Leadless Pacemakers and the Tricuspid Valve
2019; Lippincott Williams & Wilkins; Volume: 12; Issue: 5 Linguagem: Inglês
10.1161/circep.119.007375
ISSN1941-3149
AutoresJeffrey Arkles, Andrew E. Epstein,
Tópico(s)Cardiac Valve Diseases and Treatments
ResumoHomeCirculation: Arrhythmia and ElectrophysiologyVol. 12, No. 5Leadless Pacemakers and the Tricuspid Valve Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBLeadless Pacemakers and the Tricuspid ValveCan You Believe It? Can This Be True? Jeffrey S. Arkles, MD and Andrew E. Epstein, MD Jeffrey S. ArklesJeffrey S. Arkles Jeffrey S. Arkles, MD, Electrophysiology Section, Division of Cardiovascular Medicine, University of Pennsylvania, 3400 Spruce St, 9 Founders Pavilion, Philadelphia, PA 19104, Email E-mail Address: [email protected] Electrophysiology Section, Division of Cardiovascular Medicine, University of Pennsylvania, Philadelphia. and Andrew E. EpsteinAndrew E. Epstein Andrew E. Epstein, MD, Electrophysiology Section, Division of Cardiovascular Medicine, University of Pennsylvania, 3400 Spruce St, 9 Founders Pavilion, Philadelphia, PA 19104, Email E-mail Address: [email protected] Electrophysiology Section, Division of Cardiovascular Medicine, University of Pennsylvania, Philadelphia. Originally published7 May 2019https://doi.org/10.1161/CIRCEP.119.007375Circulation: Arrhythmia and Electrophysiology. 2019;12:e007375This article is a commentary on the followingImpact of Leadless Pacemaker Therapy on Cardiac and Atrioventricular Valve Function Through 12 Months of Follow-UpSee Article by Beurskens et alOne of the myriad reasons to consider a leadless pacemaker (LP) is to avoid interaction with the tricuspid valve (TV).1,2 Over the years, multiple reports have called attention to TV dysfunction related to impingement, attachment, acute damage, and chronic injury resulting from contact with transvenous leads and cardiac remodeling resulting from pacing-induced myocardial dysfunction. An increasing awareness of ventricular interdependence and right ventricular (RV) dysfunction mediating left ventricular (LV) dysfunction make these concerns ever more relevant.With the background that transvenous, endocardial, RV pacing is known to cause TV, mitral valve (MV), and cardiac dysfunction, and the assumption that lead-related adverse consequences can be mitigated by leadless pacing, in this issue of Circulation: Arrhythmia and Electrophysiology Beurskens et al3 report a study of the impact of LPs on cardiac and valvular structure and function. They compared echocardiographic studies before and after LP implantation and compared them to studies done in age- and sex-matched controls who had received dual-chamber (DDD) transvenous pacemakers. Of 53 patients receiving an LP, 28 were implanted with a Nanostim and 25 with a Micra device. TV regurgitation (TR) was graded as being more severe in 23 (43%) of patients at 12±1 months compared with baseline (P<0.001). Compared with an apical position, an RV septal position of the LP was associated with increased TR (odds ratio 5.20, P=0.03). In addition, MV regurgitation (MR) increased in 38% of the LP patients (P=0.006). LP implantation resulted in a reduction of biventricular function as measured by multiple echocardiographic measures, including tricuspid annular plane systolic excursion, the RV Tei index, the LV ejection fraction, and the LV Tei index. The changes in TR in the LP group were similar to those seen in the DDD transvenous pacemaker control group (43% versus 38%, respectively, P=0.39). Importantly, procedural characteristics (such as number of LP deployments), pacing percentage, and changes in the systolic pulmonary pressure, MR, and cardiac morphology played no significant role in the worsening of TR. The authors concluded that LP therapy was unexpectedly associated with an increase in TV dysfunction, comparable to changes seen in patients with DDD transvenous pacemaker systems, and that it adversely impacted MV and biventricular function.Yes, these observations are unexpected. They run counter to the seemingly accepted belief that leadless pacing avoids TV interaction and TR. What mechanisms can be invoked to explain how a device that does not cross the valve can interfere with its function? The authors propose some, but they are not all inclusive or necessarily independent. First, LPs may displace the papillary muscles or leaflets themselves. It is likely that different shaped LPs may have different effects: longer ones may have greater effects on the valve, and shorter ones may have greater ones on the muscles and chords. However, if so, why is septal pacing more associated with adverse outcomes than is apical pacing? Second, TR might have nothing to do with TV interaction at all but rather be more the result of RV pacing regardless of how it is done and irrespective of pacing location. Because, and as pointed out by the authors, RV pacing is known to cause TV, MV, and myocardial dysfunction, the differences in outcomes with septal versus apical pacing would have to be explained. RV pacing might also explain why the effects on the MV (MR) are the same as on the TV (TR). Not everyone with RV pacing develops MR and similarly do not develop TR.A challenge in understanding these results is the lack of an ideal control group. LPs are unique devices that fill a niche that is not equivalent to that of single chamber ventricular or DDD transvenous devices. The LP (n=53) and retrospectively identified DDD pacemaker control (n=53) patients had statistically and significantly different pacing indications including bradycardia associated with persistent or permanent atrial tachyarrhythmias (presumably including atrial fibrillation) in 53% (n=28) of the LP versus none in the DDD patients, atrioventricular (AV) block in 15% (n=8) of the LP and 55% (n=29) of the DDD patients, sinus node dysfunction in 32% (n=17) of the LP and 36% (n=19) of the DDD patients, and other in none of the LP and 9% (n=5) of the DDD patients, respectively. Based on these data, there are 2 important factors that may influence the interpretation of the results, specifically persistent atrial arrhythmias and AV dyssynchrony. MR is known to worsen in the presence of atrial fibrillation,4 and by either a direct interaction or secondary to MR, TR might worsen as well. A comparison control group with single chamber ventricular pacemakers and persistent atrial arrhythmias would allow a fairer comparison of the effects of LPs of TV and RV function. The presence of obligate AV dyssynchrony in 47% of the LP patients who had underlying sinus rhythm might have led to the degree of TV dysfunction observed in the LP patients independent of pacing location or TV apparatus interaction.Other limitations exist: How did the presence of sinus rhythm and AV dissociation in the LP patients affect interpretation of the echocardiographic findings? How long had persistent and permanent atrial tachyarrhythmias been present in the LP group? When assessing differences in RV and LV function, the duration of absent AV synchrony might have played a role just as did RV pacing itself. In addition, interpretation of the Tei index data is difficult. The index represents a measure of systolic function and efficiency and is derived from a formula incorporating the isovolumic contraction time, the ejection time, and the isovolumic relaxation time. It was not calculated in the patients with atrial fibrillation, and 36 of the 53 (68%) LP patients had the index measured which must have included some of the patients with persistent or permanent atrial tachycardias, sinus node dysfunction, or AV block in which AV synchrony was certainly absent. Because it is unlikely that any regular atrial rhythms remained constant relative to ventricular contraction in LP patients throughout the study, and because the Tei index relies on constant isovolumic and ejection times, to claim a difference is problematic as the meaning of the index in this context is uncertain. In short, if the control patients had been chosen by matching pacing indication such as bradycardia associated with persistent atrial (fibrillation) arrhythmias, the comparison might have been more robust.As also pointed out by the authors, pacemaker systems using transvenous leads that cross the TV are associated with TR because of interaction with and possibly damage to the leaflets themselves or the subvalvular apparatus. Indeed, just crossing the TV may either spear the valve with or without getting tangled in the subvalvular apparatus, including the chordae and papillary muscle.1 The authors clearly explain how entanglement of LPs with the chordae tendineae or direct interaction with the leaflets and encapsulation of LPs when abutting the leaflets all can detrimentally affect the TV. Furthermore, RV pacing can, of course, provoke dyssynchrony associated with LV dysfunction and secondary detrimental effects on right heart and TV function.5 Although LPs have traditionally been thought to have no impact on the TV, mechanical interactions deeper in the RV and on LV function have not been so much considered. However, it is notable that a further distance from the proximal end of the LP to the TV valve decreased the risk of dysfunction in keeping with the importance of direct physical contact with the valve in producing TR. Also, the percentage of RV pacing was similar in the LP and DDD groups.The primary question to be addressed is, therefore, whether LPs cause TR through mechanical interaction or if these findings are related to functional TR from progressive ventricular dysfunction. Perhaps the strongest evidence that there is a direct mechanical effect comes from the 5-fold increase in TR seen with a septal versus apical LP position. The anatomy of the TV and valvular apparatus is highly variable with multiple papillary muscles and chordal attachments. The most anatomically preserved relationship is the presence of multiple cords from the septal leaflet to the ventricular septum.6 A reasonable conclusion is that septal implantation of the LP mechanically interferes with these attachments and is a source of TR from a level beneath the valve plane. Certainly, secondary TR plays a role in the overall findings as well, and the exact contributions are unknown. Given the more favorable outcomes seen with the apical LP position, these findings may influence practice.Irrespective of the presence or absence of AV synchrony, it remains that TV and myocardial function deteriorated in both the LP and DDD pacing groups. Each had 100% opposite characteristics in 2 areas: AV synchrony (most if not all patients with LPs had AV dyssynchrony, whereas none of those with DDD devices did) and the presence or absence of a transvenous lead (none with LPs had one and all with DDD pacemakers did). These factors may have balanced each other such that after a year, worsening of TV and myocardial function occurred in both groups but for different reasons. However, it cannot be ignored that for even those with LPs, interactions with the TV cannot be ignored.As we gain more experience using LPs, the dark side may prove larger than anticipated. How will the implantation of ≥1 devices affect TV and indeed RV function? How many LPs can the RV accommodate and be implanted in an individual7 and does the size and shape of the RV make a difference? Is the numerical burden of LPs directly or exponentially related to RV and TV dysfunction? When LPs need to be removed, what damage might occur to the entire TV apparatus?8 Many questions remain unanswered in leadless pacing, especially with respect to what to expect in the future. Will the management of tricuspid insufficiency be different if the chords, leaflets or neither are involved? How can the diagnosis be made? Importantly, regardless of whether a lead crosses the TV or not, TR, MR, LV, and RV dysfunction can progress with time because of RV pacing independent of other factors.In our minds, there is a larger and tremendously important message from this article in addition to the findings specific to leadless pacing: what seems to be the truth and biologically plausible may not be. Here lies the importance and essential need for clinical investigation. We learned this from the CAST (Cardiac Arrhythmia Suppression Trial): who would have predicted that the suppression was not good but in fact detrimental?9 Our surgical colleagues ligated the internal mammary artery but without benefit when subjected to a clinical trial.10 Too bad George Washington's well-intentioned physicians bled him to death since bleeding was the standard of care.11 If only they had clinical trial evidence. So, Beurskens et al3 are to be commended for thinking outside the box, teaching us something unexpected and thereby warning us that what may seem obvious may not be true. May clinical investigation remain as the true news.Sources of FundingThis work was supported in part by the J and J Fund in Electrophysiology.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Jeffrey S. Arkles, MD, Electrophysiology Section, Division of Cardiovascular Medicine, University of Pennsylvania, 3400 Spruce St, 9 Founders Pavilion, Philadelphia, PA 19104, Email jeffrey.[email protected]upenn.eduAndrew E. Epstein, MD, Electrophysiology Section, Division of Cardiovascular Medicine, University of Pennsylvania, 3400 Spruce St, 9 Founders Pavilion, Philadelphia, PA 19104, Email andrew.[email protected]upenn.eduReferences1. Chang JD, Manning WJ, Ebrille E, Zimetbaum PJ. Tricuspid valve dysfunction following pacemaker or cardioverter-defibrillator implantation.J Am Coll Cardiol. 2017; 69:2331–2341. doi: 10.1016/j.jacc.2017.02.055CrossrefMedlineGoogle Scholar2. Salaun E, Tovmassian L, Simonnet B, Giorgi R, Franceschi F, Koutbi-Franceschi L, Hourdain J, Habib G, Deharo JC. Right ventricular and tricuspid valve function in patients chronically implanted with leadless pacemakers.Europace. 2018; 20:823–828. doi: 10.1093/europace/eux101CrossrefMedlineGoogle Scholar3. Beurskens NEG, Tjong FVY, de Bruin-Bon RHA, Dasselaar KJ, Kuijt WJ, Wilde AAM, Knops RE. Impact of leadless pacemaker therapy on cardiac and atrioventricular valve function through 12 months of follow-up.Circ Arrhythm Electrophysiol. 2019; 12:e007124. doi: 10.1161/CIRCEP.118.007124LinkGoogle Scholar4. Gertz ZM, Raina A, Saghy L, Zado ES, Callans DJ, Marchlinski FE, Keane MG, Silvestry FE. Evidence of atrial functional mitral regurgitation due to atrial fibrillation: reversal with arrhythmia control.J Am Coll Cardiol. 2011; 58:1474–1481. doi: 10.1016/j.jacc.2011.06.032CrossrefMedlineGoogle Scholar5. Khurshid S, Epstein AE, Verdino RJ, Lin D, Goldberg LR, Marchlinski FE, Frankel DS. Incidence and predictors of right ventricular pacing-induced cardiomyopathy.Heart Rhythm. 2014; 11:1619–1625. doi: 10.1016/j.hrthm.2014.05.040CrossrefMedlineGoogle Scholar6. Martinez RM, O'Leary PW, Anderson RH. Anatomy and echocardiography of the normal and abnormal tricuspid valve.Cardiol Young. 2006; 16(suppl 3):4–11.Google Scholar7. Omdahl P, Eggen MD, Bonner MD, Iaizzo PA, Wika K. Right ventricular anatomy can accommodate multiple micra transcatheter pacemakers.Pacing Clin Electrophysiol. 2016; 39:393–397. doi: 10.1111/pace.12804CrossrefMedlineGoogle Scholar8. Borgquist R, Ljungström E, Koul B, Höijer CJ. Leadless Medtronic Micra pacemaker almost completely endothelialized already after 4 months: first clinical experience from an explanted heart.Eur Heart J. 2016; 37:2503. doi: 10.1093/eurheartj/ehw137CrossrefMedlineGoogle Scholar9. Epstein AE, Hallstrom AP, Rogers WJ, Liebson PR, Seals AA, Anderson JL, Cohen JD, Capone RJ, Wyse DG. Mortality following ventricular arrhythmia suppression by encainide, flecainide, and moricizine after myocardial infarction. The original design concept of the Cardiac Arrhythmia Suppression Trial (CAST).JAMA. 1993; 270:2451–2455.CrossrefMedlineGoogle Scholar10. Benson H, McCallie DP. Angina pectoris and the placebo effect.N Engl J Med. 1979; 300:1424–1429. doi: 10.1056/NEJM197906213002508CrossrefMedlineGoogle Scholar11. Morens DM. Death of a president.N Engl J Med. 1999; 341:1845–1849. doi: 10.1056/NEJM199912093412413CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Zhang X, Wei M, Xiang R, Lu Y, Zhang L, Li Y, Zhang J, Xing Q, Tu-Erhong Z, Tang B and Zhou X (2022) Incidence, Risk Factors, and Prognosis of Tricuspid Regurgitation After Cardiac Implantable Electronic Device Implantation: A Systematic Review and Meta-analysis, Journal of Cardiothoracic and Vascular Anesthesia, 10.1053/j.jvca.2021.06.025, 36:6, (1741-1755), Online publication date: 1-Jun-2022. Razeghi O, Strocchi M, Lee A, Longobardi S, Sidhu B, Gould J, Behar J, Rajani R, Rinaldi C and Niederer S (2020) Tracking the motion of intracardiac structures aids the development of future leadless pacing systems, Journal of Cardiovascular Electrophysiology, 10.1111/jce.14657, 31:9, (2431-2439), Online publication date: 1-Sep-2020. Related articlesImpact of Leadless Pacemaker Therapy on Cardiac and Atrioventricular Valve Function Through 12 Months of Follow-UpNiek E.G. Beurskens, et al. Circulation: Arrhythmia and Electrophysiology. 2019;12 May 2019Vol 12, Issue 5 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.119.007375PMID: 31060372 Originally publishedMay 7, 2019 Keywordsmitral valvetricuspid valveatrial fibrillationEditorialsleadless pacemakerechocardiographypacemakerPDF download Advertisement SubjectsArrhythmiasElectrophysiology
Referência(s)