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In the field of cardiac electrophysiology, there is a universal desire: the discovery of a flawless diagnostic maneuver for supraventricular tachycardias (SVTs). This is not merely a wish but a shared odyssey. To improve diagnostic accuracy and achieve sufficient sensitivity and specificity, numerous diagnostic maneuvers have been proposed. However, each has its limitations and prompts a search for new diagnostic techniques. This continuous cycle of discovery and refinement, which we titled “SVT Quest” is reviewed in chronological sequence. This adventure in diagnosing narrow QRS tachycardia unfolds in 3 steps: Step 1 involves differentiating atrial tachycardia from other SVTs based on the observations such as V‐A‐V or V‐A‐A‐V response, ΔAA interval, VA linking, the last entrainment sequence, and response to the atrial extrastimulus. Step 2 focuses on differentiating orthodromic reciprocating tachycardia from atrioventricular nodal reentrant tachycardia based on the observations such as tachycardia reset upon the premature ventricular contraction during His refractoriness, uncorrected/corrected postpacing interval, differential ventricular entrainment, orthodromic His capture, transition zone analysis, and total pacing prematurity. Step 3 characterizes the concealed nodoventricular/nodofascicular pathway and His‐ventricular pathway‐related tachycardia based on observations such as V‐V‐A response, ΔatrioHis interval, and paradoxical reset phenomenon. There is no single diagnostic maneuver that fits all scenarios. Therefore, the ability to apply multiple maneuvers in a case allows the operator to accumulate evidence to make a likely diagnosis. Let's embark on this adventure! The SVT mechanism includes atrial tachycardia (AT), orthodromic reciprocating tachycardia (ORT) via an atrioventricular accessory pathway (AP), nodoventricular pathway (NVP), nodofascicular pathway (NFP) or His‐ventricular pathway, and atrioventricular nodal reentrant tachycardia (AVNRT). Diagnosis should be made in the following three steps: Step 1 involves differentiating AT from other SVTs based on observations such as V‐A‐V or V‐A‐A‐V response, ΔAA interval, VA linking, the last entrainment sequence, and response to atrial extrastimulus. Step 2 focuses on differentiating ORT from AVNRT based on observations such as tachycardia reset upon His‐refractory PVC, uncorrected/corrected postpacing interval (PPI) − tachycardia cycle length (TCL), differential ventricular entrainment, orthodromic His capture, transition zone analysis, and total pacing prematurity (TPP). Step 3 characterizes ORTs via concealed NV/NFP and HVP‐related mechanisms based on observations such as V‐V‐A response, atrioHis (AH) interval, and paradoxical reset phenomenon.

Management strategies for ventricular arrhythmias are guided by the risk of sudden death and severity of symptoms. Patients with a substantial risk of sudden death usually need an implantable cardioverter defibrillator (ICD). Although ICDs effectively end most episodes of ventricular tachycardia or ventricular fibrillation and decrease mortality in specific populations of patients, they have inherent risks and limitations. Generally, antiarrhythmic drugs do not provide sufficient protection from sudden death, but do have a role in reducing arrhythmias that cause symptoms. Catheter ablation is likewise important for reducing the frequency of spontaneous arrhythmias and is curative for some patients, usually those with idiopathic arrhythmias and no heart disease. Arrhythmia surgery is now infrequent, offered by only a few specialised centres for refractory arrhythmias. Advances in understanding of genetic arrhythmia syndromes and in technology for mapping and ablation of ventricular arrhythmias, and enhanced algorithms in implantable devices for rhythm management, have contributed to improved outcomes.

Background Although catheter ablation is an effective therapy for atrial fibrillation (AF), the most common cardiac arrhythmia encountered in clinical practice, AF ablation generates inflammation and oxidative stress in the early postoperative period predisposing to recurrence of AF. Isolevuglandins (IsoLGs) are reactive lipid mediators of oxidative stress injury that rapidly react with endogenous biomolecules to compromise their function. 2-Hydroxybenzylamine (2-HOBA), a potent small molecule scavenger of IsoLGs, sequesters the reactive species as inert adducts. This mechanism, coupled with reported safety in humans, supports the investigation of 2-HOBA as a novel therapeutic to reduce AF caused by oxidative stress, such as that which occurs after catheter ablation. Accordingly, we seek to test the hypothesis that treatment with 2-HOBA will decrease early recurrence of AF and other atrial arrhythmias following AF ablation by decreasing IsoLG adducts with native biomolecules. Methods The proposed trial will randomly assign 162 participants undergoing cryo- or radiofrequency catheter ablation for AF to 2-HOBA ( N = 81) or placebo ( N = 81). Individuals will begin the study drug 3 days prior to ablation and continue for 28 days. Participants will be given a wearable smartwatch capable of detecting and recording atrial arrhythmias. They will be instructed to record ECGs daily with additional ECGs if they experience symptoms of AF or when alerted by the smartwatch AF detection alarm. The primary clinical endpoint will be an episode of AF, atrial tachycardia, or atrial flutter lasting 30 s or more within 28 days post-AF ablation. Secondary measures will be the change in IsoLG adduct levels from blood samples collected immediately pre-ablation and post-ablation and reduction in AF burden as calculated from the smartwatch. Discussion The proposed trial will test the hypothesis that 2-HOBA reduces post-ablation atrial arrhythmias through sequestration of reactive IsoLG species. The results of this study may improve the understanding of the role of IsoLGs and oxidative stress in AF pathogenesis and provide evidence to advance 2-HOBA and related compounds as a new therapeutic strategy to treat AF. Trial registration ClinicalTrials.gov NCT04433091 . Registered on June 3, 2020.

In the last three decades, ablation of atrial fibrillation (AF) has become an evidence-based safe and efficacious treatment for managing the most common cardiac arrhythmia. In 2007, the first joint expert consensus document was issued, guiding healthcare professionals involved in catheter or surgical AF ablation. Mounting research evidence and technological advances have resulted in a rapidly changing landscape in the field of catheter and surgical AF ablation, thus stressing the need for regularly updated versions of this partnership which were issued in 2012 and 2017. Seven years after the last consensus, an updated document was considered necessary to define a contemporary framework for selection and management of patients considered for or undergoing catheter or surgical AF ablation. This consensus is a joint effort from collaborating cardiac electrophysiology societies, namely the European Heart Rhythm Association, the Heart Rhythm Society (HRS), the Asia Pacific HRS, and the Latin American HRS.

Atrial fibrillation (AF) is currently the most commonly treated cardiac arrhythmia. It is generally a progressive disease, often more difficult to control as electromechanical remodeling alters the underlying substrate. Patients typically evolve from infrequent, self-terminating episodes, to more frequent and sustained events. In addition, atrial remodeling may make sinus rhythm more challenging to achieve. Although an ablation strategy limited to pulmonary vein isolation may be curative in those with paroxysmal AF, a more extensive approach is often required in those with persistent AF. This article discusses the current approaches and most recent advances in the ablation of persistent and long-standing persistent AF.

Doc number: O88

Key Clinical PointsAtrial FibrillationAtrial fibrillation is associated with underlying heart disease and with increased risks of death, stroke, heart failure, and dementia.Therapy for conditions that are associated with a risk of atrial fibrillation, including hypertension, hyperlipidemia, diabetes mellitus, sleep apnea, obesity, and excessive alcohol consumption, may reduce the risk of recurrence of atrial fibrillation.The presence or absence of risk factors for stroke is used to estimate the risk of stroke in order to determine whether anticoagulation is indicated for paroxysmal or persistent atrial fibrillation.When atrial fibrillation has been present for 48 hours or longer or for an unknown duration and elective cardioversion is planned, a period of anticoagulation before and after cardioversion is warranted, even when risk factors for stroke are absent.Uncontrolled tachycardia can lead to deterioration of left ventricular function. Attempts to maintain sinus rhythm should be considered when atrial fibrillation has not been persistent for more than 1 year or is paroxysmal and symptomatic. Catheter ablation is more effective than antiarrhythmic drug therapy, particularly for paroxysmal atrial fibrillation.

Ibutilide is a class III antiarrhythmic agent that is used for the conversion of atrial fibrillation to sinus rhythm. 1 – 6 Ibutilide lowers the energy requirement for ventricular defibrillation, but its effect on the energy required for atrial defibrillation has not been determined. 7 – 9 We examined the effect of ibutilide on the energy requirement for atrial defibrillation and assessed whether this agent facilitates transthoracic cardioversion of atrial fibrillation that is resistant to conventional transthoracic cardioversion. Methods Patients Between August 1997 and December 1998, we enrolled 100 consecutive patients referred for cardioversion for an episode of atrial fibrillation that had lasted more . . .