Pseudomonas aeruginosa is a rare yet particularly aggressive infective endocarditis pathogen. We describe a case of successfully managed double-valve P. aeruginosa infective endocarditis, in which the presumed source of bacteremia was a long-term tunneled central venous catheter used for hemodialysis.

A 75-year-old patient who had received Evolut R 34 TAVR prosthesis for severe aortic stenosis 2 months prior, presented for dyspnea, altered mental status and abdominal pain. Three blood cultures sets tested positive for Enterococcus faecalis. Transthoracic echocardiography was limited by a poor acoustic window, prompting for transesophageal echocardiography, which revealed an echo-free gap between the prosthesis and the posterior aortic wall suggesting the possibility of a periprosthetic abscess (Panel A). Cardiac CT found an abscess between the metal structure of the prosthesis and the noncoronary aortic sinus (Panel B, arrow and Panel C, top arrow), as well as filling defects suggesting vegetations at the level of the biological valve and of the metal structure of the prosthesis (Panel C, buttom arrow and Panel D, arrow). Two aortic pseudoaneurysms in relation to the distal extremity of the endoprosthesis’s stent were also present (Panel D and E, arrowhead). Multiorgan CT scans performed as a part of the IE imaging approach revealed multiple recent ischemic lesions in the brain (Panel F), as well as hepatic, splenic and renal infarcts (Panel G). Given the severe neurological deficit caused by the stroke, the patient was not a candidate for surgical prosthesis replacement. During the monitoring, the patient presented worsening of the symptoms and he died on Day 7 of his hospitalization. Our case emphasizes the possibility of a negative outcome after TAVR, as well as the role of imaging in the diagnosis of early infective endocarditis after TAVR.^1,2

Background and Clinical Significance: The widespread use of cardiac implantable electronic devices (CIEDs) has led to an increasing number of pocket-related complications. While early hematoma and infection are common, late-onset non-infective cystic pocket collections are rare and may closely mimic infectious processes, creating significant diagnostic and therapeutic dilemmas. Case summary: We report the case of an 81-year-old woman with a complex medical history (including a previous device-related infection requiring complete pacing system extraction), with a gradually enlarging, painless elastic mass at the secondary pacemaker pocket site, without local inflammatory signs, with normal inflammatory markers, and repeated negative blood cultures. Imaging demonstrated a large cystic collection surrounding the pacemaker. Surgical exploration was performed and a large volume of odourless, thick, yellowish fluid was evacuated from a fibrous capsule. Complete extraction of the pacing system was undertaken. Fluid microbiological cultures were negative and histopathological analysis revealed a chronic, nonspecific fibro-inflammatory granulomatous process. A leadless transcatheter pacemaker was implanted with favourable clinical and procedural outcomes. Conclusions: This case highlights the complexity of decision-making in a late-onset large fluid accumulation within the device pocket when clinical and microbiological evidence of infection is lacking, and the etiology remains uncertain. The local tissue findings, after the pocket has been opened and drained, along with the distinct clinical characteristics of each case, must ultimately define the therapeutic strategy. In high-risk patients with diagnostic uncertainty, leadless pacing systems provide an effective strategy for definitive rhythm management while minimising the risk of future infection.