Significant Lead-Induced Tricuspid Regurgitation Prognosis
Significant Lead-Induced Tricuspid Regurgitation Prognosis
The main findings of this study include (1) significant lead-induced TR was observed in 38% of patients 1–1.5 years after placement of an RV lead; (2) significant lead-induced TR was associated with significant RV and right atrium enlargement, and with increased pulmonary pressures at follow-up and (3) significant lead-induced TR was independently associated with worse long-term clinical outcomes (all-cause mortality alone or combined with heart failure related events) after device implantation.
The presence of a lead through the tricuspid valve apparatus has been suggested as one of the mechanisms of TR. However, only a few studies have described the incidence of lead-induced TR acutely after implantation and no data are available from the large randomised clinical trials on cardiac devices. Kim et al evaluated the presence of TR in 248 ICD or PM recipients shortly after implantation and found in 24% of the patients an increase of TR by >1 grade. In addition, this increase in TR severity was more pronounced among patients with no or trivial TR, while patients who already were grade 1–3 TR showed only modest worsening of TR. Our study, with longer term follow-up (1–1.5 years), reported a higher incidence of significant (grade ≥2) TR progression (38%), suggesting the additional role over time of chronic lead and valvular structural and functional alterations. Similarly, we observed a trend towards a higher incidence of significant lead-induced TR among patients with only trivial TR before implantation as compared with patients with significant TR. In patients with significant TR before device implantation, with dilated tricuspid annulus and/or of leaflet malcoaptation, the presence of an RV lead may not have significant additional impact on TR severity. In contrast, in patients with new-onset significant TR, an RV lead hampering proper leaflet coaptation seems to be an important pathophysiological factor.
The exact mechanism of development and progression of TR after cardiac device placement has not been fully elucidated and may result from the mechanical interference of the RV lead with the tricuspid valve and/or from a direct effect on TR of RV pacing. In this study, no significant differences were seen in baseline clinical, echocardiography and device-related (ICD vs PM) characteristics among patients who did or did not develop significant TR after implantation, underlining the challenge of finding clear predisposing preimplantation parameters associated with lead-induced TR. These results suggest that significant lead-induced TR may result from progression of a pre-existing cardiac/valvular disease and also from interaction between the RV lead and tricuspid valve apparatus.
Although the presence of significant TR, regardless of aetiology, is a well-known prognostic factor, data on long-term outcome in patients with significant TR after RV lead implantation have not been reported. Our study demonstrated the independent association between significant lead-induced TR and all-cause mortality (combined with heart failure related events or not). Other variables independently associated with long-term outcomes (primary and secondary) were age, LVEF, percentage of RV pacing and significant mitral regurgitation, which are all known determinants of the development of heart failure and increased mortality. In particular, subanalysis according to the baseline LVEF showed that significant lead-induced TR in patients with a depressed LVEF (<40%) at baseline was associated with poor prognosis. RV pacing has been previously shown to be associated with an increased risk of LV (progressive) dysfunction and heart failure events. This detrimental effect of RV pacing might be mediated by induction of LV dyssynchrony but also by a direct negative effect on the severity of TR, as suggested by Vaturi et al. However, analyses of large trials showed that implantation of an ICD, even with minimal percentage of RV pacing, was associated with an increased risk of hospitalisations for congestive heart failure and death as compared with controls. The exact reason for this increased risk of heart failure events has not yet been elucidated but, considering the results of our study, might also be explained by lead-induced TR. Indeed, even modest grades of TR were associated with an increased risk of all-cause mortality.
These findings emphasise the importance of echocardiographic surveillance of ICD and PM recipients, enabling anticipation of the development of heart failure. Although lead repositioning or extraction might be an option only in the short-term after implantation, other therapeutic options, such as upgrade to a biventricular pacemaker, optimisation of heart failure drugs or a surgical procedure on the tricuspid valve, might be considered in patients with significant TR and/or worsening LV function.
Several limitations of this study should be mentioned. First, the exact mechanism of lead-induced TR could not be confirmed in all patients. In addition, it remains unclear whether progression of RV remodelling is the cause or the consequence of significant TR. Moreover, the time interval between echocardiographic evaluations of 1–1.5 years was chosen to ensure identification of both acute and long-term occurrence of significant TR, but might still have underestimated the incidence of this complication, particularly because patients who died within 1 year after implantation were excluded. The mode of death was not systematically available and the impact of significant lead-induced TR on cardiovascular mortality could not be assessed. Finally, prospective studies with larger patient groups and longer follow-up are needed.
In conclusion, a significantly increased incidence of TR was seen at follow-up after implantation of an RV lead in more than 35% of ICD and PM recipients. A significant lead-induced TR was associated with an impaired RV performance and with a higher incidence of long-term mortality and heart failure events. These findings suggest the importance of echocardiographic follow-up in these patients in order to optimise patient management.
Although the presence of significant TR, regardless of aetiology, is a well-known prognostic factor, data on long-term outcome in patients with significant TR after RV lead implantation have not been reported. Our study demonstrated the independent association between significant lead-induced TR and all-cause mortality (combined with heart failure related events or not). Other variables independently associated with long-term outcomes (primary and secondary) were age, LVEF, percentage of RV pacing and significant mitral regurgitation, which are all known determinants of the development of heart failure and increased mortality. In particular, subanalysis according to the baseline LVEF showed that significant lead-induced TR in patients with a depressed LVEF (<40%) at baseline was associated with poor prognosis. RV pacing has been previously shown to be associated with an increased risk of LV (progressive) dysfunction and heart failure events. This detrimental effect of RV pacing might be mediated by induction of LV dyssynchrony but also by a direct negative effect on the severity of TR, as suggested by Vaturi et al. However, analyses of large trials showed that implantation of an ICD, even with minimal percentage of RV pacing, was associated with an increased risk of hospitalisations for congestive heart failure and death as compared with controls. The exact reason for this increased risk of heart failure events has not yet been elucidated but, considering the results of our study, might also be explained by lead-induced TR. Indeed, even modest grades of TR were associated with an increased risk of all-cause mortality.
These findings emphasise the importance of echocardiographic surveillance of ICD and PM recipients, enabling anticipation of the development of heart failure. Although lead repositioning or extraction might be an option only in the short-term after implantation, other therapeutic options, such as upgrade to a biventricular pacemaker, optimisation of heart failure drugs or a surgical procedure on the tricuspid valve, might be considered in patients with significant TR and/or worsening LV function.
Several limitations of this study should be mentioned. First, the exact mechanism of lead-induced TR could not be confirmed in all patients. In addition, it remains unclear whether progression of RV remodelling is the cause or the consequence of significant TR. Moreover, the time interval between echocardiographic evaluations of 1–1.5 years was chosen to ensure identification of both acute and long-term occurrence of significant TR, but might still have underestimated the incidence of this complication, particularly because patients who died within 1 year after implantation were excluded. The mode of death was not systematically available and the impact of significant lead-induced TR on cardiovascular mortality could not be assessed. Finally, prospective studies with larger patient groups and longer follow-up are needed.
In conclusion, a significantly increased incidence of TR was seen at follow-up after implantation of an RV lead in more than 35% of ICD and PM recipients. A significant lead-induced TR was associated with an impaired RV performance and with a higher incidence of long-term mortality and heart failure events. These findings suggest the importance of echocardiographic follow-up in these patients in order to optimise patient management.
Discussion
The main findings of this study include (1) significant lead-induced TR was observed in 38% of patients 1–1.5 years after placement of an RV lead; (2) significant lead-induced TR was associated with significant RV and right atrium enlargement, and with increased pulmonary pressures at follow-up and (3) significant lead-induced TR was independently associated with worse long-term clinical outcomes (all-cause mortality alone or combined with heart failure related events) after device implantation.
Significant Lead-induced TR
The presence of a lead through the tricuspid valve apparatus has been suggested as one of the mechanisms of TR. However, only a few studies have described the incidence of lead-induced TR acutely after implantation and no data are available from the large randomised clinical trials on cardiac devices. Kim et al evaluated the presence of TR in 248 ICD or PM recipients shortly after implantation and found in 24% of the patients an increase of TR by >1 grade. In addition, this increase in TR severity was more pronounced among patients with no or trivial TR, while patients who already were grade 1–3 TR showed only modest worsening of TR. Our study, with longer term follow-up (1–1.5 years), reported a higher incidence of significant (grade ≥2) TR progression (38%), suggesting the additional role over time of chronic lead and valvular structural and functional alterations. Similarly, we observed a trend towards a higher incidence of significant lead-induced TR among patients with only trivial TR before implantation as compared with patients with significant TR. In patients with significant TR before device implantation, with dilated tricuspid annulus and/or of leaflet malcoaptation, the presence of an RV lead may not have significant additional impact on TR severity. In contrast, in patients with new-onset significant TR, an RV lead hampering proper leaflet coaptation seems to be an important pathophysiological factor.
The exact mechanism of development and progression of TR after cardiac device placement has not been fully elucidated and may result from the mechanical interference of the RV lead with the tricuspid valve and/or from a direct effect on TR of RV pacing. In this study, no significant differences were seen in baseline clinical, echocardiography and device-related (ICD vs PM) characteristics among patients who did or did not develop significant TR after implantation, underlining the challenge of finding clear predisposing preimplantation parameters associated with lead-induced TR. These results suggest that significant lead-induced TR may result from progression of a pre-existing cardiac/valvular disease and also from interaction between the RV lead and tricuspid valve apparatus.
Impact of Significant Lead-induced TR on Long-term Prognosis
Although the presence of significant TR, regardless of aetiology, is a well-known prognostic factor, data on long-term outcome in patients with significant TR after RV lead implantation have not been reported. Our study demonstrated the independent association between significant lead-induced TR and all-cause mortality (combined with heart failure related events or not). Other variables independently associated with long-term outcomes (primary and secondary) were age, LVEF, percentage of RV pacing and significant mitral regurgitation, which are all known determinants of the development of heart failure and increased mortality. In particular, subanalysis according to the baseline LVEF showed that significant lead-induced TR in patients with a depressed LVEF (<40%) at baseline was associated with poor prognosis. RV pacing has been previously shown to be associated with an increased risk of LV (progressive) dysfunction and heart failure events. This detrimental effect of RV pacing might be mediated by induction of LV dyssynchrony but also by a direct negative effect on the severity of TR, as suggested by Vaturi et al. However, analyses of large trials showed that implantation of an ICD, even with minimal percentage of RV pacing, was associated with an increased risk of hospitalisations for congestive heart failure and death as compared with controls. The exact reason for this increased risk of heart failure events has not yet been elucidated but, considering the results of our study, might also be explained by lead-induced TR. Indeed, even modest grades of TR were associated with an increased risk of all-cause mortality.
These findings emphasise the importance of echocardiographic surveillance of ICD and PM recipients, enabling anticipation of the development of heart failure. Although lead repositioning or extraction might be an option only in the short-term after implantation, other therapeutic options, such as upgrade to a biventricular pacemaker, optimisation of heart failure drugs or a surgical procedure on the tricuspid valve, might be considered in patients with significant TR and/or worsening LV function.
Several limitations of this study should be mentioned. First, the exact mechanism of lead-induced TR could not be confirmed in all patients. In addition, it remains unclear whether progression of RV remodelling is the cause or the consequence of significant TR. Moreover, the time interval between echocardiographic evaluations of 1–1.5 years was chosen to ensure identification of both acute and long-term occurrence of significant TR, but might still have underestimated the incidence of this complication, particularly because patients who died within 1 year after implantation were excluded. The mode of death was not systematically available and the impact of significant lead-induced TR on cardiovascular mortality could not be assessed. Finally, prospective studies with larger patient groups and longer follow-up are needed.
In conclusion, a significantly increased incidence of TR was seen at follow-up after implantation of an RV lead in more than 35% of ICD and PM recipients. A significant lead-induced TR was associated with an impaired RV performance and with a higher incidence of long-term mortality and heart failure events. These findings suggest the importance of echocardiographic follow-up in these patients in order to optimise patient management.
Impact of Significant Lead-induced TR on Long-term Prognosis
Although the presence of significant TR, regardless of aetiology, is a well-known prognostic factor, data on long-term outcome in patients with significant TR after RV lead implantation have not been reported. Our study demonstrated the independent association between significant lead-induced TR and all-cause mortality (combined with heart failure related events or not). Other variables independently associated with long-term outcomes (primary and secondary) were age, LVEF, percentage of RV pacing and significant mitral regurgitation, which are all known determinants of the development of heart failure and increased mortality. In particular, subanalysis according to the baseline LVEF showed that significant lead-induced TR in patients with a depressed LVEF (<40%) at baseline was associated with poor prognosis. RV pacing has been previously shown to be associated with an increased risk of LV (progressive) dysfunction and heart failure events. This detrimental effect of RV pacing might be mediated by induction of LV dyssynchrony but also by a direct negative effect on the severity of TR, as suggested by Vaturi et al. However, analyses of large trials showed that implantation of an ICD, even with minimal percentage of RV pacing, was associated with an increased risk of hospitalisations for congestive heart failure and death as compared with controls. The exact reason for this increased risk of heart failure events has not yet been elucidated but, considering the results of our study, might also be explained by lead-induced TR. Indeed, even modest grades of TR were associated with an increased risk of all-cause mortality.
These findings emphasise the importance of echocardiographic surveillance of ICD and PM recipients, enabling anticipation of the development of heart failure. Although lead repositioning or extraction might be an option only in the short-term after implantation, other therapeutic options, such as upgrade to a biventricular pacemaker, optimisation of heart failure drugs or a surgical procedure on the tricuspid valve, might be considered in patients with significant TR and/or worsening LV function.
Several limitations of this study should be mentioned. First, the exact mechanism of lead-induced TR could not be confirmed in all patients. In addition, it remains unclear whether progression of RV remodelling is the cause or the consequence of significant TR. Moreover, the time interval between echocardiographic evaluations of 1–1.5 years was chosen to ensure identification of both acute and long-term occurrence of significant TR, but might still have underestimated the incidence of this complication, particularly because patients who died within 1 year after implantation were excluded. The mode of death was not systematically available and the impact of significant lead-induced TR on cardiovascular mortality could not be assessed. Finally, prospective studies with larger patient groups and longer follow-up are needed.
In conclusion, a significantly increased incidence of TR was seen at follow-up after implantation of an RV lead in more than 35% of ICD and PM recipients. A significant lead-induced TR was associated with an impaired RV performance and with a higher incidence of long-term mortality and heart failure events. These findings suggest the importance of echocardiographic follow-up in these patients in order to optimise patient management.
