Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (963 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Inflammation of the inner lining of the heart (endocardium), the continuous membrane lining the four chambers and heart valves. It is often caused by microorganisms including bacteria, viruses, fungi, and rickettsiae. Left untreated, endocarditis can damage heart valves and become life-threatening.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Endocarditides; Infective Endocarditis; Endocarditides, Infective; Endocarditis, Infective; Infective Endocarditides.
Where it fits in the MeSH classification
- Broader topics
- Heart Diseases
- Narrower topics
- Endocarditis, Bacterial; Endocarditis, Non-Infective
Related concepts
- Endocardium
- Heart Valves
Research landscape
PubMed indexes 32,458 records tagged with the MeSH heading “Endocarditis” (counts retrieved 2026-10-29). 4,135 of them (12.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 16,197 records.
Reviews account for 3,864 records (11.9%) and meta-analyses for 119. Randomized controlled trials number 113 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 16,197 |
| 2000-2009 | 5,387 |
| 2010-2019 | 6,739 |
| 2020 onward | 4,135 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,864 | 11.9% |
| Meta-analyses | 119 | 0.4% |
| Randomized controlled trials | 113 | 0.3% |
Method: PubMed query "Endocarditis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| β-Lactam Inoculum Effect in Methicillin-Susceptible Staphylococcus aureus Infective Endocarditis | 2024 | Research article Design not recorded in structured metadata | 29 | cc by PMID 39705034 · DOI · PMC11662251 |
| Infective endocarditis: it takes a team | 2025 | Review article Design not recorded in structured metadata | 27 | cc by PMID 40214743 · DOI · PMC12193143 |
| Clinical profile and outcomes among patients with cardiac implantable electronic device presenting as isolated pocket infection, pocket-related infective endocarditis, or lead-related infective endocarditis | 2025 | Research article Design not recorded in structured metadata | 11 | cc by PMID 40083315 · DOI · PMC11982440 |
| Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41535299 · DOI · PMC12909850 |
β-Lactam Inoculum Effect in Methicillin-Susceptible Staphylococcus aureus Infective Endocarditis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- ImportanceInfective endocarditis (IE) caused by Staphylococcus aureus is associated with high mortality, approximately 20% to 30%, mostly in the first month, with no improvement in recent decades.
- Closing excerpt
- Phenotyping MSSA isolates for inoculum effect may guide β-lactam choice and improve outcomes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (389 words)
ImportanceInfective endocarditis (IE) caused by Staphylococcus aureus is associated with high mortality, approximately 20% to 30%, mostly in the first month, with no improvement in recent decades. Current opinion is that antistaphylococcal penicillin and cefazolin are equally effective in treating methicillin-susceptible S aureus (MSSA) IE, and both are recommended as possible first-line treatments. Most MSSA strains carry the β-lactamase blaZ gene, and some blaZ-positive strains exhibit an inoculum effect, meaning increased minimum inhibitory concentrations at high inoculum. This reduced susceptibility to an antibiotic at high bacterial inoculum may be particularly relevant in IE, where vegetations have very high bacterial densities.ObjectiveTo evaluate the association between phenotypic characteristics of S aureus isolates, β-lactam used, and outcome in patients with MSSA IE.Design, settings, and participantsThis retrospective case series included MSSA cases treated at 3 French university hospitals between February 2016 and February 2022. The study included patients who had clinical isolates available and had definite or possible S aureus IE that involved native or prosthetic valves. Data were analyzed from July 2023 to June 2024.Main outcomes and measuresMSSA isolates were tested for the presence of blaZ and for inoculum effects to cefazolin and oxacillin. The association between first-month mortality and the β-lactam used, the presence of blaZ, and the presence of an inoculum effect to the treatment received was evaluated.ResultsThis study included 216 patients with MSSA IE (median [IQR] age, 65 [49-73] years; 152 [70.4%] male) who were treated with antistaphylococcal penicillin (139 [64.4%]) or cefazolin (77 [35.6%]). One-month mortality of left-sided IE was 44 of 180 patients (24.4%), with no overall difference between patients treated with antistaphylococcal penicillin or cefazolin. However, 1-month mortality was higher in patients infected with blaZ-positive strains than with blaZ-negative strains (38 of 129 [29.5%] vs 6 of 51 [11.8%]; P = .01), and with strains with an inoculum effect to the β-lactam received than with strains without an inoculum effect (25 of 62 [40.3%] vs 13 of 67 [19.4%]; P = .005). On multivariable analysis, the presence of an inoculum effect was independently associated with first-month mortality (HR, 2.84; 95% CI, 1.28-6.30; P = .01).Conclusions and relevanceIn this case series of MSSA IE, the presence of an inoculum effect to the β-lactam received was a risk factor for death in the first month. Phenotyping MSSA isolates for inoculum effect may guide β-lactam choice and improve outcomes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39705034 · DOI · PMC11662251
Infective endocarditis: it takes a team [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Infective endocarditis (IE) is a relatively rare but life-threatening systemic infection, which remains associated with high morbidity and mortality.
- Closing excerpt
- In addition, implementation strategies, feasibility and options of the team approach have also been highlighted.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (185 words)
Infective endocarditis (IE) is a relatively rare but life-threatening systemic infection, which remains associated with high morbidity and mortality. The epidemiology of IE has shifted to involve an increasing numbers of older patients with both cardiovascular and other types of prosthetic devices, multiple comorbid conditions often requiring invasive procedures, increasingly virulent pathogens, in particular Staphylococcus aureus, or that can harbour anti-microbial resistance, and an escalation of injection drug use in many areas of the world. In parallel, advancements in diagnostic and therapeutic options have led to complex strategies in patients' management. Despite these epidemiologic shifts, clinical trials have been rare and most of the evidence guiding IE management derives from expert consensus or analysis of large registries. Because of this, a multi-disciplinary IE team-based approach has been recommended as the standard of care. The aim of this review is to explore the rationale for a multi-disciplinary team-based approach to the management of IE. This approach has proved to be potentially beneficial based on multiple investigations that have evaluated patient outcomes. In addition, implementation strategies, feasibility and options of the team approach have also been highlighted.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40214743 · DOI · PMC12193143
Clinical profile and outcomes among patients with cardiac implantable electronic device presenting as isolated pocket infection, pocket-related infective endocarditis, or lead-related infective endocarditis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsThe clinical spectrum of cardiac implantable electronic device (CIED) infections includes isolated pocket infection (IPI), pocket infection complicated by infective endocarditis (PIRIE), and lead-related infective endocarditis (LRIE).
- Closing excerpt
- PIRIE.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (190 words)
AimsThe clinical spectrum of cardiac implantable electronic device (CIED) infections includes isolated pocket infection (IPI), pocket infection complicated by infective endocarditis (PIRIE), and lead-related infective endocarditis (LRIE). The aim of this study was to assess the risk factors, clinical course, and outcomes in patients with CIED infections and to demonstrate differences between PIRIE and LRIE.Methods and resultsThe retrospective analysis of data from 3847 patients undergoing transvenous lead extraction for non-infectious (2640; 68.62%) and infectious (1207; 31.38%) indications, including 361 (29.91%) IPI, 472 (39.11%) PIRIE, and 374 (30.99%) LRIE, showed some differences in risk factors, clinical course, and outcomes between the subgroups. Unlike PIRIE, diabetes [hazard ratio (HR) = 1.488; 95% confidence interval (CI; 1.178-1.879), P ConclusionCardiac implantable electronic device infections share common risk factors; however, diabetes and intra-cardiac lead abrasion predispose to LRIE, whereas multiple leads and S. aureus in pocket culture are risk factors for pocket infection spread. Compared with LRIE, the clinical course of PIRIE was milder, and short- and long-term mortalities were lower, but comparable with IPI after >1 year. This may be an argument in favour of categorization into primary LRIE and secondary endocarditis, i.e. PIRIE.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40083315 · DOI · PMC11982440
Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Infective endocarditis (IE) is a severe heart infection caused predominantly by Gram-positive bacteria forming biofilm on heart valves.
- Closing excerpt
- Overall, our findings provide insights into how host blood flow impacts QS activation, which, in turn, regulates pathogenesis in IE, and highlight the Fsr QS as a potential determinant of clinical disease course.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Infective endocarditis (IE) is a severe heart infection caused predominantly by Gram-positive bacteria forming biofilm on heart valves. While biofilm formation is central to disease progression, the underlying bacterial mechanisms remain poorly understood. Here, we identify the Fsr quorum sensing (QS) system of Enterococcus faecalis as an unexpected negative regulator of biofilm and pathogenesis in IE. Using microfluidic and in vivo models, we show that blood flow prevents Fsr activation in early IE, with Fsr induction occurring only later, once bacteria form biofilm microcolonies and become shielded from flow. Deletion of Fsr promotes robust biofilm growth, driven partly through the downregulation of GelE and SprE proteases, reprograms metabolism by upregulating lrgAB to enhance pyruvate utilization, and increases gentamicin tolerance in vivo. Furthermore, we show that GelE cleaves the human pro-IL-1β into an active form, suggesting a species-specific mechanism for inflammation modulation by QS. In support of these findings, analysis of IE patient cohorts shows that naturally occurring Fsr-deficient E. faecalis strains are associated with prolonged bacteremia. Overall, our findings provide insights into how host blood flow impacts QS activation, which, in turn, regulates pathogenesis in IE, and highlight the Fsr QS as a potential determinant of clinical disease course.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41535299 · DOI · PMC12909850
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Infective endocarditis epidemiology over five decades: a systematic review [5]
- Research article Right-Sided Infective Endocarditis 2020: Challenges and Updates in Diagnosis and Treatment [6]
- Research article Prevention of Viridans Group Streptococcal Infective Endocarditis: A Scientific Statement From the American Heart Association [7]
- Research article Update on Cardiovascular Implantable Electronic Device Infections and Their Prevention, Diagnosis, and Management: A Scientific Statement From the American Heart Association: Endorsed by the International Society for Cardiovascular Infectious Diseases [8]
- Research article Meta-analysis of 18F-FDG PET/CT in the diagnosis of infective endocarditis [9]
- Research article Oral Is the New IV. Challenging Decades of Blood and Bone Infection Dogma: A Systematic Review [10]
References
- Jean B, Crolle M, Pollani C, Le Guilloux A, Martin-Blondel G, Tattevin P, et al.. β-Lactam Inoculum Effect in Methicillin-Susceptible Staphylococcus aureus Infective Endocarditis. . 2024. PMID 39705034 · DOI · PMC11662251
- Lau L, Baddour L, Fernández Hidalgo N, Brothers TD, Kong WKF, Borger MA, et al.. Infective endocarditis: it takes a team. . 2025. PMID 40214743 · DOI · PMC12193143
- Jacheć W, Polewczyk A, Nowosielecka D, Kutarski A. Clinical profile and outcomes among patients with cardiac implantable electronic device presenting as isolated pocket infection, pocket-related infective endocarditis, or lead-related infective endocarditis. . 2025. PMID 40083315 · DOI · PMC11982440
- Antypas H, Schmidtchen V, Staiger WI, Yanhong LI, Tan RJW, Ng KKF, et al.. Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis. . 2026. PMID 41535299 · DOI · PMC12909850
- Slipczuk L, Codolosa JN, Davila CD, Romero-Corral A, Yun J, Pressman GS, et al.. Infective endocarditis epidemiology over five decades: a systematic review. PLoS One. 2013. PMID 24349331 · DOI · PMC3857279
- Shmueli H, Thomas F, Flint N, Setia G, Janjic A, Siegel RJ. Right-Sided Infective Endocarditis 2020: Challenges and Updates in Diagnosis and Treatment. J Am Heart Assoc. 2020. PMID 32700630 · DOI · PMC7792231
- Wilson WR, Gewitz M, Lockhart PB, Bolger AF, DeSimone DC, Kazi DS, et al.. Prevention of Viridans Group Streptococcal Infective Endocarditis: A Scientific Statement From the American Heart Association. Circulation. 2021. PMID 33853363 · DOI
- Baddour LM, Esquer Garrigos Z, Rizwan Sohail M, Havers-Borgersen E, Krahn AD, Chu VH, et al.. Update on Cardiovascular Implantable Electronic Device Infections and Their Prevention, Diagnosis, and Management: A Scientific Statement From the American Heart Association: Endorsed by the International Society for Cardiovascular Infectious Diseases. Circulation. 2024. PMID 38047353 · DOI
- Mahmood M, Kendi AT, Ajmal S, Farid S, O'Horo JC, Chareonthaitawee P, et al.. Meta-analysis of 18F-FDG PET/CT in the diagnosis of infective endocarditis. J Nucl Cardiol. 2019. PMID 29086386 · DOI
- Wald-Dickler N, Holtom PD, Phillips MC, Centor RM, Lee RA, Baden R, et al.. Oral Is the New IV. Challenging Decades of Blood and Bone Infection Dogma: A Systematic Review. Am J Med. 2022. PMID 34715060 · DOI · PMC8901545
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.