Introduction

Prosthetic valve endocarditis (PVE) after surgical aortic valve replacement and transcatheter aortic valve replacement (TAVR) carries significant morbidity/mortality. The initial infectious nidus on the prosthetic valve is typically the sewing ring, which can lead to dehiscence and/or leaflet dysfunction.

Although TAVR is most often performed via the femoral artery in a less invasive manner than conventional sternotomy, it is offset with a specific set of infection risks related to the entry site and device/procedure: non-standardized protocols for infection control outside of a standard/hybrid operating room, valve crimping injury, paravalvular leak turbulence, neo?leaflet stress with mal-aligned commissures, intact/calcified native leaflets, and intracardiac hardware (ie., pacemaker leads).

The study is done to compare incidence, predisposing factors, microbiology, diagnostic modalities, studies, management, and outcomes of PVE in SAVR and TAVR to better understand the pathology, as TAVR is now approved in lower risk, younger patients.

To compare incidence, predisposing factors, microbiology, diagnostic modalities, studies, management, and outcomes of PVE in SAVR and TAVR to better understand the pathology.

A comprehensive database search from PubMed and Embase to identify published studies from January 1, 2015 to March 13, 2020. Key words were indexed for original reports, clinical studies, and reviews. Reports were evaluated by 2 authors against a priori inclusion/exclusion criteria.

Studies were included if they reported incidence and outcomes related to surgical aortic valve replacement/TAVR PVE and excluded if they were published pre?2015 or included a small population. Followed the Cochrane methodology and Preferred Reporting Items for Systematic Reviews and Meta?Analyses guidelines for all stages of the design and implementation. Study quality was based on the Newcastle?Ottawa Scale.

 

Results

Thirty?three studies with 311 to 41?025 patients contained relevant information. The majority found no significant difference in incidence of surgical aortic valve replacement/TAVR PVE (reported as 0.3%–1.2% per patient?year versus 0.6%–3.4%), but there were key differences in pathogenesis. TAVR has a specific set of infection risks related to entry site, procedure, and device, including non-standardized protocols for infection control, valve crimping injury, paravalvular leak, neo?leaflet stress, intact/calcified native leaflets, and intracardiac hardware.

There are several risk factors for SAVR PVE, including male sex, prolonged cardiopulmonary bypass time, previous native valve endocarditis, and type of valve prosthesis implanted. Modifiable sources of infection in the postoperative period are sternal wound infections, intravascular catheter infections, urinary tract infections, and pneumonia.

Additional risks may be associated with the TAVR procedure itself: crimping of valve leaflets during valve loading and post-dilatation following deployment can lead to microscopic cellular damage that predisposes to inflammation and bacterial organism adhesion.

 

Conclusion

PVE is a serious consequence of bacterial seeding in both SAVR and TAVR that comes with high risk of morbidity and mortality. Although culprit bacteria have typically been Streptococci and Staphylococci, Enterococci has become a predominant agent with transfemoral TAVR.

Utilization of an endocarditis team consisting of a surgeon, cardiologist, and infectious disease specialist can improve institutional results and provide bespoke care for these complex patients.

With the expansion of TAVR to lower risk and younger patients, a better understanding of pathogenesis, patient presentation, and guideline?directed treatment is paramount. When operative intervention is necessary, mortality remains high at 20% to 30%. Unique TAVR infection risks present opportunities for PVE prevention, therefore, further investigation is imperative.

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