Abstract:The incidence of increased TR postendocardial lead placement was 10.0%; this is lower than prior estimates. Predevice RA area and RVSP are predictors of increased TR after lead placement.
“…There was a significant increase in the amount and grade of TR in a paced state compared to when the subjects were using their intrinsic conduction system, without any changes in RV ejection fraction or estimated RV systolic pressure . However, the association between pacing burden and amount of TR has not been demonstrated in other retrospective analyses, and the location of the RV lead in one randomized clinical trial of patients who were pacemaker‐dependent (apical vs septal position) was not found to affect the rates of TR …”
Section: Mechanisms Of Tv Dysfunctionmentioning
confidence: 96%
“…Risk factors for device‐related TR appear to include predevice right atrial area and elevated RV systolic pressures, as well as older age, abnormal left ventricular relaxation, and pulmonary hypertension after device implant . Multiple transvalvular leads in the RV has fairly consistently been shown to associate with increased rates of TV dysfunction .…”
Section: Incidence Predictors and Clinical Relevancementioning
Although thought to be a rare event, permanent pacemakers and implantable cardioverter-defibrillators with right ventricular intracardiac leads have the potential to induce tricuspid valve dysfunction. Adverse lead-valve interactions can take place through a variety of mechanisms including damage at the time of implantation, leaflet pinning, or long-term fibrosis encapsulating the leaflet tissue. Clinical manifestations can display a wide range of severity, as well as a highly variable time span between implantation and hemodynamic deterioration. This review aims to describe the potential pathophysiologic effects of intracardiac device leads on the tricuspid valve, with a focus on ideal diagnostic strategies and treatment options once lead-induced valvular dysfunction is suspected.
“…There was a significant increase in the amount and grade of TR in a paced state compared to when the subjects were using their intrinsic conduction system, without any changes in RV ejection fraction or estimated RV systolic pressure . However, the association between pacing burden and amount of TR has not been demonstrated in other retrospective analyses, and the location of the RV lead in one randomized clinical trial of patients who were pacemaker‐dependent (apical vs septal position) was not found to affect the rates of TR …”
Section: Mechanisms Of Tv Dysfunctionmentioning
confidence: 96%
“…Risk factors for device‐related TR appear to include predevice right atrial area and elevated RV systolic pressures, as well as older age, abnormal left ventricular relaxation, and pulmonary hypertension after device implant . Multiple transvalvular leads in the RV has fairly consistently been shown to associate with increased rates of TV dysfunction .…”
Section: Incidence Predictors and Clinical Relevancementioning
Although thought to be a rare event, permanent pacemakers and implantable cardioverter-defibrillators with right ventricular intracardiac leads have the potential to induce tricuspid valve dysfunction. Adverse lead-valve interactions can take place through a variety of mechanisms including damage at the time of implantation, leaflet pinning, or long-term fibrosis encapsulating the leaflet tissue. Clinical manifestations can display a wide range of severity, as well as a highly variable time span between implantation and hemodynamic deterioration. This review aims to describe the potential pathophysiologic effects of intracardiac device leads on the tricuspid valve, with a focus on ideal diagnostic strategies and treatment options once lead-induced valvular dysfunction is suspected.
“…These mechanical factors were reproduced in the subsequent series . More recent studies have identified the predictors that are not directly related to PM leads, such as the age, an enlarged RA or RV, the RV systolic pressure, and mitral valve surgery . However, most prior studies had the common limitation of a cross‐sectional design and insufficient patient numbers and failed to determine the “modifiable” factors.…”
Section: Discussionmentioning
confidence: 99%
“…[2][3][4][5][6] Prior studies have determined the incidence of TR after a pacemaker (PM) implantation is 7-39%. [7][8][9][10][11][12] This is expected to escalate as the number of devices increases in line with a greater proportion of older people in the overall population. However, despite its growing clinical significance, large clinical data focused on the chronological aspect of TR development with sufficient patient numbers and follow-up information are not available.…”
Introduction
The incidence and predictors of tricuspid regurgitation (TR) after permanent pacemaker (PM) implantations have not been well evaluated. We attempted to determine TR's natural course and predictors, especially focusing on the influence of atrial fibrillation (AF).
Methods
Data from 530 patients with dual‐chamber PMs were evaluated. The main study outcomes were moderate to severe TR and isolated TR (moderate to severe TR without other structural heart diseases [SHDs]) in follow‐up echocardiography.
Results
Over a median follow‐up period of 7.6 years, moderate to severe TR developed in 14.5% patients. Of those, concomitant SHD was observed in 51.9% of patients, and 48.1% presented with isolated TR. A multivariable analysis identified the independent predictors of moderate to severe TR (diabetes mellitus [DM], chronic lung disease, preexisting mild TR, peripheral artery disease, moderate to severe aortic regurgitation, and persistent AF [PeAF]) and isolated TR (DM, preexisting mild TR, and PeAF). PeAF (n = 67, 12.6%) was an independent predictor of both moderate to severe TR (hazard ratio [HR] 2.59, 95% confidence interval [CI]: 1.22–5.51) and isolated TR (HR 4.54, 95% CI: 1.60–12.90). The patients with PeAF exhibited a higher incidence of moderate to severe TR (21.8% vs 12.9% vs 11.6% PeAF, paroxysmal AF, and without AF, respectively) and isolated TR (18.6% vs 6.6% vs 4.2%, respectively) during the follow‐up.
Conclusion
Moderate to severe TR after PM implantations developed with or without the influence of concomitant SHD. Patients with PeAF exhibited a higher risk of moderate to severe TR after PM implantations.
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