Effects of ICD Leads on Tricuspid Valve and Right Ventricle
Quick Takes
- Six months following device implantation, a transvenous device led to a 7-fold increase in the likelihood of worsening TR, which was moderate or severe in 7% of TV-ICD recipients.
- However, there was no evidence of RV dilatation or systolic dysfunction 6 months following TV-ICD insertion.
- While there was no observed impact of TV-ICD leads on RV size and function, 6 months may be too short an interval to detect a difference.
Study Questions:
What is the effect of a transvenous implantable cardioverter-defibrillator (TV-ICD) on tricuspid regurgitation (TR) severity, and secondarily, on right ventricular (RV) size and function?
Methods:
The ATLAS (Avoid Transvenous Leads in Appropriate Subjects) investigators evaluated TR severity before and 6 months after ICD insertion in a post hoc analysis of adults randomized to receive a TV-ICD (n = 252) or subcutaneous ICD (S-ICD) (n = 251) device. TR and RV size and systolic function were assessed by echocardiographic images analyzed in a core laboratory. Changes in echocardiographic parameters between baseline and 6 months were evaluated using linear mixed models.
Results:
At baseline, at least mild TR was present in 30% of individuals. At 6 months, the proportion of participants with any TR in the TV-ICD group was 42% versus 19% in the S-ICD group (p < 0.001). The proportion with moderate or severe TR was 7% in the TV-ICD group versus 2% in the S-ICD group (p = 0.021). At 6 months, the odds ratio of ≥1 grade worsening of TR in the TV-ICD group as compared with the S-ICD group was 7.2 (95% confidence interval, 3.3-15.8; p < 0.001). There were no differences between groups with respect to RV size or systolic function.
Conclusions:
The authors report that 6 months following TV-ICD insertion, there was a 7-fold increase in the risk of ≥1 grade worsening of TR, with 7% of individuals having TR that was moderate or severe.
Perspective:
This study reports that 6 months following device implantation, a transvenous device led to a 7-fold increase in the likelihood of worsening TR, which was moderate or severe in 7% of TV-ICD recipients. However, there was no evidence of RV dilatation or systolic dysfunction 6 months following TV-ICD insertion. Thus, it appears that insertion of a TV-ICD lead causes TR, which in many cases is clinically significant. While there was no observed impact of TV-ICD leads on RV size and function, 6 months may be too short an interval to detect a difference. Additional longer-term prospective studies are indicated to assess the extent to which the TR caused by transvenous leads may result in RV dilatation, dysfunction, or adverse clinical outcomes.
Clinical Topics: Arrhythmias and Clinical EP, Implantable Devices, SCD/Ventricular Arrhythmias, Valvular Heart Disease
Keywords: Defibrillators, Implantable, Tricuspid Valve Insufficiency
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