalities (such as TWA). Moreover, acute electrotonic uncoupling during ischemia was shown to be modulated by interventions affecting autonomic balance, as passive electrical derangements were blunted by complete/partial β-adrenoreceptor blockade and/or vagal nerve stimulation, but enhanced by exercise. iii In conclusion, these experiments establish post-MI passive electrical heterogeneities and their modulation by autonomic changes and/or acute ischemia, as a risk/prognostic factor for SCD/arrhythmic susceptibility in vivo. iv A mis padres, Pedro Luis y María de los Ángeles. A mi hijito Javier, and to Sarah, my soulmate. v Acknowledgments While a single paragraph cannot fully express my appreciation for their support, I would nonetheless like to document my gratitude to Dr. Bradley Clymer, Dr. George Billman, Dr. Furrukh Khan, Dr. Michael Howie, and Mr. Roger Dzwonczyk. Their friendship and invaluable guidance as professors, scientists, and engineers have taught me that passion, collaboration, and dedication can make the unthinkable a reality. Additionally, I will always treasure Dr. Robert Hamlin’s brilliance, eagerness, and endless desire to learn. To all of you, my dear professors, and to all of the other friends and collaborators that I have had the pleasure of meeting, please receive my most sincere and eternal gratitude. vi Vita 1998................................................................B.S. (summa cum laude), Electrical Engineering, Universidad Simón Bolívar (Caracas, Venezuela) 2005................................................................M.S. Electrical & Computer Engineering, The Ohio State University (OH, USA) Publications Dzwonczyk R, del Rio C, Brown DA, Michler RE, Wolf RK, Howie MB. Myocardial Electrical Impedance Responds to Ischemia and Reperfusion in Humans. Comput Cardiol. 2002; 29: 541−543. del Río CL, Dzwonczyk R, Clymer BD, McSweeney TD, Awad H, Czerwinski P, Howie MB. Use of Myocardial Electrical Impedance to Assess the Efficacy of Preconditioning. Comput Cardiol. 2002; 29: 489−492. Dzwonczyk R, del Rio CL, Brown DA, Michler RE, Wolf RK, Howie MB. Myocardial Electrical Impedance Responds to Ischemia and Reperfusion in Humans. IEEE Trans Biomed Eng 2004; 51:2206-09. vii del Río CL, Dzwonczyk R, McConnell PI, Clymer BD, Howie MB, Billman GE. Beta- Adrenergic Receptor Blockade Attenuates the Electronic Uncoupling Induced by Coronary Artery Occlusion. Comput Cardiol 2004; 31: 405−408. Dzwonczyk R, del Rio CL, Sun B, Michler RE, Howie MB. Devices used to expose the posterior coronary artery in OPCABG surgery may cause ischemia. Proc. IEEE Northeast Bioengineering Conference, April 2005: 148 – 149. McConnell PI, del Rio CL, Jacoby DB, Pavlicova M, Kwiatkowski P, Zawadzka A, Dinsmore JH, Astra L, Wisel S, Michler RE. Correlation of Autologous Skeletal Myoblast Survival with Changes in Left Ventricular Remodeling in Dilated Ischemic Heart Failure. J Thorac Cardiovasc Surg. 2005 Oct; 130(4):1001. del Rio CL, McConnell PI, Clymer BD, Dzwonczyk R, Michler RE, Billman GE, Howie MB. Early Time Course of Myocardial Electrical Impedance During Acute Coronary Artery Occlusion in Pigs, Dogs And Man. J Appl Physiol. 2005 Oct; 99(4):1576-81. Dzwonczyk R, del Rio CL, Sai-Sudhakar C, Sirak JH, Michler RE, Sun B, Kelbick N, Howie MB. Vacuum-assisted apical suction devices induce passive electrical changes consistent with myocardial ischemia during off-pump coronary artery bypass graft surgery. Eur J Cardiothorac Surg. 2006 Dec; 30(6):873-876. Dzwonczyk R, del Rio CL, Sun B, Howie MB. Myocardial Electrical Impedance Correlates with Ischemic ECG ST-Segment Changes in Humans. Conf Proc IEEE Eng Med Biol Soc. 2006; 1: 2568-2569. viii McConnell PI, del Rio CL, Kwiatkowski P, Farrar DJ, Sun BC. Assessment of cardiac function during axial-flow left ventricular assist device support using a left ventricular pressure-derived relationship: comparison with pre-load recruitable stroke work. J Heart Lung Transplant. 2007 Feb; 26(2):159-66. del Rio CL, McConnell PI, Kukielka M, Dzwonczyk R, Clymer DB, Howie MB, Billman GE. Electrotonic Remodeling following Myocardial Infarction in Dogs Susceptible and Resistant to Sudden Cardiac Death. J Appl Physiol. 2008 Feb;104(2):386-93. del Rio CL, Dawson TA, Clymer BD, Paterson DJ, Billman GE. Acute Vagal Nerve Stimulation Attenuates Early Passive Electrical Changes Induced by Myocardial Ischemia: Heart Rate Mediated Attenuation. Exp Physiol. 2008 Aug; 93(8):931-44. Dzwonczyk R, del Rio C, McSweeney TD, Zhang X, Howie MB. Myocardial electrical activity does not affect myocardial electrical impedance measurements. J Clin Monit Comput. 2009 Aug; 23(4):217-22. Howie M, del Río C, Khan F, Lopez L, Dzwonczyk R, Bergese S. (2009). A Secure and Expandable Electronic Patient Record System Using Web-based Technology. Ibnosina Journal Of Medicine And Biomedical Sciences, IJMBS. 2009; 1(3): 73-9. Kijtawornrat A, Panyasing Y, Del Rio C, Hamlin RL. Assessment of ECG interval and restitution parameters in the canine model of short QT syndrome. J Pharmacol Toxicol Methods. 2010 May-Jun;61(3):231-7. ix Hamlin RL, del Rio C. An approach to the assessment of drug-induced changes in non- electrophysiological properties of cardiovascular function. J Pharmacol Toxicol Methods. 2010 Jul-Aug;62(1):20-9. Zwijnenberg RJ, del Rio CL, Pollet RA, Muir III WW. Effects of perzinfotel on the minimum alveolar concentration of isoflurane in dogs when given as a pre-anesthetic IV, IM or SQ and in combination with butorphanol. Am J Vet Res. 2010 Jun;71(6):604-9. Zwijnenberg RJ, del Rio CL, Pollet RA, Muir III WW. Effects of perzinfotel, butorphanol and a butorphanol-perzinfotel combination on the minimum alveolar concentration of isoflurane in cats. Am J Vet Res. 2010 Jun;71(11):1270-6. Panyasing Y, Kijtawornrat A, del Rio C, Carnes C, Hamlin RL. Uni- or bi-ventricular hypertrophy and susceptibility to drug-induced torsades de pointes. J Pharmacol Toxicol Methods. 2010 Sep-Oct;62(2):148-56
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