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............................................................................................................................................................................. 21 Areas for further research

With the advent of catheter ablation in the 1990s, resulting in the successful elimination of APs in symptomatic patients, AVRT now represents <20% of all SVTs.11,13 The frequency of AVNRT, which used to account for 50% of all SVT cases,14 has changed to 30%,11,13 and the proliferation of AF ablation will unavoidably result in more iatrogenic left atrial MRAT. Moreover, the prolonged survival of paediatric and ACHD patients is expected to impose a further challenge on electrophysiologists, who will encounter even more complex MRATs. Several important advances in the field of anatomical and electrical mapping, as well as our appreciation of scar tissue and the transmurality of ablation lesions, should improve our efficiency in treating these patients. The past decade has witnessed a rapid evolution of ablation equipment and electrode-guiding systems, which has resulted in more controllable and safer procedures. Intracardiac echocardiography, robotic techniques, and sophisticated anatomical navigation systems have been developed, and it is now possible to perform ablation without exposing the operator to radiation and ergonomically unfavourable positions.581 New materials for electrodes and other equipment have allowed the concept of a radiation-free electrophysiology laboratory with the use of CMR. The vision of a fully radiation-free, magnetic laboratory in the future is not science fiction anymore.582 The revolution in computer technology offers not only improved mapping and electrode-moving systems, but also the enhancement of specific SVT classification schemes with fully automated algorithms that may greatly assist emergency departments, ambulances, and monitored patients.583 Mathematical modelling and numerical analyses have also been employed in the investigation of the circuit of AVNRT.317,329 Further analysis of recorded ECGs using fast Fourier and Gaussian models may also provide useful diagnostic information about the nature of the tachycardia. Novel electroanatomical mapping systems are being developed to assist the identification of the tachycardia mechanism and optimal ablation site of SVT, and, especially, complex atrial macro-re-entrant tachycardias, with reduced fluoroscopy times.584589 Systems are now available that allow the simultaneous visualization of activation and voltage. The implications that these may have on characterizing the tachycardia substrate, and not just the circuit, require future research. New data on the genetics of SVT continually appear since the identification of a missense mutation in the PRKAG2 gene, which encodes the regulatory c-subunit of adenosine monophosphate (AMP)-activated protein kinase, as a cause of familial WPW syndrome.590,591 The R302Q mutation in PRKAG2 has been associated with Mahaim fibers.592 A novel form of WPW syndrome is associated with microdeletion of the BMP2 gene, which encodes bone morphogenetic protein-2, a member of the transforming growth factor-beta gene superfamily, and affects the development of annulus fibrosus.593 Other rare, genetic forms of pre-excitation have also been described.398 Whether this kind of genetic predisposition translates into a higher ventricular fibrillation risk remains to be seen. Genetic animal models of WPW that express mutations (such as of the gene encoding the AMP-activated protein kinase) responsible for a familial form of WPW syndrome with a phenotype identical to that of the human syndrome have been developed, and may provide insight into the development and properties of the cardiac conduction system and APs.594 Spontaneous AVNRT has also been identified as a potential first clinical manifestation of concealed Brugada syndrome, particularly in female patients.595 It has been postulated that genetic variants that reduce the sodium current may predispose individuals to expression of both phenotypes. Cellular electrophysiology is now being integrated into genetic analysis. The coupling of wholeexome sequencing with cellular electrophysiological functional analysis may elucidate the underlying pathophysiological mechanism responsible for certain phenotypes.596 Recently, a familial form of IST was shown to be associated with a gain-of-function mutation in the HCN4 pacemaker channel (R524Q), conferring an increased sensitivity to the second messenger cyclic AMP, which is a key mediator in sympathetic modulation.597 These developments may have important implications for a more specific diagnostic and personalized therapeutic approach in SVT. Future research should define actionable patient-specific molecular arrhythmia mechanisms, clarify the responses of the underlying substrates to interventions, and achieve selective supraventricular targeting of specific arrhythmic mechanisms with drugs.

SVTs are not only an everyday clinical problem, with AVNRT being the most common regular arrhythmia in humans. They also provide the background for proper training of future electrophysiologists by means of their well-defined circuits, in most cases, and predictable responses in the electrophysiology laboratory. In the era of computerized approaches that are now available for AF, complex AT, and VT ablation, this is very important for a rational, Aristotelian approach to the art of medicine.598

22 Supplementary data

Supplementary Data with additional Supplementary Figures and text complementing the full text, as well as sections on the electrophysiological mechanisms of SVT, tachycardia circuits, and cardiac anatomy for the electrophysiologist, along with the related supplementary references, are available on the European Heart Journal website and via the ESC website at www.escardio.org/guidelines.

23 Appendix

Author/Task Force Member Affiliations Elena Arbelo, Arrhythmia Unit, Cardiovascular Institute, Hospital Clinic de Barcelona, Universitat de Barcelona, Spain; Cardiovascular Institute, Hospital Clınic, Universitat de Barcelona, Barcelona, Spain; and Institut d’Investigacio August Pi i Sunyer (IDIBAPS), Centro de Investigacion Biome ́dica en Red de Enfermedades; Barcelona, Spain; Fernando Arribas, Department of Cardiology, Hospital 12 de Octubre, Madrid, Spain; Jeroen J. Bax, Cardiology, Leiden University Medical Center, Leiden, Netherlands; Carina Blomstro ̈m- Lundqvist, Department of Medical Science and Cardiology, Uppsala University, Uppsala, Sweden; Hugh Calkins, Cardiology, John Hopkins Medical Institutions, Baltimore, United States of America; Spyridon G. Deftereos, 2nd Department of Cardioloy, National and Kapodistrian University of Athens, Athens, Greece; Gerhard-Paul Diller, Cardiology III, University Hospital Muenster, Muenster, Germany; Juan J. Gomez-Doblas, Cardiology, Hospital Universitario Virgen de la Victoria, CIBERG, Malaga, Spain; Bulent Gorenek, Cardiology Department, Eskisehir Osmangazi University, Turkey; Andrew Grace, Department of Cardiology, Royal Papworth Hospital NHS Foundation Downloaded from academic.oup.com/eurheartj/article/41/5/655/5556821 by guest on 07 October 2026