Blood culture-negative infective endocarditis poses considerable clinical and diagnostic challenges because of its atypical manifestations and the difficulty in identifying the responsible pathogens. The involvement of Bartonella henselae, a rare etiologic agent of blood culture-negative infective endocarditis, further complicates diagnosis and management. Dissemination of Bartonella across multiple organ systems is a recognized feature of the disease. A 73-year-old female with a one-year history of prosthetic mitral valve replacement for mitral valve stenosis secondary to rheumatic fever presented with a one-year history of self-remitting fevers and worsening anemia. In the months preceding admission, she also experienced a cerebrovascular accident involving the left frontal lobe. She was known to care for feral cats, coming into close contact with them through feeding and combing their fur for fleas. CT (computed tomography) imaging on admission was concerning for a left renal infarction, prompting an embolic workup. The transesophageal echocardiogram was notable for irregular thickening of the bioprosthetic mitral valve and mobile, filamentous densities, suggestive of a vegetation. Bartonella henselae IgG titers were markedly elevated at 1:32,768, raising concerns for infective endocarditis secondary to Bartonella henselae with dissemination to the bone marrow and left kidney. This report emphasizes the need for increased awareness, thorough diagnostic imaging, and thoughtful treatment approaches for a patient with widespread bartonellosis. Early identification of Bartonella henselae should be considered in blood culture-negative endocarditis cases, especially in patients with relevant epidemiological exposure.

Background and Objectives: The optimal timing for surgical intervention in acute aortic valve infective endocarditis (IE) remains debated. Although European guidelines distinguish emergency, urgent, and delayed indications, some centres postpone surgery, concerned that operating before sufficient antibiotic sterilization could increase IE relapse risk. Materials and Methods: This retrospective, observational, multicenter study included patients with acute aortic valve IE. Patients who were not operated, had non-aortic valve IE, or underwent emergency surgery were excluded. Surgery within 7 days of starting targeted antibiotics was classified as "early"; surgery between 7 and 30 days as "late." Primary outcomes were in-hospital mortality and 30-day permanent pacemaker implantation. Secondary endpoints included reinfection, reoperation for IE relapse, and mid-term survival. Results: A total of 203 patients included: 104 early and 99 late. In-hospital mortality was comparable (early: 16 patients, 15.4%; late: 16 patients, 16.2%; p = 0.90). Permanent pacemaker implantation was higher in the late group (early: 9 patients, 8.7%; late: 18 patients, 18.2%; p = 0.046). Mid-term survival at four years was similar (early: 67.1 ± 5.8%; late: 59.7 ± 8.1%; p = 0.71). Recurrence of IE (early: 5.7%; late: 4.8%; p > 0.9) and reoperation for recurrent IE (early: 5.7%; late: 4.8%; p > 0.9) did not differ. Conclusions: Delaying surgery for acute aortic valve IE does not improve procedural safety, as in-hospital mortality is similar. Early intervention does not increase reinfection or reoperation risk, and may reduce permanent pacemaker implantation, likely by preventing progressive fibrosis of the cardiac conduction system caused by infection and prolonged antibiotic exposure.

Infective endocarditis (IE) continues to represent a major challenge for global health systems. In 2019, its annual incidence was estimated at 13.8 cases per 100,000 individuals, contributing to approximately 66,300 deaths worldwide. Due to its high morbidity and mortality rates, enhancing preventive measures has become a priority in both clinical practice and ongoing research efforts. Since the publication of the 2015 ESC Guidelines for the management of IE, several pivotal studies have emerged, prompting a re-evaluation and potential update of the existing recommendations. One growing concern is the increasing antibiotic resistance among oral streptococci, particularly to macrolides such as azithromycin and clarithromycin, which now show higher resistance levels than penicillin. Changes in national antibiotic stewardship programs may have inadvertently contributed to a rise in IE incidence, in part due to altered prophylactic practices. At the same time, advances in diagnostic modalities-including more widespread and targeted use of echocardiography in patients with positive blood cultures for organisms like Enterococcus faecalis, Staphylococcus aureus, and various streptococci-have likely improved detection rates. Additionally, innovations in imaging, particularly computed tomography (CT) and nuclear medicine techniques, have enhanced the diagnosis of IE, especially among patients with prosthetic heart valves or implantable cardiac devices. This has allowed for better characterization of patient populations, aiding in the refinement of diagnostic criteria and therapeutic approaches. Furthermore, updated antibiotic treatment protocols, informed by EUCAST's antimicrobial susceptibility data, have helped tailor antimicrobial regimens to current resistance trends. The combination of improved diagnostic sensitivity and evolving microbial resistance patterns has also led to an increased number of patients being considered for cardiac surgery as part of their treatment pathway. This review seeks to synthesize the latest findings and guideline revisions, offering an integrated overview of recent progress in the diagnosis, medical treatment, and surgical management of infective endocarditis. It will also explore current therapeutic strategies and operative indications in light of the most recent evidence.

Background/Objectives: Infective endocarditis (IE) is a life-threatening cardiovascular infection with in-hospital mortality of 15-30% despite modern therapy. Contemporary IE demonstrates non-random valve involvement: aortic and mitral 35-45%, tricuspid 5-10% (30-50% in intravenous drug users [IVDU]), and pulmonary < 1%. These patterns implicate valve-specific anatomy and hemodynamics as central determinants of susceptibility. This narrative review examines the reported distribution of IE across the aortic, mitral, tricuspid and pulmonary valves and summarises the anatomical, haemodynamic, structural, microbial and patient-related factors associated with valve-specific susceptibility. Methods: A structured narrative review of English-language literature was conducted using PubMed/MEDLINE, Embase, Scopus, and Google Scholar (January 1990-March 2026). Search terms included "infective endocarditis," "valve anatomy," "hemodynamics," "bicuspid aortic valve," "prosthetic valve endocarditis," and "transcatheter aortic valve replacement (TAVR) endocarditis." We included anatomical studies, clinical cohorts, surgical series, imaging research, and international guidelines. Evidence was synthesized narratively using Oxford Centre for Evidence-Based Medicine (CEBM) levels. Results: IE susceptibility follows a biologically coherent gradient determined by the interaction between valve anatomy, hemodynamic stress, endothelial injury, and structural substrate. The aortic valve is most vulnerable because of high shear stress, congenital abnormalities such as bicuspid aortic valve, and direct continuity with the cardiac fibrous skeleton, predisposing to peri-annular extension. Mitral valve IE is largely conditional upon pre-existing structural disease, particularly mitral valve prolapse, rheumatic heart disease, and mitral annular calcification, and is characterized by a high risk of systemic embolization. Tricuspid valve IE reflects the interaction between low-pressure hemodynamics and acquired patient-specific modifiers, including intravenous drug use, cardiovascular implantable electronic devices, and congenital heart disease. Pulmonary valve IE remains uncommon because of favorable native hemodynamics but occurs predominantly in repaired congenital heart disease, right ventricular outflow tract reconstruction, and prosthetic pulmonary valves. Across all valve types, multimodality imaging and anatomical assessment consistently influence complication detection, surgical planning, and long-term surveillance. Conclusions: IE involvement is unevenly distributed among the cardiac valves. Aortic and mitral involvement predominate, tricuspid involvement is strongly influenced by injection drug use and intracardiac devices, and pulmonary-valve IE remains rare and is principally associated with congenital abnormalities or prosthetic material. These patterns highlight the possible contributions of haemodynamic stress, pre-existing structural abnormalities, and age-related valvular changes to the greater susceptibility of left-sided valves.

Balloon valvuloplasty is a commonly performed catheter-based procedure in dogs with congenital pulmonic stenosis. Worldwide, veterinary cardiologists often administer peri- and postoperative prophylactic antimicrobials to prevent infectious complications, like bacterial endocarditis. Infective endocarditis of the pulmonary valve is, however, extremely rare in dogs, and it has never been reported after balloon valvuloplasty. The objective of this retrospective case series was to investigate the incidence of infective endocarditis, if balloon dilatation of pulmonic stenosis was performed without antimicrobial prophylaxis. Medical records of dogs operated at a university teaching hospital in a 20-year period from 2006 to 2025 were reviewed for clinical signs and echocardiographic changes that could be caused by infective endocarditis. Of the 83 dogs that were operated without peri- or postoperative antimicrobial prophylaxis, survived the surgery, and had at least three weeks of follow-up, none developed infective endocarditis. Follow-up in 68 dogs was based on medical history, physical examination and echocardiography during rechecks at the authors' institution. Follow-up information from the remaining 15 dogs was gained from the owners and/or the referring veterinarians. Our study demonstrated zero event rate in dogs that underwent balloon dilatation of congenital pulmonic stenosis without antimicrobial prophylaxis.