4.3 Article

Risk factors for infective endocarditis following transcatheter pulmonary valve replacement in patients with congenital heart disease

Journal

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
Volume 94, Issue 4, Pages 625-635

Publisher

WILEY
DOI: 10.1002/ccd.28474

Keywords

TCPVR complications; IE; pulmonary valve disease

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Objectives We sought to delineate the risk factors for infective endocarditis (IE) in patients undergoing transcatheter pulmonary valve replacement (TCPVR). Background Despite the therapeutic benefits of TCPVR for treatment of dysfunctional right ventricular outflow tracts, IE is a major complication of the approach. Specific hemodynamic gradients and patient immune status as predisposing factors for IE are largely unexplored. Methods We performed a retrospective review of patients who had undergone TCPVR at UCLA between October 2010 and October 2017. Cases of IE were diagnosed based on the modified Duke criteria. Results Two hundred and thirty-five cases of TCPVR were performed with a mean follow-up of 2.6 years (range 0.0-8.0 years). Sixteen distinct IE events developed in 13 patients (Melody (TM) n = 12, SAPIEN n = 1), with a median time from implant to IE of 3.3 years (range 2.0-7.2 years). Univariate Cox regression showed that immunocompromised status was significantly associated with the development of IE hazard ratios (HR 5.43 [1.80-16.4], p = .003). Kaplan-Meier curves show that the 5-year freedom from IE among immunocompetent patients was 87% (95% CI 78-96%) versus 64% (95% CI 39-89%) among immunocompromised patients (log-rank p = .02). Postimplant right ventricular systolic pressure was higher among immunocompromised patients (p = .03). The risk of IE post-TCPVR in immunocompromised patients with residual pulmonary stenosis was 43%. Conclusions Among the risk factors examined in this study, immunocompromised status was the most significant predictor of IE development post-TCPVR. Patients with the lowest risk of IE are those with competent immune systems, without a history of IE, and with minimal residual pulmonary valve gradients post-TCPVR.

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