Table 1.
Definitions of definite, possible and rejected infective endocarditis [7].
Fig 1.
“Transcatheter heart valve (THV) endocarditis.
A. Long-axis transesophageal view showing typical vegetation attached to the ventricular side of a THV (red arrow). B. Short-axis transesophageal view showing de novo peri-prosthetic echo-free cavities and thickened areas (red arrow). C. 4 fluoro-deoxyglucose positron emission tomography (FDG-PET) depicting cells with an enhanced glucose metabolism at the level of THV, thus corroborating the diagnosis of endocarditis” [29].
Fig 2.
“The JenaValve transcatheter heart valve (THV) prosthesis (JenaValve Technology GmbH, Munich, Germany), a trileaflet porcine root tissue valve attached to a nitinol stent (A) and its implantation in illustration (B to D) and fluoroscopy (E to H). Release of the positioning feelers and placement into the aortic sinuses enables anatomic orientation (B and F). After correct orientation has been verified in 2 different fluoroscopic angulations, release of the lower stent part facilitates the clipping of the native aortic valve leaflets to the device and expansion of the stent allowing for secure anchoring even in the absence of valve calcium (C and G). Release of the upper stent part completes deployment of the valve prosthesis (D and H)” [18].
Fig 3.
PRISMA flow diagram.
Table 2.
Risk of bias in individual studies.
Table 3.
Characteristics of included studies.
Fig 4.
Percentage of post-TAVI infective endocarditis in studies included in the systematic review.
The microbiological profile of post-TAVI infective endocarditis is reported in 8 studies. Enterococci are the most common causative organism isolated from 25.9% of cases followed by Staphylococcus aureus (16.1%), coagulase-negative Staphylococcus species (14.7%), other Streptococcus species (12.5%), Viridans streptococci (8.5%), gram negative rods/HACEK/candida species (11%) and polymicrobial (0.42%).The cultures were negative in 6.7% of cases. The causative organisms of infective endocarditis are shown in Fig 5.
Fig 5.
Causative organisms of post-TAVI infective endocarditis.
The in-hospital mortality and mortality at follow-up were assessed in 7 studies with the mean incidence of 29.5% in-hospital mortality and 29.9% mortality at follow-up. The incidence of heart failure after post-TAVI infective endocarditis was reported in 5 studies making a cumulative incidence of 37.1%. Two studies determined the incidence of stroke with the stroke occurring in 10.5% and 0% post-TAVI infective endocarditis patients. Major bleeding was reported in 2 studies with an average of 11.3%. Only a single study by Martinez-Selles et al. reported arrhythmias in 20% cases. The septic shock occurred in 10% and 27.7% post-TAVI infective endocarditis patients according to 2 studies. The surgical intervention for the treatment of post-TAVI infective endocarditis was reported in 7 studies with the mean of 11.4%. Four studies revealed the valve-in-valve procedure performed in an average of 6.4% cases. The clinical outcomes of post-TAVI infective endocarditis are shown in Fig 6.
Fig 6.
Clinical outcomes in patients of post-TAVI infective endocarditis.
The incidence of infective endocarditis in the included studies with its causative organisms are summarized in Table 4.
Table 4.
Incidence of post-TAVI infective endocarditis in the included studies with its causative organisms.
Table 5.
Clinical outcomes of post-TAVI infective endocarditis.
Table 6.
Antibiotics used for treatment of post-TAVI IE in 5 studies.