|Year : 2020 | Volume
| Issue : 4 | Page : 129-132
Incidence and Severity of Tricuspid Regurgitation after Permanent Pacemaker: Single-Center Cohort in the Philippines
Erdie Cruz Fadreguilan MD 1, Janine Paola T Rangel MD 2, Berwyn Viannely F Flores MD 1
1 Non-Invasive Electrophysiology Section, Philippine Heart Center, Philippines
2 Clinical Research Fellow, Non-Invasive Cardiology Division, Philippine Heart Center, Philippines
|Date of Submission||28-Apr-2020|
|Date of Decision||27-Jul-2020|
|Date of Acceptance||11-Aug-2020|
|Date of Web Publication||09-Feb-2021|
Dr. Erdie Cruz Fadreguilan
Philippine Heart Center, Quezon City
Source of Support: None, Conflict of Interest: None
Background: Tricuspid regurgitation related to permanent pacemaker (PPM) lead can occur in 25-29% of patients compared to individuals who did not undergo such procedure, with symptoms of right heart failure developing from six months to ten years after PPM implantation. Early detection is necessary as prompt intervention maybe required to prevent morbidity and even mortality. Aim: This study has been carried out to determine the incidence and severity of pacemaker lead-related tricuspid regurgitation (TR) immediately after the procedure and 1–3 months after permanent pacemaker implantation. Methods: This is a prospective cohort study on 60 patients who underwent permanent pacemaker implantation. Baseline demographic, electrocardiographic and echocardiographic parameters were collected. Patients underwent follow-up 2D- and 3Dechocardiogram within three days or prior to discharge and within one to three months after permanent pacemaker insertion to determine the development of tricuspid regurgitation (TR) or increase in its severity from baseline. Results: The mean age was 65.2 ± 13.5 years, majority were females (58%) who underwent permanent pacemaker implantation predominantly due to advanced atrioventricular block (75%). Three patients developed mild TR and one patient developed moderate TR within three days postoperatively. On follow-up within one to three months postoperatively, thirteen patients (22%) developed moderate TR and one patient developed severe TR, which required removal of the RV lead with improvement thereafter. Conclusion: In this study cohort, nearly one-fourth of patients who underwent implantation of permanent pacemaker developed at least moderate TR within one to three months of the procedure. Follow-up echocardiogram 3 months after pacemaker implantation may be warranted to detect this complication early.
Keywords: Pacemaker complication, permanent pacemaker, right heart failure, tricuspid regurgitation, tricuspid valve echocardiogram
|How to cite this article:|
Fadreguilan EC, T Rangel JP, F Flores BV. Incidence and Severity of Tricuspid Regurgitation after Permanent Pacemaker: Single-Center Cohort in the Philippines. J Clin Prev Cardiol 2020;9:129-32
|How to cite this URL:|
Fadreguilan EC, T Rangel JP, F Flores BV. Incidence and Severity of Tricuspid Regurgitation after Permanent Pacemaker: Single-Center Cohort in the Philippines. J Clin Prev Cardiol [serial online] 2020 [cited 2022 Jan 18];9:129-32. Available from: https://www.jcpconline.org/text.asp?2020/9/4/129/308972
| Introduction|| |
Tricuspid regurgitation (TR) is one of the potential complications after implantation of permanent pacemaker endocardial leads. Studies have shown the presence of lead-related TR in 25%–29% of patients who underwent permanent pacemaker insertion compared to age-matched controls who did not undergo such procedure. In patients with preexisting TR, the severity of TR has been shown to worsen after the procedure.
The presence of moderate-to-severe TR portends a poor prognosis. It may increase right-sided heart preload and central venous pressure, which may eventually lead to right ventricular (RV) dilatation. Chronic increases in right-sided heart volume and pressures may culminate in RV failure. Early detection of de novo or worsening lead-related TR is, therefore, necessary to prevent disease progression. This study has been carried out to determine the incidence and severity of pacemaker lead-related TR immediately after the procedure and 1–3 months after permanent pacemaker implantation.
| Methodology|| |
This was a prospective cohort study of adult patients who underwent permanent pacemaker insertion in a tertiary cardiac center in the Philippines. The study was carried out at the Philippine Heart Center from September 1, 2017, to December 31, 2017. The study was approved by the institutional ethics review board and was conducted in accordance with the applicable International Conference on Harmonization Guidelines on Good Clinical Practice Guidelines. A written consent was secured from the patients or a legally authorized representative before inclusion in the study.
Inclusion criteria met by the participants of the study were consenting male or female patients, >19 years of age, admitted at the Philippine Heart Center with an indication for permanent pacemaker implantation. Exclusion criteria were previous endocardial lead placement, presence of congenital structural heart disease, valvular and/or rheumatic heart disease with moderate-to-severe TR, and patients with known pulmonary hypertension.
Baseline demographic data including gender, age, and presence of comorbidities (i.e., hypertension, diabetes mellitus, smoking status, dyslipidemia, and coronary artery disease) and electrocardiographic and echocardiographic parameters were collected before permanent pacemaker insertion.
Two-dimensional (2D) echocardiograms were performed using the Siemens Acuson S2000 Ultrasound Machine. Standard echocardiographic views were acquired, and the presence of any regurgitant jet from the tricuspid valve (TV) was measured on three occasions – before the procedure, 3 days after the procedure, and after 1–3-month postimplantation. The largest jet area (ratio of the TR area to the right atrial area), vena contracta width, and regurgitant fraction were recorded and graded as none, trivial, mild, moderate, or severe. The degree of TR was assessed as the ratio of the maximal TR jet area to the corresponding right atrial area: <20% was defined as mild TR, 20%–40% as moderate TR, and >40% as severe TR. A change in TR was defined as a change of at least one grade (for example, from none to mild, mild to moderate, or moderate to severe). Assessment of the lead in relation to the TV plane was attempted in multiple planes. The datasets were digitally stored and transferred to a workplace computer for off-line analysis.
The primary end point of the study was the absolute difference in the incidence of mild, moderate, or severe TR after pacemaker implantation, compared to predevice implantation, as measured by 2D and 3D echocardiography. Secondary end points included the absolute difference in RV diastolic diameters and RV function (fractional area and tricuspid annular plane systolic excursion [TAPSE]) and systolic pressures pre- and postdevice implantation. Clinical and echocardiographic data were compared preoperatively, at 3 days postoperatively, and within 1–3-month postdevice implantation.
Descriptive statistics were used to summarize the clinical characteristics of the patients. Frequency and proportion were used for nominal variables, median and interquartile range for ordinal variables, and mean and standard deviation for interval/ratio variables. Stata software version 13.0 (SataCorp Texas, US) was used for data analysis.
| Results|| |
From September 1, 2017, to December 31, 2017, sixty patients underwent implantation of permanent pacemaker. The mean age was 65.2 ± 13.5 years and 35 (58%) were females. Atrioventricular (AV) heart block (75%) was the most common indication for pacemaker implantation, and all the patients received dual-chamber pacing. Forty-eight (80%) patients had hypertension, 28 (47%) had diabetes mellitus, and 14 (23%) had experienced myocardial infarction in the past [Table 1].
Baseline echocardiographic parameters for the right atrium and right ventricle were within normal limits for age and body surface area for the patients. Before pacemaker implantation, 23 (38%) patients had mild TR, and the remaining had none to trivial TR [Table 2]. After pacemaker implantation, repeat echocardiogram within 3 days, three (5%) patients developed new-onset mild TR and one patient developed moderate TR. On follow-up, 2D echocardiogram within 1–3 months postoperatively, the TR of the same patient became severe [Figure 1]. The patient had a marked decrease in RV systolic function with tricuspid annular dilatation and was readmitted with acute heart failure. The patient underwent removal of the RV lead and conversion to atrial-based single-chamber pacing (AAIR-atrial paced, atrial sensed, inhibited, rate responsive) after confirmation of normal AV node function with the observation of 1:1 AV conduction with rapid atrial pacing. On further follow-up, the patient's TR resolved with marked clinical improvement. Thirteen patients (22%) progressed to moderate TR from trivial to mild TR but had adequate RV systolic function at the time of examination, whereas 21 (35%) patients developed mild TR from none at baseline. As a result, after lead implantation, compared to preimplantation levels, TR was worsened by at least 1 grade in 35% and 2 grades in 22% of the whole study population during the follow-up (Fisher's exact value <0.005).
|Figure 1: Two-dimensional transthoracic echocardiogram. RV inflow view showing the presence of a pacemaker lead (arrow) and associated posteriorly directed tricuspid regurgitation. (RV = Right ventricular, AL = Anterior tricuspid leaflet, PL = Posterior tricuspid leaflet, SL = Septal tricuspid leaflet)|
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|Table 2: Incidence of tricuspid valve regurgitation after permanent pacemaker insertion|
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In the immediate postoperative period after pacemaker insertion, RV diastolic diameters, fractional area, TAPSE, systolic pressures were unchanged. There was, however, a significant increase in RV wall thickness with no change in RV function. On the other hand, left ventricular (LV) function was observed to have significantly decreased from baseline (P < 0.05) [Table 3]. These changes were, however, not observed 1–3-month postimplantation with seemingly decrease in the RV wall thickness and improvement in LV function back to baseline values [Table 4].
|Table 3: Echocardiographic parameters at baseline and within 3 days after proton-pump inhibitors|
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|Table 4: Echocardiographic parameters at baseline and within 1–3 months after proton-pump inhibitors|
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| Discussion|| |
In the patient cohort included in this study, 23.3% of patients developed at least moderate TR as early as 1–3 months after implantation of a permanent pacemaker with 35% of patients shown to have an increase in severity of preexisting TR by at least 1 grade. These figures are similar to previous studies in a literature review, which have shown the presence of lead-related TR in up to 39% of patients who underwent permanent pacemaker insertion. Similarly, in another study, the worsening of preexisting TR by 1–2 grades in up to 25% of patients was seen.
The period of development of endocardial lead-related TR varies from as early as 6 months to as late as several years later. In our series of patients, new-onset and worsening of preexisting TR were already observed to occur as early as 1–3 months after pacemaker implantation. Although the earlier onset could not be explained based on the other findings in this study, the earlier development of significant TR emphasizes the value of early follow-up of patients after pacemaker implantation to look for the development of this complication. In a country like the Philippines where still the majority of leads used are tined, lead extraction is not performed, the value of recognition before lead fibrosis develops and could not be overemphasized.
Reported mechanisms for TR are scar formation or thrombus on the leads impairing TV leaflet closure, neoendocardium formation leading to fibroses and adhesions, thrombosis or edema of TV leaflets, perforation or laceration of TV leaflets, chordal entrapment, and altered RV activation or geometry owing to RV pacing. In this study, however, the quality of the images acquired was not adequate to analyze these possible mechanisms.
Early intervention is recommended once this complication is detected as mortality is increased in patients who developed significant TR after pacemaker implantation. In this study, one patient developed severe TR and RV failure 3 months after implantation. Removal of the ventricular lead resulted in decreased TR severity and marked clinical improvement emphasizing the importance of early detection and management of this important complication. None of the patients with moderate TR developed symptoms and required intervention. Whether some of these patients' TR would progress with time remain to be further investigated. Chang et al. have proposed a decision tree for lead intervention for the indication of TR in the absence of associated infection.
An interesting finding in this study was the observed decline in LV ejection fraction immediately after pacemaker implantation, which improved after 1–3 months. Chronic RV pacing has been associated with the development of significant LV dysfunction in 9% of patients in a previous study, with 10% or more reduction in LV ejection fraction resulting in an EF of <45% – pacing-induced cardiomyopathy. This decline in LV function is attributed to RV pacing-induced dyssynchrony. The significance of the observed immediate asymptomatic decline in LV ejection fraction, followed by improvement in this study is unclear and warrants further investigation.
Limitations of the study
Limitations of this study include lack of details regarding the expertise of the implanting surgeons and cardiac electrophysiologists or whether trainees under supervision did the implants. Lead manipulation and possible trauma to the TV may correlate with the level of expertise of the implanter. In addition, the use of transesophageal echocardiogram may define the mechanism of lead-related TR after permanent pacemaker implantation.
Clearly, a larger sample size will better define the incidence of TR and its impact on the clinical outcome of patients. Long-term follow-up is also needed to evaluate the impact of lead-related TR on cardiac hemodynamics and prognosis more comprehensively.
| Conclusion|| |
This study has shown the development of TR of at least moderate severity in nearly one-fourth of the patients who underwent pacemaker implantation for various indications. The diagnosis was established by echocardiogram done as early as 1–3 months after the procedure. Follow-up echocardiogram within this period may be warranted to detect this important complication for early intervention before the development of fibrosis in tined pacemaker leads.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Paniagua D, Aldrich HR, Lieberman EH, Lamas GA, Agatston AS. Increased prevalence of significant tricuspid regurgitation in patients with transvenous pacemakers leads. Am J Cardiol 1998;82:1130-2.
Kim JB, Spevack DM, Tunick PA, Bullinga JR, Kronzon I, Chinitz LA, et al
. The effect of transvenous pacemaker and implantable cardioverter defibrillator lead placement on tricuspid valve function: An observational study. J Am Soc Echocardiogr 2008;21:284-7.
Nath J, Foster E, Heidenreich PA. Impact of tricuspid regurgitation on long-term survival. J Am Coll Cardiol 2004;43:405-9.
Ramirez FD, Almutairi A, Stadnick E, Nair GM, Sadek MM, Birnie DH. Late resolution of pacemaker lead-related severe tricuspid regurgitation and right ventricular dysfunction after percutaneous lead extraction: A case report and review of the literature. HeartRhythm Case Rep 2016;2:324-7.
Fischman D. Pacemaker-associated right heart failure: An under-recognized problem. J Innov Cardiac Rhythm Manag 2015;6:2217-20.
Al-Bawardy R, Krishnaswamy A, Bhargava M, Dunn J, Wazni O, Tuzcu EM, et al
. Tricuspid regurgitation in patients with pacemakers and implantable cardiac defibrillators: A comprehensive review. Clin Cardiol 2013;36:249-54.
Delling FN, Hassan ZK, Piatkowski G, Tsao CW, Rajabali A, Markson LJ, et al
. Tricuspid regurgitation and mortality in patients with transvenous permanent pacemaker leads. Am J Cardiol 2016;117:988-92.
Chang JD, Manning JW, Ebrille E, Zimetbaum PJ. Tricuspid valve dysfunction following pacemaker or cardioverter-defibrillator implantation. J Am Coll Cardiol 2017;69:2331-41.
Yu CM, Chan JY, Zhang Q, Omar R, Yip GW, Hussin A, et al
. Biventricular pacing in patients with bradycardia and normal ejection fraction. N Engl J Med 2009;361:2123-34.
[Table 1], [Table 2], [Table 3], [Table 4]