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Device Lead–Associated Tricuspid Regurgitation
According to the American Heart Association (AHA) heart disease and stroke statistics, in the year 2014, more than 300,000 pacemakers (PMs) and 60,000 intracardiac defibrillators (ICDs) were implanted in United States. As the population continues to age, the number of cardiac implantable electronic device (CIED) leads, which includes PMs, ICDs, and cardiac resynchronization therapy (CRT), will most likely increase. The first reports of device lead–mediated interference with the tricuspid valve (TV) apparatus were published in the late 1900s. Subsequently, multiple case reports, case series, and retrospective cohort studies have shown an association between the presence of a device lead and worsening tricuspid regurgitation (TR). With the recent surge in percutaneous options for valvular dysfunction and the realization that TR is not a benign condition, , the interest in this topic has soared among both echocardiographers and interventionalists. All currently available device leads have been documented to interfere with the TV apparatus, and the resultant TR is classified as primary (organic) TV dysfunction. This chapter reviews the existing evidence behind CIED-mediated TR, discusses the potential mechanisms of CIED-mediated interference of the TV apparatus, and provides an overview on how to diagnose CIED-mediated interference using echocardiography.
Cardiac Implantable Electronic Devices and Tricuspid Regurgitation
The reported frequency of significant TR after CIED placement is variable, ranging anywhere from 7% to 45% in selected studies. Initial studies using two-dimensional (2D) echocardiography reported conflicting results with early studies being mostly negative, showing no difference in TR severity before and after right ventricular (RV) lead implantation, while later studies suggested an increase in TR severity after CIED implantation. , , , Some studies even suggested an improvement in TR after CIED implantation. This was in part believed to be attributable to improvement in right heart hemodynamics with pacing. , One might ask why reports of CIED-related TR were so conflicting in the early studies. In part, this could be caused by limitations of study design. Many of these studies were retrospective and observational and without control groups, and minimal data were reported on outcomes. Furthermore, the assessment of TR severity was largely qualitative instead of objective, based on measured parameters. These limitations are further compounded by the challenges associated with TR assessment on 2D echocardiography. Comparison of TR degree before and after device lead implantation is frequently confounded by the strong reflectivity of the device lea das well as lead-generated acoustic artifact, both of which may lead to underestimation of TR severity by color Doppler. Device leads are fully visualized as they traverse the TV annulus in only 15% of cases on 2D echocardiography. Finally, many of these patients (at least those with ICD and CRT devices) have underlying left ventricular (LV) dysfunction, which, over time may lead to RV enlargement, tricuspid annular dilatation, and functional TR, a situation that may confound the underlying cause of TR in a cross-sectional study. More recently, studies have incorporated outcomes into their methods and have shown that CIED-induced TR is associated with a poorer prognosis. , , One single-center study examined the prevalence of significant TR in 634 consecutive patients over a 6-year period. PM leads were associated with a higher risk of developing significant TR and higher likelihood of death even after adjustment for LV dysfunction and pulmonary hypertension.
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