Accessory Atrioventricular Pathways

Abstract

HomeCirculationVol. 117, No. 12Accessory Atrioventricular Pathways Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBAccessory Atrioventricular PathwaysGetting to the Origins Siew Yen Ho, PhD, FRCPath, FESC Siew Yen HoSiew Yen Ho From Cardiac Morphology, National Heart & Lung Institute, Imperial College London and Royal Brompton Hospital, London, United Kingdom. Search for more papers by this author Originally published25 Mar 2008https://doi.org/10.1161/CIRCULATIONAHA.107.764035Circulation. 2008;117:1502–1504By definition, accessory atrioventricular pathways are aberrant muscle bundles that connect the atrium to a ventricle outside of the regular atrioventricular conduction system. Clinically, they may manifest as substrates for ventricular preexcitation. The first accessory pathway in a patient who suffered from Wolff-Parkinson-White syndrome was described in 1943 by Wood, Wolferth, and Geckler.1 Shortly after, Öhnell created a reconstruction of an accessory pathway that very elegantly showed the close proximity of the pathway to the fibrous attachment of the mitral valve and its relationship with the sulcus coronarius (Figure, A).2 Subsequent histological studies have demonstrated unequivocally that these pathways are the anatomic substrates for the classical Wolff-Parkinson-White variety of preexcitation. Download figureDownload PowerPointFigure. A, Öhnell’s depiction of an accessory bundle in the left atrioventricular groove.2 Reprinted with permission from Blackwell Publishing. B, Histological section stained with Masson’s trichrome (fibrous tissue in green and myocardium in red) to show an accessory left-sided pathway (arrow) skirting the mitral annulus. C, Histological section showing a broad right-sided accessory pathway (arrow) that is formed by a myocardial pouch extending from the right atrial appendage to the ventricle and ultimately traced to a small right ventricular vein. This pathway is some distance from the fibrous annulus of the tricuspid valve. *Valvar annulus.Article p 1508Accessory atrioventricular pathways are found most often in the parietal atrioventricular junctional areas, including the paraseptal areas. They breach the insulation provided by the fibrofatty tissues of the atrioventricular groove (sulcus tissue) and the hingelines (fibrous annulus) of the valves. They are rarely found in the area of fibrous continuity between the aortic and mitral valves because in this area, there is usually a wide gap between the atrial myocardium and ventricular myocardium to accommodate the aortic outflow tract. On the left parietal side, the accessory pathways tend to pass close to the hingeline of the mitral valve (Figure, B). In the right atrioventricular junction, the atrioventricular groove is much deeper than on the left side, and the accessory muscle bundles can cross at any depth. Cardiac surgeons have suggested that the deep groove may itself allow the atrial wall to fold over the ventricular wall, thereby producing atrial-ventricular myocardial continuity.3 Most of the pathways identified through the use of microscopy have been working myocardium, with only a few reported to contain histologically specialized cells.4 Whether comprising working myocardium or abnormal myocytes, these pathways have normal gap junctions with a pattern suggestive of working ventricular myocardium.5 Morphologically, these threads of musculature are thicker at their atrial origins and they branch into finer strands at the ventricular insertions. They are up to 3 mm in width but may be 10 mm or more long.2,4,6Other types of accessory atrioventricular pathways found in certain circumstances are well recognized. One of the 7 pathways in the study conducted by Becker and colleagues4 was a specialized bundle that had its atrial insertion in a node of specialized tissues in the parietal margin of the tricuspid annulus, forming an atriofascicular tract.7 Multiple pathways can occur in the setting of so-called Purkinje cell tumors, often with additional tumors within the ventricles. Another type of pathway related to coronary veins is usually manifested in the form of extensive myocardial cuffs around the veins crossing the atrioventricular junction or expanded as diverticulums into the ventricular mass. Others are related to the atrial appendages overlying ventricular masses (Figure, C).For several decades, accessory pathways have been avulsed successfully through surgery using conventional dissection or by cryothermy or radiofrequency ablation. In the past 2 decades, advancements in precision mapping and ablation of accessory pathways via the transcatheter route have made it possible for many patients to be cured. Although rare, sudden death may be the first presenting sign in patients with undiagnosed and/or asymptomatic preexcitation syndrome. This is particularly worrisome for families with an affected child. The majority of cases have no clear familial involvement, but a small number of patients have affected relatives. Recently, the transcatheter procedure has been deemed safe and effective in experienced hands, but whether it should be used as a prophylactic measure against life-threatening events remains controversial.8,9 Clearly, there is a need to know more about how these pathways develop so as to guide further therapeutic strategies.In the embryonic human heart, a ring of musculature at the atrioventricular canal provides myocardial continuity between developing atrial and ventricular myocardium in the early stages. This canal myocardium was shown initially to have slow conduction properties in the chick.10 The canal myocardium is sandwiched by sulcus tissue on the outside and endocardial cushions on the inside. Kim and colleagues11 showed that the bulk of the canal myocardium was incorporated into the vestibules making up the atrial walls leading toward the valvar orifices, but it did not contribute to ventricular myocardium. A small part of the canal myocardium becomes the atrioventricular node, and normally this is the only site of myocardial continuity, with the developing ventricular conduction bundles at completion of cardiac septation. In their earlier study, however, Wessels and colleagues12 noted strands of myocardial continuity between atrial and ventricular tissues in all human fetal hearts and many normal neonatal hearts.Pivotal to the understanding of accessory atrioventricular pathways is knowledge of how the insulating tissue plane at the sulcus and annulus came into being. Wessels and colleagues,13 among others, offered the explanation that sulcus tissue joins with endocardial cushion tissues at the ventricular margin of the canal. According to this study,13 the valvar leaflets were formed by cushion tissue, without contribution or real inward growth of sulcus tissue. Instead, the ventricular walls distal to the atrioventricular canal bulged like shoulders toward the atria. They suggested that accessory pathways resulted from incomplete fusion between sulcus and cushion tissues. It is not clear from their study, however, how myocardial discontinuity was effected so as to allow sulcus tissue to meet cushion tissue. In contrast, a simpler explanation was put forward by others who suggested that invagination of sulcus tissue like a wedge through the muscular canal wall was part of the process for development of valvar leaflets, with little contribution from the cushions.14,15 Be that as it may, there is consensus that the insulating tissues came from the epicardial side.It was while studying the embryologic origins of the coronary vessels in chicken-quail chimeras that Gittenberger-de Groot and coworkers identified and traced the migration of a novel population of cells termed epicardial-derived cells (EPDCs) into the myocardial interstitium and endocardial cushions.16 Observing a close relationship between EPDCs and cardiac fibroblasts, they suggested a potential role of migrating EPDCs in the formation of the insulating tissue plane between atrial and ventricular myocardium. This concept, based on exquisite experimental techniques, differs from their earlier work describing infolding of the epicardial tissues to form the core of the developing leaflets.15 The latest article from this group17 examines the role of EPDCs in formation of the insulating plane (annulus fibrosis) by comparing wild-type quail embryos with EPDC-inhibited embryos. In normal development, EPDCs migrate through the atrioventricular canal myocardium to populate the endocardial cushions.16 By impeding EPDC migration, Gittenberger-de Groot et al observed persistence of broad bundles of accessory atrioventricular myocardial connections that resulted in ventricular preexcitation. In agreement with the previous findings of this group, the accessory bundles in wild-type embryos were smaller, and there was no correlation with ECG recordings.17,18 In the previous study,18 the accessory bundles identified as myocardial on myosin light chain 2a positivity were noted to be broad and multiple and in various locations in young hearts (Hamburger-Hamilton stages 35–39), whereas in older embryos (Hamburger-Hamilton stages 40–44), the bundles were small and mainly located on the right side. By way of comparison, fibrous insulation was complete in the adult quail. Coincidentally, they observed that MLC2a-positive pathways were also stained with periostin, a fibroblast marker that has a role in regulating fibroblast-myocyte interaction.19 In the present report,17 the small pathways in both wild-type and EPDC-inhibited hearts stained positive for both MLC2a and periostin. Broad pathways were only found in EPDC-inhibited hearts, but these were associated with local interruption of periostin staining. An important observation of the present study17 is the interplay between EPDCs, periostin, and accessory pathways. The investigators proposed the concept that impeded migration of EPDCs through the myocardium to the endocardial cushions delayed the development of the fibrous annulus. Although the study has given us a glimpse of pathways that are candidates for premature ventricular activation in the quail, the question of why some accessory pathways produce a functional effect, occasionally devastatingly so, whereas others do not, remains to be clarified. In his monograph, Öhnell2 considered that some may have been acquired, for instance after myocarditis, a view also put forward more recently by Basso and her colleagues.6Developmentally, the work of Kolditz and colleagues would appear to support the notion that accessory pathways resulted from incomplete interruption of canal myocardium resulting from late arrival of EPDCs.17 Although incomplete interruption due to sulcus tissue stopping short of the annulus can account for accessory atrioventricular pathways that pass close to the annulus, it is difficult to picture the same process being involved in pathways that are in peripheral locations or in other morphologies as described above. The conundrum of whether those develop later by growing through holes in the tissue plane remains. For those related to coronary veins, what causes the walls to become muscularized (or remain muscularized)? Do the multipotent EPDCs and periostin have a role in those, too? We await further insights into this intriguing area of study.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Sources of FundingThe Cardiac Morphology unit at the Royal Brompton Hospital receives funding support from the Royal Brompton and Harefield Hospital Charitable Fund.DisclosuresNone.FootnotesCorrespondence to Siew Yen Ho, PhD, FRCPath, FESC, Cardiac Morphology, National Heart & Lung Institute, Dovehouse St, London, United Kingdom, SW3 6LY. E-mail [email protected] References 1 Wood FC, Wolferth CC, Geckeler GD. Histologic demonstration of accessory muscular connections between auricle and ventricle in a case of short P-R interval and prolonged QRS complex. Am Heart J. 1943; 25: 454–462.CrossrefGoogle Scholar2 Öhnell RF. Pre-excitation, cardiac abnormality, pathophysiologycal, patho-anatomical and clinical studies of excitatory spread phenomenon bearing upon the problem of the WPW (Wolff, Parkinson and White) electrocardiogram and paroxysmal tachycardia. Acta Med Scand. 1944; 152: 1–167.Google Scholar3 Ferguson TB Jr, Cox JL. Surgical management of the Wolff-Parkinson-White syndrome. In: Mandel WJ, ed. Cardiac Arrhythmias. 3rd ed. Philadelphia, Pa: JB Lippincott Co; 1995: 1154–1156.Google Scholar4 Becker AE, Anderson RH, Durrer D, Wellens HJ. The anatomical substrates of Wolff-Parkinson-White syndrome: a clinicopathologic correlation in seven patients. Circulation. 1978; 57: 870–879.CrossrefMedlineGoogle Scholar5 Peters NS, Rowland E, Bennett JG, Green CR, Anderson RH, Severs NJ. The Wolff-Parkinson-White syndrome: the cellular substrate for conduction in the accessory atrioventricular pathway. Eur Heart J. 1994; 15: 981–987.CrossrefMedlineGoogle Scholar6 Basso C, Corrado D, Rossi L, Thiene G. Ventricular preexcitation in children and young adults: atrial myocarditis as a possible trigger of sudden death. Circulation. 2001; 103: 269–275.CrossrefMedlineGoogle Scholar7 Tchou P, Lehmann MH, Jazayeri M, Akhtar M. Atriofascicular connection or a nodoventricular Mahaim fiber? Electrophysiologic elucidation of the pathway and associated reentrant circuit. Circulation. 1988; 77: 837–848.CrossrefMedlineGoogle Scholar8 Pappone C, Manguso F, Santinelli R, Vicedomini G, Sala S, Paglino G, Mazzone P, Lang CC, Gulletta S, Augello G, Santinelli O, Santinelli V. Radiofrequency ablation in children with asymptomatic Wolff-Parkinson-White syndrome. N Engl J Med. 2004; 351: 1197–1205.CrossrefMedlineGoogle Scholar9 Wellens HJ. Catheter ablation for cardiac arrhythmias. N Engl J Med. 2004; 351: 1172–114.CrossrefMedlineGoogle Scholar10 de Jong F, Opthof T, Wilde AAM, Janse MJ, Charles R, Lamers WH, Moorman AFM. Persisting zones of slow impulse conduction in developing chicken hearts. 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J Anat. 1979; 128: 427–428.Google Scholar15 Wenink AC, Gittenberger-de Groot AC. Embryology of the mitral valve. Int J Cardiol. 1986; 11: 75–84.CrossrefMedlineGoogle Scholar16 Gittenberger-de Groot AC, Vrancken Peeters MP, Mentink MM, Gourdie RG, Poelmann RE. Epicardium-derived cells contribute a novel population to the myocardial wall and the atrioventricular cushions. Circ Res. 1998; 82: 1043–1052.CrossrefMedlineGoogle Scholar17 Kolditz DP, Wijffels MCEF, Blom NA, van der Laarse A, Hahurij ND, Lie-Venema H, Markwald RR, Poelmann RE, Schalij MJ, Gittenberger-de Groot AC. Epicardium-derived cells in development of annulus fibrosis and persistence of accessory pathways. Circulation. 2008; 117: 1508–1517.LinkGoogle Scholar18 Kolditz DP, Wijffels MC, Blom NA, van der Laarse A, Markwald RR, Schalij MJ, Gittenberger-de Groot AC. Persistence of functional atrioventricular accessory pathways in postseptated embryonic avian hearts: implications for morphogenesis and functional maturation of the cardiac conduction system. Circulation. 2007; 115: 17–26.LinkGoogle Scholar19 Oka T, Xu J, Kaiser RA, Melendez J, Hambleton M, Sargent MA, Lorts A, Brunskill EW, Dorn GW 2nd, Conway SJ, Aronow BJ, Robbins J, Molkentin JD. Genetic manipulation of periostin expression reveals a role in cardiac hypertrophy and ventricular remodeling. Circ Res. 2007; 101: 313–21.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Katritsis D and Morady F (2022) Wolff-Parkinson-White syndrome and atrioventricular reentrant tachycardias Clinical Cardiac Electrophysiology, 10.1016/B978-0-323-79338-4.00024-8, (276-305.e1), . Larsen J, Andrade J, Glover B and Brugada P (2021) Accessory Pathway (AP) Conduction Clinical Handbook of Cardiac Electrophysiology, 10.1007/978-3-030-74319-2_5, (105-125), . 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Mohanan Nair K, Namboodiri N and Valaparambil A (2020) Syncope in a young woman, BMJ, 10.1136/bmj.l6877, (l6877) March 25, 2008Vol 117, Issue 12 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.107.764035PMID: 18362241 Originally publishedMarch 25, 2008 KeywordsWolff- Parkinson-White syndromearrhythmiaEditorialsmorphogenesisPDF download Advertisement SubjectsAnimal Models of Human DiseaseArrhythmiasDevelopmental Biology