MAPs have undergone a fascinating history, beginning with injury potentials in 1883, and undergoing a remarkable renaissance over the last 30 years in many areas of electrophysiology research, both basic and clinical. Since 1986, the contact electrode technique has provided a unique means to test basic research concepts in the intact or in vivo human heart. Even so, observations in clincal elctrophysiology still warrant further exploration in basic science. Scientific experts in the field have contributed to this volume their latest data on myocardial repolarization and the many factors that modulate normal and abnormal repolorization, to the benefit of electrophysiologists, cardiologists, clinicians as well as pharmaceutical researchers involved in the development of aniarrhythmic drugs. By concentrating on the electrical activity of the in situ heart, this timely and informative reference brings to light information that cannot be obtained by any other means. This work's detailed overview of MAP techniques highlights: how to use the technique properly in patients to obtain high-quality signals and avoid artifacts how to use computers for automated analyses of the MAP signals a thorough evaluation of the basic theory underlying the genesis of the monophasic action potential signal direct comparison, in an intact heart, of the direct myocardial action potential with the body surface ECG the limitations and possible new frontiers of this techniqueAlong with new techniques, such as single-catheter MAP recording, chapters feature new understandings about heart rate, antiarrhythmic drugs, mechanoelectrical feedback, dispersion of ventricular repolarization, detection of arrhythmia triggers, ventricular fibrillation, and antiarrhythmic device-related uses of MAP recordings.

Table of Contents:
Foreword from the Basic Scientist's ViewB. F. Hoffman Foreword from the Clinical Electrophysiologist's Point of View: Potential Future Uses of Monophasic Action Potential RecordingsM. M. Scheinman Section I. Monophasic Action Potential Methodology 1. Theory Underlying the Suction Electrode Method and Early Use in Clinical ResearchS. B. Olsson, S. Yuan 2. Monophasic Action Potentials Recorded by Contact Electrode Method: Genesis, Measurements and InterpretationM. R. Franz 3. Computer Model of Monophasic Action Potential GenesisN. Trayanova, L. Malden, E. Atkinson 4. Multiple Monophasic Action Potential Recording With a Single Magnetocardiographically Localizable Amagnetic CatheterR. Fenici, P. Fenici 5. The Monophasic Action Potential-Pacing Combination Catheter: Assessing The Relationship Between Repolarization and Excitability In VivoM. R. Franz 6. The Monophasic Action Potential as a Guide and Clinical Teaching Tool During Electrophysiology StudiesP. E. Karasik, M. E. Chavez, R. D. Fletcher, M. R. Franz 7. How to Record High-Quality Monophasic Action Potential TracingsP. T. Sager 8. Computer-Assisted Real-Time Monophasic Action Potential AnalysisB. C. Knollman Section II. Rate-Dependent Modulation of Action Potential Duration in Normal and Ischemic Myocardium 9. Activation-Repolarisation Sequence Memory in the Isolated Rabbit HeartA. Costard-Jaeckle, M. Antz, M. R. Franz 10. Tachycardia Superimposed on Bradycardia Prolongs Ventribular Refractoriness and Facilitates Arrhythmia InductionT. Satoh, D. P. Zipes 11. Cardiac Memory in the AtriaM. A. Wood 12. Use of Cardiac Action Potentials to Investigate Cardiac Memory: From Bedside to Computer ModelR. Goyal, F. Morady 13. Action Potential Alternans, Electrical Restitution, Repolarisation Dispersion and Arrhythmia Vulnerability in the Isolated Ischemic Rabbit HeartR. W. Kurz, M. R. Franz 14. The Role of Cytosolic Calcium in Electrical and Mechanical Alternans During IschemiaW. T. Clusin 15. Action Potential Duration Restitution and Graded Response Mechanisms of Ventricular Vulnerability to Reentry and Fibrillation: Role of Monophasic Action Potential RecordingsH. S. Karagueuzian, Y-H. Kim, M. Yashima, T-J. Wu, P-S. Chen 16. Physiologic Mechanisms Underlying the Link Between T Wave Alternans and Vulnerability to Ventricular FibrillationR. L. Verrier, B. D. Nearing 17. Changes in Monophasic Action Potential Configuration and Prevalence of Ventricular Fibrillation During Regional Ischemia and Reperfusion in the Intact Canine Heart: Effects of Preconditioning Ischemia and Potassium Channel ModulatorsT. Miyazaki, S. Ogawa, D. P. Zipes Section III. Dispersion of Ventricular Repolarization and Refractoriness 18. High Resolution Management of Ventricular Repolarisation Using Voltage-Sensitive DyesI. Libbus, K. R. Laurita, D. S. Rosenbaum 19. Effects of Heart Rate and Antiarrhythmic Drugs on Dispersion Of Ventricular Repolarization Measured by Multiple Monophasic Action Potential RecordingsM. Zabel, S. H. Hohnloser, M. R. Franz 20. Dispersion of Ventricular Repolarisation and Arrhythmias: Basic and Clinical CorrelatesD. P. Higham, R. W. F. Campbell 21. Validation of Electrocardiographic Variables of Dispersion of Ventricular Repolarisation with Direct Myocardial Repolarisation MeasurementsM. Zabel, P. R. Lichtlen, A. Haverich, M. R. Franz 22. Mapping of the Spatial Correlation Between the Activation and Repolarisation Properties in the Normal VentricleL. Gepstein, G. Hayam, S. A. Ben-Haim 23. Abnormal Relationship Between Activation and Repolarisation in Human Left Ventricular HypertrophyM. R. Franz, K. Bargheer Section IV. Evaluation of Antiarrhythmic Drug Effects 24. Frequency Dependence of Class I and Class III Antiarrhythmic Agents Explaining Their Antiarrhythmic and Proarrhythmic PropertiesL. Hondeghem 25. Effect of d-Sotalol on the Vulnerable Window of Ventricular Fibrillation and a Definition of the "Area of Vulnerability"P. F. Kirchhof, C. L. Fabritz 26. Are Newer Class III Antiarrhythmic Drugs Better? Experimental and Clinical DataC. Schmitt, J. Schreieck, B. Zrenner 27. Frequency Dependence of Class III Antiarrhythmic Drugs and Reversal by Sympathetic StimulationP. T. Sager, A. E. Shalaby 28. Modification of the Ventricular Tachyarrhythmia Substrate by Combined Class Ia and Class III Drug Treatment: Role of Use DependencyS. D. Lee, P. Dorian, D. M. Newman 29. Post-Repolarisation Refractoriness: Could It Be Why Antiarrhythmic Drugs Work?P. F. Kirchhof, C. L. Fabritz, M. R. Franz 30. Mechanism of Atrial Flutter Conversion by Class III Antiarrhythmic DrugsG. Fenelon, K. A. Ellenbogen, M. A. Wood, B. S. Stambler Section V. Torsades de Pointes and Other Triggered Ventricular Arrhythmias 31. New Theories on the Genesis of Early and Delayed After-DepolarisationsB. Szabo, W. M. Jackman, R. Lazzara 32. Early After-Depolarisations in the In Situ Canine Heart: Mechanistic Insights Into Acquired Torsades de Pointes ArrhythmiasM. A. Vos, S. C. Verduyn, H. J. Wellens 33. Delayed After-Depolarisation in the In Situ Canine Heart: The Role of the Diastolic UpslopeM. A. Vos, M. de Groot, H. J. Wellens 34. Electrophysiologic Characteristics of M Cells and Their Roles in ArrhythmiasC. Antzelevitch, G-X. Yan, W. Shimizu, S. Sicouri, G. Eddlestone, A. C. Zygmunt 35. Monophasic Action Potentials and Torsades de Pointes: Bridging the Gap Between Experimental Studies and Clinical DataL. Eckhardt, R. Johna, M. Borggrefe, G. Breithardt, W. Haverkamp 36. Disorders of Cardiac Repolarisation and ArrhythmogenesisN. El-Sherif, E. B. Caref 37. Early Afterdepolarisations and Polymorphic Ventricular Arrhythmias in Acquired and Congenital Long QT Syndrome: Observations from Clinical and Experimental StudiesW. Shimizu, T. Ohe, C. Antzelevitch 38. Gender as a Risk Factor for Acquired Torsades de PointesS. N. Ebert, X-K. Liu, R. L. Woosley Section VI. Mechanoelectrial Feedback 39. Effects of Ventricular Dilatation on Conduction, Repolarisation, and Defibrillation Thresholds in Isolated Rabbit HeartsM. J. Reiter 40. Mechanisms of Load-Induced Changes in Ventricular Repolarisation and RefractorinessB. B. Lerman. E. D. Engelstein 41. Time and Voltage Dependence of Electrophysiologic Stretch Effects in the Intact HeartM. Zabel, F. Sachs, M. R. Franz Section VII. Ventricular Fibrillation and Defibrillation 42. Nonuniform Repolarisation and the Wavelet Hypothesis of Cardiac FibrillationJ. A. Abildskov, R. L. Lux 43. Monophasic Action Potential Recordings During Ventricular Fibrillation Compared To Intracellular RecordingsC. L. Fabritz, P. Kirchhof, R. Coronel, T. Opthof, M. R. Franz, M. Janse 44. Extension of Refractoriness Mechanism for Ventricular DefibrillationO. H. Tovar, J. L. Jones 45. Mechanisms of Induction and Termination of Ventricular FibrillationS. Behrens, M. R. Franz 46. Effects of Monophasic and Biphasic Defibrillation Shocks on Dispersion of Ventricular Depolarisation and RepolarisationP. C. Fotuhi, X. Zhou, S. B. Knisley, R. E. Ideker Section VIII. Antiarrhythmic Device-Related Uses of Monophasic Action Potential Recording 47. Real-Time Monitoring of Radiofrequency-Induced Myocardial Lesions by Simultaneous Recording of Monophasic Action PotentialsM. R. Franz, H. Sharkey, S. Edwards, M. M. Scheinman 48. Electrophysiologic Basis for and Clinical Experience with Multisite Atrial Pacing for Prevention of Atrial FibrillationS. Saksena, A. Prakash, R. B. Krol 49. Local Capture by Atrial Pacing in Chronic Atrial Fibrillation Monitored by Monophasic Action Potential RecordingsC. Pandozi, M. Villani, M. Santini 50. A Novel Automated Method to Detect FF Intervals During Atrial Fibrillation Using the Monophasic Action Potential TechniqueM. Adam, V. Barbaro, P. Bartolini, G. Calcagnini, S. Morelli, F. Bellocci, P. Zecchi, A. S. Montenero