Материал: 2019 ESC - supraventricular tachycardia

with either biventricular or His-bundle pacing is appropriate.569 572 Long-term medical therapy with beta-blockers, and angiotensinconverting enzyme inhibitors or angiotensin II receptor blockers, is indicated before and after successful ablation for the known beneficial effects of these drugs on the LV remodelling process. Given the risk of recurrence of arrhythmias, long-term monitoring of patients is recommended.

16 Supraventricular tachycardia in sports

Athletes with frequent supraventricular arrhythmias should be assessed to exclude the presence of an underlying cardiac disease, electrolyte imbalance, thyroid dysfunction, and the use of stimulants or performance-enhancing drugs. Table 13 outlines the recommendations for sports eligibility of patients with SVT.573,574

Ventricular pre-excitation (WPW syndrome) is a rare cause of sudden cardiac death in young athletes.575 Although many individuals with ventricular pre-excitation remain asymptomatic throughout their lives, symptomatic AVRT may occur. Patients with WPW may also develop other arrhythmias, such as AF, which could degenerate into ventricular fibrillation and sudden cardiac death. Because sports activity has been associated with an increased risk of AF,576 athletes with ventricular pre-excitation have an increased risk of sudden cardiac death if the AP has the potential for fast antegrade conduction. Thus, catheter ablation of the AP is currently recommended in symptomatic athletes with ventricular pre-excitation. Asymptomatic athletes with intermittent pre-excitation (at rest or during exercise) or abrupt disappearance of pre-excitation during stress testing may be considered to be at low risk (see section 11.3.11 for reservations), but should be further evaluated as they may be eligible for competitive sports activity. In asymptomatic athletes with ventricular pre-excitation, invasive risk stratification should be conducted as described in section 11.3.11 and catheter ablation should be

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performed in those with high-risk features.577 Asymptomatic patients stratified at low risk are allowed to practice competitive sports.

AVNRT, orthodromic AVRT over a concealed AP, and AT are not listed among the causes of sudden cardiac death during exercise in patients with a structurally normal heart. However, their occurrence during sports activity may be associated with very high heart rate because of sympathetic stimulation and may cause haemodynamic impairment even in patients with structurally normal hearts. Accordingly, catheter ablation should generally be recommended for all athletes with a history of paroxysmal SVT. Athletes with SVT who do not wish to undergo catheter ablation, or in whom the procedure has been unsuccessful, may be considered eligible for competitive sports activity if the arrhythmia is sporadic, unrelated to cardiac disease, well tolerated, and unrelated to exercise, and when the sports activity does not have a high intrinsic risk of loss of consciousness (such as divers, pilots, horse riders, etc.).578

Treatment of paroxysmal SVT with beta-blockers or sodium channel blockers is discouraged in athletes, because these drugs may reduce performance during sports and have limited ability to prevent arrhythmia recurrence during sports activity. Moreover, betablockers are listed by the World Anti-Doping Agency as prohibited drugs in particular sports.

17 Supraventricular tachycardia and driving restrictions

The frequency of which medical causes contribute to motor vehicle accidents is not precisely known. Data on arrhythmias as a cause of motor vehicle accidents are hard to obtain due to the difficulty of documenting such events in the general population. However, the proportion is believed to be small, with 1 - 3% of all motor vehicle accidents established as being due to a driver’s sudden incapacitation.579 Of these accidents, 5 - 10% are related to cardiac causes, with

or without syncope, while <2% of cases of reported sudden driver incapacitation have resulted in injury or death to bystanders, or other road users.579

In 2013, a Working Group of the ESC published detailed recommendations on driving restriction in patients with SVT (Table 14).580 Two groups of drivers are considered. Group 1 comprises drivers of motorcycles, cars, and other small vehicles with and without a trailer. Group 2 includes drivers of vehicles over 3500 kg or passengercarrying vehicles exceeding eight seats excluding the driver. Drivers of taxicabs, small ambulances, and other vehicles form an intermediate category between the ordinary private driver and the vocational driver.

18 Key messages

•Not all SVTs are arrhythmias of the young.

•Vagal manoeuvres and adenosine are the treatments of choice for the acute therapy of SVT, and may also provide important diagnostic information.

•Verapamil is not recommended in wide QRS-complex tachycardia of unknown aetiology.

•Consider using ivabradine, when indicated, together with a betablocker.

•In all re-entrant and most focal arrhythmias, catheter ablation should be offered as an initial choice to patients, after having explained in detail the potential risks and benefits.

•Patients with macro-re-entrant tachycardias following atrial surgery should be referred to specialized centres for ablation.

•In post-AF ablation ATs, focal or macro-re-entrant, ablation should be deferred for >3 months after AF ablation, when possible.

•Ablate AVNRT, typical or atypical, with lesions in the anatomical area of the nodal extensions, either from the right or left septum.

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•AVNRT, typical or atypical, can now be ablated with almost no risk of AV block.

•Do not use sotalol in patients with SVT.

•Do not use flecainide or propafenone in patients with LBBB, or ischaemic or structural heart disease.

•Do not use amiodarone in pre-excited AF.

•One in five patients with asymptomatic pre-excitation will develop an arrhythmia related to their AP during follow-up.

•The risk of cardiac arrest/ventricular fibrillation in a patient with asymptomatic pre-excitation is 2.4 per 1000 person-years.

•Non-invasive screening may be used for risk stratification of patients with asymptomatic pre-excitation, but its predictive ability remains modest.

•Invasive assessment with an EPS is recommended in patients with asymptomatic pre-excitation who either have high-risk occupations or are competitive athletes.

•If a patient undergoes assessment with an EPS and is found to have an AP with ‘high-risk’ characteristics, catheter ablation should be performed.

•If possible, avoid all antiarrhythmic drugs during the first trimester of pregnancy. If beta-blockers are necessary, use only beta-1 selective agents (but not atenolol).

•If ablation is necessary during pregnancy, use non-fluoroscopic mapping.

•Consider TCM in patients with reduced LV function and SVT.

•Ablation is the treatment of choice for TCM due to SVT. AV nodal ablation with subsequent biventricular or His-bundle pacing (‘ablate and pace’) should be considered if the SVT cannot be ablated.

19 Gaps in the evidence

•The distinction between triggered activity and enhanced automaticity is not straightforward, as the two mechanisms share many similar responses and characteristics, such as enhancement by

adrenergic activation and suppressed by L-type Ca2þ current blockade.

•Re-entrant circuits may be microscopic or simulate foci by surface ‘breakthrough’ of transmural propagation. Thus, mapping may be inadequate to distinguish them from automatic/triggered activity.

•The exact circuit of AVNRT, the most common regular arrhythmia in the human, remains unresolved.

•The potential role of connexin proteins in AVNRT, and SVT in general, is under investigation.

•Both invasive and non-invasive tests for the risk assessment of patients with asymptomatic pre-excitation have limitations, being dependent on the autonomic tone. More accurate risk-stratifica- tion models are needed.

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•The proper management of asymptomatic pre-excitation and strict catheter ablation indications have not been established.

•The genetics of SVT have not been adequately studied. There has been evidence for familial forms of AVNRT, AVRT, sinus tachycardia, and AT, but data are scarce.

•Novel electroanatomical mapping systems now allow the simultaneous visualization of activation and voltage. The implications that this may have on characterizing the tachycardia substrate, and not just the circuit, require future research.

•Mathematical modelling and numerical analysis of recorded ECGs, using fast Fourier and Gaussian models, may be helpful for the future of artificial intelligence applications in the differential diagnosis of narrow and wide QRS-complex tachycardias, but experience is limited.

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 to30%,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,

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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.584 589 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

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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 Trust, Cambridge University Health Partners, Cambridge, United Kingdom; Siew Yen Ho, Cardiac Morphology, Royal Brompton Hospital, London, United Kingdom; Juan-Carlos Kaski, Molecular and Clinical Sciences Research Institute, St George’s University of London, London, United Kingdom; Karl-Heinz Kuck, Cardiology, Asklepios Klinik St. Georg, Hamburg, Germany; Pier David Lambiase, Cardiology, UCL & Barts Heart Centre, London, United Kingdom; Frederic Sacher, Service de Rythmologie, IHU LIRYC/Bordeaux University Hospital, Bordeaux, France; Georgia Sarquella-Brugada, Arrhythmia, Inherited Cardiac Disease and Sudden Death Unit, Hospital Sant Joan de De´u, Barcelona, Spain; Piotr Suwalski, Central Clinical Hospital of the Ministry of Interior and Administration, Centre of Postgraduate Medical Education, Warsaw, Poland; Antonio Zaza, Universita degli Studi Milano-Bicocca, Dipartimento di Biotecnologie e Bioscienze, Bldg U3, p.za della Scienza 2, 20126 Milano, Italy.

ESC Committee for Practice Guidelines (CPG): Stephan Windecker (Chairperson) (Switzerland), Victor Aboyans (France), Colin Baigent (United Kingdom), Jean-Philippe Collet (France), Veronica Dean (France), Victoria Delgado (Netherlands), Donna Fitzsimons (United Kingdom), Chris P. Gale (United Kingdom), Diederick E. Grobbee (Netherlands), Sigrun Halvorsen (Norway), Gerhard Hindricks (Germany), Bernard Iung (France), Peter Ju¨ni (Canada), Hugo

A.Katus (Germany), Ulf Landmesser (Germany), Christophe Leclercq (France), Maddalena Lettino (Italy), Basil S. Lewis (Israel), Bela Merkely (Hungary), Christian Mueller (Switzerland), Steffen E. Petersen (United Kingdom), Anna Sonia Petronio (Italy), Dimitrios J. Richter (Greece), Marco Roffi (Switzerland), Evgeny Shlyakhto (Russian Federation), Iain

A.Simpson (United Kingdom), Miguel Sousa-Uva (Portugal), Rhian M. Touyz (United Kingdom).