Dr. Madison Spach has been one of the most influential thought leaders in the field of cardiac electrophysiology over the past four decades. He received his undergraduate and medical degrees from Duke University. After serving internships in Medicine and Pediatrics he completed his General Pediatrics training and then did a fellowship in Pediatric Cardiology. He then joined the faculty at Duke in Pediatric Cardiology, becoming the Chief of that Division as an Assistant Professor in 1960. He rose to the rank of Professor of Pediatrics, Physiology and Cell Biology. He is currently the James B. Duke Professor of Pediatrics, Emeritus. He has been widely recognized and honored by the Pediatrics, Cardiology and Electrophysiology communities as an outstanding researcher, clinician and teacher. He has served as the President of a number of societies including the Cardiology Section of the American Academy of Pediatrics, North Carolina Heart Association, the Society of Pediatric Research and the Cardiac Electrophysiology Society. He has been honored as the Helen B. Taussig Lecturer at the American Heart Association scientific sessions, the ALZA Distinguished Lecturer of the Biomedical Engineering Society, the Distinguished Scientist Awardee of the North American Society of Pacing and Electrophysiology (NASPE), and the Anlyan Lifetime Achievement Awardee at Duke University. He has enjoyed continuous funding from the National Institutes of Health for nearly 4 decades.

Dr. Spach has made a number of important contributions to the field of Pediatric Cardiology among the most numerous and seminal are those in cardiac electrophysiology. A central focus of his investigative interests is the mechanism of electrical conduction in the heart. He performed a number of critical studies that examined the origin of surface electrocardiographic deflections and the relationships of intracellular to extracellular potentials in the heart.

His group was the first to demonstrate that conduction in the myocardium was discontinuous with components of cytoplasmic and junctional resistance. These observations laid the foundation for the contemporary understanding of anisotropic conduction in the myocardium and functional reentry.

The microscopic anisotropic passive conduction properties were shown to be significant determinants of the propagation response to modification of the sodium conductance by premature depolarizations and by sodium channel-blocking drugs. In nonuniform anisotropic muscle bundles premature action potentials produced unidirectional or longitudinal conduction block, or a dissociated longitudinal conduction (a safer type of propagation, similar to transverse propagation). Directional differences in the velocity conduction of premature action potentials were necessary for the generation of reentrant circuit. Na channel blockade produced a similar use-dependent dissociated longitudinal conduction in nonuniform anisotropic bundles. The electrical events at microscopic level demonstrated that conditions leading to obliteration of side-to-side electrical coupling between fibers provide a primary mechanism for reentry to occur.

His group defined multiple regional differences in the action potential profile in the atria with the longest action potentials in the area of the sinus node, and decreasing duration with increasing distance from the node area. Additionally, multiple conduction abnormalities in the right atrium were identified and conspired with heterogeneous repolarization as the mechanisms of reentry in the atrium.

Dr. Spach’s work explored the importance of the microarchitecture of the heart. His group demonstrated that the myocardial architecture creates inhomogeneities of the cellular electrical load that cause cardiac propagation to be stochastic in nature with the direction and delays in excitation during propagation are constantly changing. The appearance of continuous conduction at the macroscopic level results from spatial and temporal averaging of the microscopic events. The microscopic features of normal propagation provide a protective effect against arrhythmias by reestablishing the general trend of wave-front movement after small variations in excitation events occur.

More recent work has explored the influence of cell size as gap junction distribution as determinants of anisotropic conduction in normally developing myocardial cells and arrhythmogenic pathological substrates. Cell size is as important as gap junction distribution in determining transverse conduction properties in normal developmental hypertrophy of the ventricular myocardium.

Overall, the body of work from Dr. Spach’s laboratory has provided key insights into the nature of electrical conduction in the heart, the mechanisms of cardiac arrhythmias, action of clinically used antiarrhythmic drugs and the susceptibility of the diseased heart to potentially lethal cardiac rhythm disturbances. Those who were fortunate enough to train with Dr. Spach and many of us, who were “taught” through the literature and scientific meetings, are extremely grateful for the wisdom and the grace with which it was imparted.

We are fortunate and honored to have Dr. Madison S. Spach as the 14th Annual Gordon K. Moe Lecturer.