Targeted Treatment of Inappropriate Sinoatrial Node Tachycardia Based on Electrophysiological and Structural Mechanisms

Abstract

The purpose of this review is to determine the causal mechanisms and treatment of inappropriate sinoatrial tachycardia (IST), defined as a non-physiological elevation in resting heart rate. IST is defined as a resting daytime sinus rate >100 beats/minute and an average 24-hour heart rate >90 beats/minute. Potential causal mechanisms include sympathetic receptor hypersensitivity, blunted parasympathetic tone, or enhanced intrinsic automaticity within the sinoatrial node (SAN) pacemaker-conduction complex. These anomalies may coexist in the same patient. Recent ex-vivo near-infrared transmural optical imaging of the SAN in human and animal hearts provides important insights into the functional and molecular features of this complex structure. In particular, it reveals the existence of preferential sinoatrial conduction pathways that ensure robust SAN activation with electrical conduction. The mechanism of IST is debated because even high-resolution electroanatomical mapping approaches cannot reveal intramural conduction in the 3-dimensional SAN complex. It may be secondary to enhanced automaticity, intranodal re-entry, or sinoatrial conduction pathway re-entry. Different pharmacological approaches can target these mechanisms. Long-acting β blockers in IST can act on both primarily increased automaticity and dysregulated autonomic system. Ivabradine targets sources of increased SAN automaticity. Conventional or hybrid ablation may target all the described abnormalities. This review provides a state-of-the-art overview of putative IST mechanisms. In conclusion, based on current knowledge, pharmacological and ablation approaches for IST, including the novel hybrid SAN sparing ablation, are discussed. The purpose of this review is to determine the causal mechanisms and treatment of inappropriate sinoatrial tachycardia (IST), defined as a non-physiological elevation in resting heart rate. IST is defined as a resting daytime sinus rate >100 beats/minute and an average 24-hour heart rate >90 beats/minute. Potential causal mechanisms include sympathetic receptor hypersensitivity, blunted parasympathetic tone, or enhanced intrinsic automaticity within the sinoatrial node (SAN) pacemaker-conduction complex. These anomalies may coexist in the same patient. Recent ex-vivo near-infrared transmural optical imaging of the SAN in human and animal hearts provides important insights into the functional and molecular features of this complex structure. In particular, it reveals the existence of preferential sinoatrial conduction pathways that ensure robust SAN activation with electrical conduction. The mechanism of IST is debated because even high-resolution electroanatomical mapping approaches cannot reveal intramural conduction in the 3-dimensional SAN complex. It may be secondary to enhanced automaticity, intranodal re-entry, or sinoatrial conduction pathway re-entry. Different pharmacological approaches can target these mechanisms. Long-acting β blockers in IST can act on both primarily increased automaticity and dysregulated autonomic system. Ivabradine targets sources of increased SAN automaticity. Conventional or hybrid ablation may target all the described abnormalities. This review provides a state-of-the-art overview of putative IST mechanisms. In conclusion, based on current knowledge, pharmacological and ablation approaches for IST, including the novel hybrid SAN sparing ablation, are discussed. The purpose of this review is to determine the causal mechanisms and treatment of inappropriate sinoatrial tachycardia (IST), defined as a nonphysiological elevation in resting heart rate. IST is a chronic condition in which the sinus rate exceeds physiological needs and is otherwise unexplained by any specific trigger. IST is defined as a resting daytime sinus rate >100 beats/minute and average 24-hour heart rate >90 beats/minute.1Olshansky B Sullivan RM. Inappropriate sinus tachycardia.J Am Coll Cardiol. 2013; 61: 793-801Crossref PubMed Scopus (103) Google Scholar,2Olshansky B Sullivan RM. Inappropriate sinus tachycardia.Europace. 2019; 21: 194-207Crossref PubMed Scopus (29) Google Scholar Symptoms are heterogenous and may include palpitations, exercise intolerance, dyspnea, fatigue, syncope, chest pain, anxiety, and depression. Up to 90% of IST patients are young women with an average age of approximately 30 years.3Still AM Raatikainen P Ylitalo A Kauma H Ikäheimo M Antero Kesäniemi Y Huikuri HV Prevalence, characteristics and natural course of inappropriate sinus tachycardia.Europace. 2005; 7: 104-112Crossref PubMed Scopus (90) Google Scholar, 4Lopera G Castellanos A Moleiro F Huikuri HV Myerburg RJ. Chronic inappropriate sinus tachycardia in elderly females.Ann Noninvasive Electrocardiol. 2003; 8: 139-143Crossref PubMed Scopus (20) Google Scholar, 5Pellegrini CN Scheinman MM. Epidemiology and definition of inappropriate sinus tachycardia.J Interv Card Electrophysiol. 2016; 46: 29-32Crossref PubMed Scopus (8) Google Scholar, 6Morillo CA Klein GJ Thakur RK Li H Zardini M Yee R. Mechanism of “inappropriate” sinus tachycardia. Role of sympathovagal balance.Circulation. 1994; 90: 873-877Crossref PubMed Scopus (175) Google Scholar Despite several basic and clinical studies, the electrophysiological mechanisms of IST remain heterogeneous. The increased heart rate is due to dysfunctional intrinsic sinoatrial node (SAN) pacemaker automaticity, abnormal function of the cardiac autonomic nerves, and/or various forms of macro or micro-reentry.7Antzelevitch C Burashnikov A. Overview of basic mechanisms of cardiac arrhythmia.Card Electrophysiol Clin. 2011; 3: 23-45Abstract Full Text Full Text PDF PubMed Scopus (197) Google Scholar,8Baruscotti M Bianco E Bucchi A DiFrancesco D. Current understanding of the pathophysiological mechanisms responsible for inappropriate sinus tachycardia: role of the If “funny” current.J Interv Card Electrophysiol. 2016; 46: 19-28Crossref PubMed Scopus (22) Google Scholar These anomalies may coexist in the same patient. Potential etiologies of IST require patient-specific treatments, with highly variable long-term success and safety.9Rodríguez-Mañero M Kreidieh B Al Rifai M Ibarra-Cortez S Schurmann P Álvarez PA Fernández-López XA García-Seara J Martínez-Sande L González-Juanatey JR Valderrábano M Ablation of inappropriate sinus tachycardia: a systematic review of the literature.JACC Clin Electrophysiol. 2017; 3: 253-265Crossref PubMed Scopus (26) Google Scholar The aim of this review is to provide a state-of-the-art overview of the putative mechanisms of IST. Furthermore, based on current knowledge, pharmacological and ablation strategies for IST are discussed (Figure 1, Figure 2).Figure 2Inappropriate sinus node mechanism: re-entry. The SAN is represented with SACPs extending towards SVC, IVC and RAA, that is separated from the SAN by the CT. Re-entry can be secondary to anatomic or functional block in SACPs, block related to sink source mismatch, fibrosis and slow conduction. Hypothesized re-entrant mechanism through SACPs is shown: from the SAN the impulse travels towards SACPs (red arrows, right side), it blocks in one SACP that provides the pathway for the re-entrant wavefront (blue arrow, right side). RAA = right atrial appendage.View Large Image Figure ViewerDownload Hi-res image Download (PPT) The SAN, located at the junction of the superior vena cava (SVC) and the right atrium, is a complex, multi-compartmental structure located at an intramural depth of approximately 1 to 3 mm and composed of small clusters of pacemaker myocytes arranged in parallel rows that frequently anastomose.10James TN. Anatomy of the human sinus node.Anat Rec. 1961; 141: 109-139Crossref PubMed Scopus (152) Google Scholar, 11Sánchez-Quintana D Cabrera JA Farré J Climent V Anderson RH Ho SY. Sinus node revisited in the era of electroanatomical mapping and catheter ablation.Heart. 2005; 91: 189-194Crossref PubMed Scopus (143) Google Scholar, 12Csepe TA Zhao J Hansen BJ Li N Sul LV Lim P Wang Y Simonetti OP Kilic A Mohler PJ Janssen PML Fedorov VV. Human sinoatrial node structure: 3D microanatomy of sinoatrial conduction pathways.Prog Biophys Mol Biol. 2016; 120: 164-178Crossref PubMed Scopus (64) Google Scholar, 13Li N Hansen BJ Csepe TA Zhao J Ignozzi AJ Sul LV Zakharkin SO Kalyanasundaram A Davis JP Biesiadecki BJ Kilic A Janssen PML Mohler PJ Weiss R Hummel Fedorov VV. and intranodal and conduction pathways the human sinoatrial node from 2017; PubMed Scopus Google Scholar It is that the SAN is the SAN is of pacemaker are and within of and to a SAN pacemaker TN. Anatomy of the human sinus node.Anat Rec. 1961; 141: 109-139Crossref PubMed Scopus (152) Google Scholar, 11Sánchez-Quintana D Cabrera JA Farré J Climent V Anderson RH Ho SY. Sinus node revisited in the era of electroanatomical mapping and catheter ablation.Heart. 2005; 91: 189-194Crossref PubMed Scopus (143) Google Scholar, 12Csepe TA Zhao J Hansen BJ Li N Sul LV Lim P Wang Y Simonetti OP Kilic A Mohler PJ Janssen PML Fedorov VV. Human sinoatrial node structure: 3D microanatomy of sinoatrial conduction pathways.Prog Biophys Mol Biol. 2016; 120: 164-178Crossref PubMed Scopus (64) Google Scholar, 13Li N Hansen BJ Csepe TA Zhao J Ignozzi AJ Sul LV Zakharkin SO Kalyanasundaram A Davis JP Biesiadecki BJ Kilic A Janssen PML Mohler PJ Weiss R Hummel Fedorov VV. and intranodal and conduction pathways the human sinoatrial node from 2017; PubMed Scopus Google Scholar These SAN pacemaker clusters as that electrical Recent ex-vivo human heart with intramural near-infrared optical mapping that sinoatrial conduction pathways and the SAN with the near-infrared optical mapping is a imaging that or in the heart and optical Fedorov B cardiac pacemaker of the sinoatrial node optical PubMed Scopus Google Scholar These that the SAN is from the by fibrosis and for 3 to SACPs that electrical to the atrial and to atrial activation sinus N Hansen BJ Csepe TA Zhao J Ignozzi AJ Sul LV Zakharkin SO Kalyanasundaram A Davis JP Biesiadecki BJ Kilic A Janssen PML Mohler PJ Weiss R Hummel Fedorov VV. and intranodal and conduction pathways the human sinoatrial node from 2017; PubMed Scopus Google N Kalyanasundaram A Hansen BJ R G PJ Zakharkin S S Janssen Biesiadecki BJ F Hummel Mohler PJ H Zhao J Fedorov VV. intranodal conduction and in human sinoatrial PubMed Scopus Google Scholar In several are to the SACP in the SAN and the TA Zhao J Hansen BJ Li N Sul LV Lim P Wang Y Simonetti OP Kilic A Mohler PJ Janssen PML Fedorov VV. Human sinoatrial node structure: 3D microanatomy of sinoatrial conduction pathways.Prog Biophys Mol Biol. 2016; 120: 164-178Crossref PubMed Scopus (64) Google Scholar This structure of the SACP is to function of the SAN by the SAN pacemaker and the The SAN and the function a resting with atrial to This to 30 in of an current with a of the SAN and automaticity. 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A in the cardiac pacemaker is with inappropriate sinus 2017; PubMed Scopus Google Scholar (Figure from the various autonomic as the mechanism of increased automaticity in IST (Figure may be by SAN with an abnormal to the physiological autonomic or a dysregulated autonomic F R C Chronic sinus tachycardia in otherwise 91: PubMed Scopus Google Scholar In a of IST, of into the at the of the right superior autonomic the SAN, IST for and autonomic BJ R R of inappropriate sinus tachycardia: and Interv Card Electrophysiol. 2005; PubMed Scopus Google Scholar the SAN require in and the of the the junction with the right atrium, in the JA S and of the human intrinsic cardiac Rec. PubMed Scopus Google Scholar Furthermore, in the of from the right the to the IST and the SAN activation and J BJ G Y Y Y R Anatomy and of the right for the of inappropriate sinus tachycardia.J Electrophysiol. PubMed Scopus Google Scholar on clinical CA Klein GJ Thakur RK Li H Zardini M Yee R. Mechanism of “inappropriate” sinus tachycardia. Role of sympathovagal balance.Circulation. 1994; 90: 873-877Crossref PubMed Scopus (175) Google Scholar in patients by IST, a to a by and a intrinsic heart rate autonomic with and is with a of in the to J S A and autonomic in patients with tachycardia PubMed Scopus Google Scholar The heart at in patients with IST that mechanism primarily in the SAN, and the autonomic can as a is the CA Klein GJ Thakur RK Li H Zardini M Yee R. Mechanism of “inappropriate” sinus tachycardia. Role of sympathovagal balance.Circulation. 1994; 90: 873-877Crossref PubMed Scopus (175) Google P J Noninvasive of autonomic in patients with inappropriate sinus J Cardiol. 2013; Full Text Full Text PDF PubMed Scopus Google Scholar (Figure The of IST in a heart this M PJ Inappropriate sinus tachycardia in a insights into 2011; 8: Full Text Full Text PDF PubMed Scopus Google Scholar The cardiac is a of this in the heart with IST. 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PubMed Scopus Google Scholar with or are for IST catheter ablation (Figure that may be a and heart rate in IST. ablation strategies the and the hybrid sparing The to target the SAN with or approaches to heart rate from the or a of M Kreidieh B Al Rifai M Ibarra-Cortez S Schurmann P Álvarez PA Fernández-López XA García-Seara J Martínez-Sande L González-Juanatey JR Valderrábano M Ablation of inappropriate sinus tachycardia: a systematic review of the literature.JACC Clin Electrophysiol. 2017; 3: 253-265Crossref PubMed Scopus (26) Google Scholar in review a of of IST catheter ablation that at a of of the patients of this SAN is with a pacemaker rate as as D J C M A J P R S C A P Y D S L A A R Sinus node sparing hybrid ablation in patients with inappropriate sinus tachycardia Full Text Full Text PDF PubMed Scopus Google Scholar SAN ablation in patients with IST can be of SAN ablation may be because of transmural that the intramural SAN pacemaker within superior or because of the of the M Kreidieh B Al Rifai M Ibarra-Cortez S Schurmann P Álvarez PA Fernández-López XA García-Seara J Martínez-Sande L González-Juanatey JR Valderrábano M Ablation of inappropriate sinus tachycardia: a systematic review of the literature.JACC Clin Electrophysiol. 2017; 3: 253-265Crossref PubMed Scopus (26) Google Scholar A R sinus node ablation ablation for the treatment of inappropriate sinus tachycardia.J Electrophysiol. 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PubMed Scopus Google Scholar The of this be because of of increased automaticity of within the the of and right SAN SVC, IVC and ablation or electrical of and in a by M Kreidieh B Al Rifai M Ibarra-Cortez S Schurmann P Álvarez PA Fernández-López XA García-Seara J Martínez-Sande L González-Juanatey JR Valderrábano M Ablation of inappropriate sinus tachycardia: a systematic review of the literature.JACC Clin Electrophysiol. 2017; 3: 253-265Crossref PubMed Scopus (26) Google Scholar the of ablation for IST This is important as with the novel ablation is are to the of the hybrid IST at long-term The electrophysiological mechanisms for IST are and clinical an intrinsic of sinus node automaticity and autonomic that be or secondary to IST. Different pharmacological approaches can target these mechanisms. Long-acting β blockers in IST can act on both increased automaticity and dysregulated autonomic system. Ivabradine targets sources of increased SAN automaticity. Conventional or hybrid ablation may target all the described abnormalities. SAN ablation is with pacemaker in to of hybrid SAN sparing ablation a rate of pacemaker as as with success rate and at are to specific mechanisms of forms to and ablation Furthermore, novel of enhanced automaticity including and pacemaker with enhanced automaticity the SAN and through SACPs, in

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