Background Delays in performing urgent coronary artery bypass graft (CABG) surgery are increasing across the UK, with national wait times now exceeding guideline targets. Prolonged preoperative admissions contribute to hospital bed pressures, increased costs and negative psychosocial effects for patients. Virtual wards using remote patient monitoring (RPM) may enable safe early discharge for clinically stable patients awaiting surgery.Objectives To evaluate the feasibility, safety and outcomes of a virtual ward pathway using RPM for patients awaiting urgent CABG surgery.Methods A prospective, multicentre, single-arm study was conducted across three UK cardiac centres (December 2022-May 2025). Eligible patients were discharged home with daily symptom reporting via a digital platform and structured clinician review. The primary outcome was preoperative major adverse cardiovascular events (MACE). Secondary outcomes included 30-day mortality, resternotomy, time to surgery, postoperative stay, readmissions and patient experience.Results 128 patients were enrolled (mean age 61 years; 87% male). No preoperative MACE occurred (0%; 95% CI 0.0% to 2.3%). 30-day mortality was 0% (95% CI 0.0% to 2.9%), and resternotomy occurred in 2.3%, comparable to national rates. Median time from discharge to surgery was 10 days, saving an estimated 1152 inpatient bed-days. Postoperative length of stay was 7.0 days compared with a national average of 8.0 (p=0.084). Patient experience was favourable: 95% felt safe at home, and 89% found the platform easy to use.Conclusions A virtual ward pathway with remote monitoring for selected patients awaiting urgent CABG was safe, feasible and associated with high patient acceptability and major reductions in inpatient utilisation. These findings support this model as a scalable approach to managing urgent surgical pathways while preserving safety and surgical timelines.

BACKGROUND:Prosthetic valve infective endocarditis (PVE) is one of the most severe complications after valve implantation. Early diagnosis and identification of paravalvular complications are essential to determine optimal timing of surgery. Our aim is to assess the diagnostic performance of Computed Tomography Coronary Angiography (CTCA) versus Transoesophageal echocardiography (TOE) for the detection of valvular and paravalvular complications of PVE against the reference standard of surgical inspection. METHODS:Fifty-two patients who underwent pre-operative CTCA and TOE for the assessment of prosthetic valve IE were included. Imaging findings of vegetation, abscess/pseudoaneurysm, leaflet perforation and dehiscence were compared with intra-operative findings. Significant ancillary findings on CTCA likely to impact surgical planning were also reported. RESULTS:Median age was 64 years and 66 ​% were male. Surgical inspection revealed vegetations in 39 cases; CTCA had a sensitivity of 81.6 ​% specificity 90.9 ​%, AUC 0.876; TOE had a sensitivity of 97.4 ​%, specificity 72.7 ​%, AUC 0.807. Surgical inspection revealed abscess/pseudoaneurysm in 29 cases; CTCA had a sensitivity of 86.2 ​%, specificity 95.2 ​%, AUC 0.886; TOE had a sensitivity of 55.2 ​%, specificity 90.5 ​% (p ​< ​0.001), AUC 0.749. Significant ancillary findings on CTCA were identified in 24 (46 ​%) of patients. CONCLUSION:CTCA demonstrates higher diagnostic accuracy for paravalvular complications of PVE compared to TOE; a critical finding that necessitates early surgical intervention. Additionally, CTCA provides valuable ancillary information that can influence surgical planning. CTCA demonstrates comparable performance to TOE in identifying vegetations. Echocardiography remains superior for evaluating valve perforation, and dehiscence. A combined approach utilising both echocardiography and CTCA is recommended.

Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have been shown to reduce cardiovascular rehospitalisation in heart failure with reduced ejection fraction (HFrEF) patients. However, it is unknown whether initiating SGLT2i during an inpatient stay for a HFrEF exacerbation results in better outcomes versus initiation post-discharge in a cohort of diabetic and non-diabetic patients. This study compares cardiovascular rehospitalisation, heart failure specific rehospitalisation, cardiovascular death, and all-cause death between patients initiated on SGLT2i as an inpatient versus post-discharge. A retrospective study of four hospitals in England involving 184 patients with HFrEF exacerbations between March 2021 and June 2022 was performed. Cardiovascular rehospitalisation, heart failure specific rehospitalisation, cardiovascular death, and all-cause death were compared between the two groups using Cox regression. A Cox proportionalhazards model was fitted to determine predictors of cardiovascular rehospitalisation. There were 148 (80.4%) individuals who received SGLT2i as an inpatient, while 36 (19.6%) individuals received SGLT2i post-discharge. Median followup was 6.5 months for inpatients and 7.5 months for post-discharge patients (p=0.522). SGLT2i inpatients had significantly reduced cardiovascular rehospitalisations (22.3%) versus post-discharge patients (44.4%) (p=0.005), and significantly reduced heart failure specific rehospitalisations (10.1%) versus post-discharge patients (27.8%) (p=0.018). There was no significant difference in all-cause death (p=0.743) and cardiovascular death (p=0.816) between the two groups. Initiating SGLT2i post-discharge was an independent predictor of cardiovascular rehospitalisation (hazard ratio 2.40, 95% confidence interval 1.31 to 4.41, p=0.005). In conclusion, inpatient SGLT2i initiation for HFrEF exacerbations may reduce cardiovascular and heart failure specific rehospitalisation versus initiation postdischarge. In the absence of contraindications, clinicians should consider initiating SGLT2i once patients are clinically stable during inpatient HFrEF admissions.

Background Infective endocarditis (IE) is a rare, highly morbid condition with 17% in-hospital mortality. A total of 25–30% require surgery and there is ongoing debate with regard to markers predicting patient outcomes and guiding intervention. This systematic review aims to evaluate all IE risk scores currently available. Methods Standard methodology (PRISMA guideline) was used. Papers with risk score analysis for IE patients were included, with attention to studies reporting area under the receiver-operating characteristic curve (AUC/ROC). Qualitative analysis was carried out, including assessment of validation processes and comparison of these results to original derivation cohorts where available. Risk-of-bias analysis illustrated according to PROBAST guidelines. Results Of 75 articles initially identified, 32 papers were analyzed for a total of 20 proposed scores (range 66–13,000 patients), 14 of which were specific for IE. The number of variables per score ranged from 3 to 14 with only 50% including microbiological variables and 15% including biomarkers. The following scores had good performance (AUC > 0.8) in studies proposing the score (often the derivation cohort); however fared poorly when applied to a new cohort: PALSUSE, DeFeo, ANCLA, RISK-E, EndoSCORE, MELD-XI, COSTA, and SHARPEN. DeFeo score demonstrated the largest discrepancy with initial AUC of 0.88, compared to 0.58 when applied to different cohorts. The inflammatory response in IE has been well documented and CRP has been found to be an independent predictor for worse outcomes. There is ongoing investigation on alternate inflammatory biomarkers which may assist in IE management. Of the scores identified in this review, only three have included a biomarker as a predictor. Conclusion Despite the variety of available scores, their development has been limited by small sample size, retrospective collection of data and short-term outcomes, with lack of external validation, limiting their transportability. Future population studies and large comprehensive registries are required to address this unmet clinical need.

HomeJournal of the American Heart AssociationVol. 11, No. 16Infective Endocarditis Remains a Deadly Disease—It's Bad News, Especially When Staphylococci and Enterococci Are Involved: A Call to Action Open AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citations ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toOpen AccessEditorialPDF/EPUBInfective Endocarditis Remains a Deadly Disease—It's Bad News, Especially When Staphylococci and Enterococci Are Involved: A Call to Action Christopher P. Primus and Simon Woldman Christopher P. PrimusChristopher P. Primus *Correspondence to: Christopher P. Primus, MBBS, Specialised Cardiology Division, Barts Heart Centre, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, United Kingdom. Email: E-mail Address: [email protected] https://orcid.org/0000-0002-7464-5210 , Barts Heart Centre, , St Bartholomew's Hospital, Barts Health NHS Trust, , London, , United Kingdom, and Simon WoldmanSimon Woldman https://orcid.org/0000-0003-2156-4019 , Barts Heart Centre, , St Bartholomew's Hospital, Barts Health NHS Trust, , London, , United Kingdom, , University College London, , London, , United Kingdom, Originally published10 Aug 2022https://doi.org/10.1161/JAHA.122.026788Journal of the American Heart Association. 2022;11:e026788This article is a commentary on the followingTemporal Changes, Patient Characteristics, and Mortality, According to Microbiological Cause of Infective Endocarditis: A Nationwide StudyOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 10, 2022: Ahead of Print In this issue of the Journal of the American Heart Association (JAHA), Østergaard and colleagues present data drawn from national registries across Denmark, providing clear insight to the common pathogens and associated outcomes following a first episode of infective endocarditis (IE).1 Understanding the predictors of poor outcome and identifying modifiable patient‐ and disease‐related factors are key to building an evidence‐based approach to tackle the high morbidity and mortality associated with IE. Danish registries provide a unique opportunity to achieve this, with individual citizens traceable across pseudoanonymized national databases.The Danish National Patient Registry holds information on every hospital admission in Denmark since 1977, with International Classification of Diseases, Tenth Revision (ICD‐10) coded diagnoses obtained from patient discharge paperwork. Although coding relating to IE is not without pitfalls, the authors identified patients with a first diagnosis of IE from 2010 to 2017 with a combination of ICD‐10 codes previously identified as having good positive predictive value for IE.2 This allowed linking of patients with first‐time IE to clinical, microbiological, and outcome registries, containing key demographic and comorbidity data. Over the 8 years of study, 4123 admissions with IE were included in analyses, with no significant difference in incidence. Outcome data were available for both inpatient stay and in the medium term, with a median follow‐up period of 2.3 years (interquartile range 0.4–4.6 years). This allowed for identification of trends over time, accounting for captured patient characteristics and causative organism. Interestingly, in the more recent quartile of study, patients were older, had proportionally more prosthetic valve IE, and were more likely to have a past history of cancer and diabetes compared with earlier time periods.1Staphylococci were the leading causative organism in IE (28.1%), followed by Streptococci (26.0%) and Enterococci (15.5%) with blood culture negative IE (BCNIE) accounting for 18.9% of cases.1 This is in line with international registries showing falling rates of streptococcal IE and climbing staphylococcal and enterococcal IE.3, 4 However, there was no temporal change in the proportion of IE secondary to these organisms in the period of study. This does, however, reflect the shift in causative organism over the past 20 years, associated with the climbing incidence of invasive procedures and a population with a longer life expectancy.5, 6, 7 These relate not only to cardiac interventions with climbing rates of valve surgery, the evolution of transcatheter aortic valve implantation, and cardiac implantable devices but also to indwelling vascular catheters associated with dialysis and the management of cancer.3, 5Given the important role of viridans streptococci in IE, an increased population health focus on improving oral health and dental hygiene may also contribute to falling rates of streptococcal disease.8, 9 An inevitable impact of this change in causative organism has been a shift from subacute bacterial IE to rapid deterioration with an acute presentation for staphylococcal disease, in particular. This demands new treatment paradigms for the diagnosis and management of IE, with many patients seeking evaluation of fever later in their illness. This is despite guidance for patients deemed at high risk, including those with valvular heart disease, prosthetic heart valves, and previous IE; this has been particularly evident during the COVID‐19 pandemic.10, 11, 12, 13 Although Staphylococcus aureus is a known predictor of poor outcome in IE, only 13.6% of patients underwent operative intervention in the current study, compared with 20.1% of those with streptococcal IE, 24.3% with enterococcal IE, and 21.1% with BCNIE.1Despite high rates of morbidity and mortality, IE remains a rare disease, and this may explain in part why health care services are ill equipped to deliver rapid diagnostics to patients with IE that may well be life saving. This is highlighted in the current study, and other large international registries, where almost 1 in 5 cases were BCNIE (18.9%).1, 3, 4 This is despite established diagnostic pathways to identify the causative pathogen in this scenario, including the use of 16S rDNA polymerase chain reaction technology.3, 12, 13 This phenomenon is reflected in the current study, with a statistically significant decline in the proportion of BCNIE over the period of study from 24.1% in 2010 to 18.4% in 2017.1 Further promising work continues in this area, with the emerging technologies of both metagenomics to identify bacterial DNA in resected valve tissue and proteomics to capture proteins pathognomonic of certain bacteria and fungi.14, 15 Critically, identifying the causative organism will allow more targeted therapeutics, reducing toxicity and improving outcomes for this group in particular.The paradigm shift in the timing of surgery in IE has been adopted in international guidelines, with a move away from the concept of achieving sterility and operating late, toward early surgery to avoid heart failure, intractable sepsis, irreversible structural damage, and death.12, 13 This move led to reduced all‐cause mortality in a large meta‐analysis, favoring surgery before 7 days compared with 8 to 21 days, with an odds ratio (OR) of 0.61 (95% CI, 0.50–0.74), albeit with a possible higher rate of recurrence in the early surgery group.16 The modern approach to the management of IE is to therefore actively identify the established indications for surgical intervention in every patient at the time of diagnosis, and regularly thereafter, as a part of a multidisciplinary expert IE team.12, 17, 18 Despite this, the EuroENDO (European Infective Endocarditis) registry identified 69.3% of patients had an indication for surgery, with only 51.2% of patients actually undergoing surgical intervention; the remaining 18.1% had the highest rates of mortality.3 Of those undergoing surgery, just 31.5% went to the operating theater emergently or urgently, with 32.0% operated beyond the first week and 36.5% electively. In the current study, the population statistics preclude identification of surgical indications; however operative rates declined steadily from 24.8% in 2010 to 2011 to 17.6% in 2016 to 2017.1 If we are to reduce mortality in IE further, it is imperative we reconfigure our services to improve response times, training a cohort of cardiologists to identify IE early and manage it aggressively, and a further cohort of cardiac surgeons and anesthetists who operate upon these patients on a regular basis.The most striking findings from Østergaard and colleagues however, relate to in‐hospital versus medium‐term mortality.Overall in‐hospital mortality was comparable to other European countries in the contemporary era at 18.7%, with highest mortality rates in S. aureus IE (28.2%) compared with just 11.1% in streptococcal IE.1 This translated to an OR of 3.5 (95% CI, 2.7–4.4) for S. aureus IE, OR of 2.0 (95% CI, 1.5–2.6) for BCNIE, OR of 1.8 (95% CI, 1.2–2.7) for coagulase negative Staphylococci (CoNS), and OR of 1.5 (95% CI, 1.0–2.3) for enterococcal IE. A similar distribution of risk was seen for 1‐year mortality, albeit ≈10% higher in absolute values.1However, at a median follow‐up of 2.3 years (interquartile range 0.4–4.6 years) mortality rates were astounding: 74.4% for enterococcal IE, 70.1% for S. aureus, 62.4% for BCNIE and coagulase negative Staphylococci IE, and 58.5% for streptococcal IE. This higher rate of mortality for patients with enterococcal disease, compared with S. aureus, was identified only when differentiating mortality at time from discharge compared with admission.1 This suggests that although S. aureus IE is high risk at presentation, if patients survive their admission, they do better compared with their counterparts with enterococcal disease, who are older with more comorbidities.To put these findings in context, mortality rates in observational studies of patients with heart failure between 2000 and 2009 to 2010 show a 1‐year mortality of 20% and a 5‐year mortality of 53% to 67%.19, 20 Even without the anticipated real‐world reduction in mortality with novel heart failure pharmacotherapy, the mortality in IE is significantly worse than in heart failure. Yet most countries spend very little on the organization of IE services in comparison with heart failure.In conclusion, the present study highlights significant mortality in IE, with Staphylococci as the leading causative organism in an unselected cohort of patients with IE. When adjusting for inpatient mortality, the prognosis following enterococcal IE is also poor. Patient characteristics are important factors in relation to the causative organism, particularly in relation to intracardiac prosthetic material and indwelling long‐term vascular catheters.The very high rates of medium‐term mortality are a serious concern, and as a community we must strive to identify and address modifiable risk factors to improve outcome. To achieve this, we must innovate in diagnostics, adopt a mindset of active consideration and adoption of early surgery, and develop robust pathways that facilitate working in expert teams.DisclosuresNone.Footnotes*Correspondence to: Christopher P. Primus, MBBS, Specialised Cardiology Division, Barts Heart Centre, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, United Kingdom. Email: christopher.primus@nhs.netThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.See Article by Østergaard et al.For Disclosures, see page 3.References1 Østergaard L, Voldstedlund M, Bruun NE, Bundgaard H, Iversen K, Køber N, Christensen JJ, Rosenvinge FS, Jarløv JO, Moser C, et al. Temporal changes, patient characteristics, and mortality, according to microbiological cause of infective endocarditis: a nationwide study. J Am Heart Assoc. 2022; 11:e025801. doi: 10.1161/JAHA.122.025801LinkGoogle Scholar2 Fawcett N, Young B, Peto L, Quan TP, Gillott R, Wu J, Middlemass C, Weston S, Crook DW, Peto TEA, et al. 'Caveat emptor': the cautionary tale of endocarditis and the potential pitfalls of clinical coding data—an electronic health records study. BMC Med. 2019; 17:169. doi: 10.1186/s12916-019-1390-xCrossrefMedlineGoogle Scholar3 Habib G, Erba PA, Iung B, Donal E, Cosyns B, Laroche C, Popescu BA, Prendergast B, Tornos P, Sadeghpour A, et al. Clinical presentation, aetiology and outcome of infective endocarditis. Results of the ESC‐EORP EURO‐ENDO (European infective endocarditis) registry: a prospective cohort study. Eur Heart J. 2019; 40:3222–3232. doi: 10.1093/eurheartj/ehz620CrossrefMedlineGoogle Scholar4 Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG, Bayer AS, Karchmer AW, Olaison L, Pappas PA, Moreillon P, et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century. Arch Intern Med. 2009; 169:463.CrossrefMedlineGoogle Scholar5 Cahill TJ, Prendergast BD. Infective endocarditis. Lancet. 2016; 387:882–893. doi: 10.1016/S0140-6736(15)00067-7CrossrefMedlineGoogle Scholar6 Talha KM, Baddour LM, Thornhill MH, Arshad V, Tariq W, Tleyjeh IM, Scott CG, Hyun MC, Bailey KR, Anavekar NS, et al. Escalating incidence of infective endocarditis in Europe in the 21st century. Open Heart. 2021; 8:e001846. doi: 10.1136/openhrt-2021-001846CrossrefMedlineGoogle Scholar7 Pant S, Patel NJ, Deshmukh A, Golwala H, Patel N, Badheka A, Hirsch GA, Mehta JL. Trends in infective endocarditis incidence, microbiology, and valve replacement in the United States from 2000 to 2011. J Am Coll Cardiol. 2015; 65:2070–2076. doi: 10.1016/j.jacc.2015.03.518CrossrefMedlineGoogle Scholar8 GBD 2017 Oral Disorders Collaborators , Bernabe E, Marcenes W, Hernandez CR, Bailey J, Abreu LG, Alipour V, Amini S, Arabloo J, Arefi Z, Arora A, et al. Global, regional, and national levels and trends in burden of oral conditions from 1990 to 2017: a systematic analysis for the Global Burden of Disease 2017 Study. J Dent Res. 2020; 99:362–373. doi: 10.1177/0022034520908533CrossrefMedlineGoogle Scholar9 Lockhart PB, Brennan MT, Thornhill M, Michalowicz BS, Noll J, Bahrani‐Mougeot FK, Sasser HC. Poor oral hygiene as a risk factor for infective endocarditis–related bacteremia. J Am Dent Assoc. 2009; 140:1238–1244. doi: 10.14219/jada.archive.2009.0046CrossrefMedlineGoogle Scholar10 Havers‐Borgersen E, Fosbøl EL, Butt JH, Petersen JK, Dalsgaard A, Kyhl F, Schou M, Phelps M, Kragholm K, Gislason GH, et al. Incidence of infective endocarditis during the coronavirus disease 2019 pandemic: a nationwide study. Int J Cardiol Heart Vasc. 2020; 31:100675. doi: 10.1016/j.ijcha.2020.100675CrossrefMedlineGoogle Scholar11 Escolà‐Vergé L, Cuervo G, de Alarcón A, Sousa D, Barca LV, Fernández‐Hidalgo N; IE COVID‐19 Investigators . Impact of the COVID‐19 pandemic on the diagnosis, management and prognosis of infective endocarditis. Clin Microbiol Infect. 2021; 27:660–664. doi: 10.1016/j.cmi.2020.11.022CrossrefMedlineGoogle Scholar12 Habib G, Lancellotti P, Antunes MJ, Bongiorni MG, Casalta J‐P, Del Zotti F, Dulgheru R, El Khoury G, Erba PA, Iung B, et al. 2015 ESC guidelines for the management of infective endocarditis. Eur Heart J. 2015; 36:3075–3128. doi: 10.1093/eurheartj/ehv319CrossrefMedlineGoogle Scholar13 Baddour LM, Wilson WR, Bayer AS, Fowler VG, Tleyjeh IM, Rybak MJ, Barsic B, Lockhart PB, Gewitz MH, Levison ME, et al. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications. Circulation. 2015; 132:1435–1486. doi: 10.1161/CIR.0000000000000296LinkGoogle Scholar14 Million M, Gaudin M, Melenotte C, Chasson L, Edouard S, Verdonk C, Prudent E, Amphoux B, Meresse S, Dorent R, et al. Metagenomic analysis of microdissected valvular tissue for etiological diagnosis of blood culture‐negative endocarditis. Clin Infect Dis. 2020; 70:2405–2412. doi: 10.1093/cid/ciz655CrossrefMedlineGoogle Scholar15 Snipsøyr MG, Wiggers H, Ludvigsen M, Stensballe A, Vorum H, Poulsen SH, Rasmussen LM, Petersen E, Honoré B. Towards identification of novel putative biomarkers for infective endocarditis by serum proteomic analysis. Int J Infect Dis. 2020; 96:73–81. doi: 10.1016/j.ijid.2020.02.026CrossrefMedlineGoogle Scholar16 Anantha Narayanan M, Mahfood Haddad T, Kalil A, Kanmanthareddy A, Suri R, Mansour G, Destache C, Baskaran J, Mooss A, Wichman T, et al. Early versus late surgical intervention or medical management for infective endocarditis: a systematic review and meta‐analysis. Heart. 2016; 102:950–957. doi: 10.1136/HEARTJNL-2015-308589CrossrefMedlineGoogle Scholar17 Botelho‐Nevers E, Thuny F, Casalta JP, Richet H, Gouriet F, Collart F, Riberi A, Habib G, Raoult D. Dramatic reduction in infective endocarditis–related mortality with a management‐based approach. Arch Intern Med. 2009; 169:1290–1298. doi: 10.1001/archinternmed.2009.192CrossrefMedlineGoogle Scholar18 Chirillo F, Scotton P, Rocco F, Rigoli R, Borsatto F, Pedrocco A, De Leo A, Minniti G, Polesel E, Olivari Z. Impact of a multidisciplinary management strategy on the outcome of patients with native valve infective endocarditis. Am J Cardiol. 2013; 112:1171–1176. doi: 10.1016/J.AMJCARD.2013.05.060CrossrefMedlineGoogle Scholar19 Gerber Y, Weston SA, Redfield MM, Chamberlain AM, Manemann SM, Jiang R, Killian JM, Roger VL. A contemporary appraisal of the heart failure epidemic in Olmsted County, Minnesota, 2000 to 2010. JAMA Intern Med. 2015; 175:996–1004. doi: 10.1001/jamainternmed.2015.0924CrossrefMedlineGoogle Scholar20 Tsao CW, Lyass A, Enserro D, Larson MG, Ho JE, Kizer JR, Gottdiener JS, Psaty BM, Vasan RS. Temporal trends in the incidence of and mortality associated with heart failure with preserved and reduced ejection fraction. JACC Heart Fail. 2018; 6:678–685. doi: 10.1016/j.jchf.2018.03.006CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesTemporal Changes, Patient Characteristics, and Mortality, According to Microbiological Cause of Infective Endocarditis: A Nationwide StudyLauge Østergaard, et al. Journal of the American Heart Association. 2022;11 August 16, 2022Vol 11, Issue 16 Article InformationMetrics Copyright © 2022 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley BlackwellThis is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.https://doi.org/10.1161/JAHA.122.026788PMID: 35946465 Originally publishedAugust 10, 2022 Keywordsheart valve diseaseinfective endocarditismortalityorganismpopulation studynationwide studyEditorialsblood stream infectionPDF download SubjectsCardiovascular SurgeryEpidemiologyInfectious EndocarditisMortality/SurvivalRisk Factors

Background The first wave of the COVID-19 pandemic required rapid reconfiguration and reallocation of resources. We triaged all cardiac imaging requests from our referral network serving 2.5 million people, to our tertiary centre, performing only clinically urgent studies and cancelling non-urgent studies. Requesters received notification of cancellation in the same format as test reports and were encouraged to repeat their request when pandemic conditions had improved. The impact of this cancellation on patient outcomes is assessed. Methods Retrospective analysis of routinely collected clinical and administrative data from the institutional data warehouse determined patient outcomes for those with cancelled and performed stress echocardiography, nuclear stress perfusion studies, cardiac CT angiography and cardiac MRI. Mortality data was drawn from the NHS spine. Data analysis was performed using R. Results 1600 cardiac studies for 1592 patients were cancelled in April 2020, and 2234 cardiac studies were performed for 2184 patients between April and July 2020, representing high-risk outpatient requests. 41 patients who had cancelled scans died, and 105 patients with performed scans died (table 1). Of cancelled scans, 787 patients had a subsequent scan in some modality, of which 701 were the same modality as the original test. 761 patients had no repeat outpatient testing until October 2021. Mortality was higher in patients for whom scans were performed (log-rank p = 0.03, figure 1A). Non-elective admissions were higher in patients who had scans performed (4% in cancelled vs. 8% performed after 574 days of follow-up, log-rank p <0.001 figure 1B). Over the course of the pandemic, our wait-times for cardiac testing did not exceed the national standard of 16 weeks.Limitations: Data was not collected prospectively, due to the level of emergency; cancellation data may not be complete. All cause mortality under pandemic conditions cannot be extrapolated to non-pandemic situations. Conclusion Our approach to diagnostic testing in cardiology during the first wave of the COVID-19 pandemic accurately identified and tested high-risk patients without causing harm to those at lower risk, demonstrated by higher admission rates in patients in whom tests were performed, and the absence of an adverse impact on mortality. 49% of patients underwent subsequent cardiac testing after a cancelled test. We maintained low waiting times throughout the pandemic. Conflict of Interest None

BACKGROUND:Patients with acute severe aortic regurgitation (AR) due to infective endocarditis can progress rapidly from the hemodynamically stable patient to pulmonary edema and cardiogenic shock. We sought to identify patients at risk of decompensation where emergent surgery should be undertaken. METHODS:We identified 90 patients with acute severe AR from the echocardiography laboratory database. Baseline clinical, hemodynamic (heart rate (HR) and blood pressure (BP)), and echocardiographic data including mitral filling, premature mitral valve closure (PMVC), and diastolic mitral regurgitation (DMR) were identified. The primary endpoint was subsequent development of pulmonary edema or severe hemodynamic instability. RESULTS:Patients who met the primary endpoint had a higher HR (98.5 bpm vs 80.5 bpm), lower diastolic BP (54 mm Hg vs 61.5 mm Hg), higher mitral E-wave velocity (113 cm/s vs 83 cm/s), higher E/e' ratio (12.4 vs 8), higher proportion of DMR (27.8% vs 7.4%), and PMVC (25% vs 9.3%) than patients who did not meet the endpoint. The proportion of patients with the primary endpoint increased as HR increased ((≤81 bpm) 3/30 (10%), (81-94 bpm) 11/31 (35.5%), (≥94 bpm) 22/29 (75.9%), P < .0001) and as the diastolic BP reduced ((≤54 mm Hg) 19/31 (61.3%), (54-63 mm Hg) 12/31 (38.7%), (≥63 mm Hg) 5/28 (17.9%), P = .003). Independent predictors were a higher HR (OR 1.08 (95% CI 1.04-1.13) P = .0003) and DMR (OR 4.71 (95% CI 1.23-18.09), P = .02). CONCLUSION:Decompensation in acute severe AR is common. Independent predictors of decompensation are increasing HR(≥94 bpm) and the presence of DMR. Those with these adverse markers should be considered for emergent surgery.

ABSTRACT Background Disparities between weekend and weekday care, termed 'the weekend effect', have led to a UK government pledge to provide 7-day services. Despite this, poor outcomes have led to criticism of the programme. This study consequently sought to evaluate consultant-led virtual review as a model for 7-day cardiology services. Methods Over 4 weekends, cardiology patients underwent virtual review alongside in-person teams. Outcomes included length of stay, same-day discharge and 30-day mortality rates, as well as duration of ward rounds and change in patient management. Patients were surveyed on attitudes towards virtual review. Results Statistical analysis revealed no significant difference in clinical outcomes, while virtual review was noted to significantly decrease time taken (p<0.0001). Attitudes towards virtual review were broadly favourable. Conclusion By demonstrating comparable outcomes compared with conventional review, as well as high acceptability, this study identified virtual review as an effective substitute for in-person care.

International guidance recognizes the shortcomings of the modified Duke Criteria (mDC) in diagnosing infective endocarditis (IE) when transoesophageal echocardiography (TOE) is equivocal. 18F-FDG PET/CT (PET) has proven benefit in prosthetic valve endocarditis (PVE), but is restricted to extracardiac manifestations in native disease (NVE). We investigated the incremental benefit of PET over the mDC in NVE. Dual-center retrospective study (2010-2018) of patients undergoing myocardial suppression PET for NVE and PVE. Cases were classified by mDC pre- and post-PET, and evaluated against discharge diagnosis. Receiver Operating Characteristic (ROC) analysis and net reclassification index (NRI) assessed diagnostic performance. Valve standardized uptake value (SUV) was recorded. 69/88 PET studies were evaluated across 668 patients. At discharge, 20/32 had confirmed NVE, 22/37 PVE, and 19/69 patients required surgery. PET accurately re-classified patients from possible, to definite or rejected (NRI: NVE 0.89; PVE 0.90), with significant incremental benefit in both NVE (AUC 0.883 vs 0.750) and PVE (0.877 vs 0.633). Sensitivity and specificity were 75% and 92% in NVE; 87% and 86% in PVE. Duration of antibiotics and C-reactive Protein level did not impact performance. No diagnostic SUV cut-off was identified. PET improves diagnostic certainty when combined with mDC in NVE and PVE.

Abstract Background Infective endocarditis (IE) is a known but uncommon cause of cardioembolic stroke and there are rare but recognized cases of IE without an inflammatory response. Cutibacterium acnes is an increasingly recognized source of invasive infections, including IE, but diagnosis is challenging due to its low virulence and fastidious nature. Case summary A 47-year-old man presented with a multi-focal stroke suggestive of a cardioembolic source. Outpatient transoesophageal echocardiography (TOE) was concerning for vegetation or thrombus associated with his previous mitral valve repair. He remained clinically well, with no evidence of an inflammatory response and sterile blood cultures. Computed tomography–positron emission tomography (CT-PET) corroborated the TOE findings, however, given the atypical presentation, he was treated for valvular thrombus. Following discharge, he quickly re-presented with further embolic phenomena and underwent emergency mitral valve replacement. Intraoperative findings were consistent with prosthetic valve IE (PVE) and a 6-week course of antibiotics commenced. C. acnes was identified on molecular testing. Eighteen months later, he re-presented with further neurological symptoms. Early TOE and CT–PET were consistent with IE. Blood cultures grew C. acnes after prolonged incubation. Given the absence of surgical indications, he was managed medically, and the vegetation resolved without valvular dysfunction. He continues to be followed up in an outpatient setting. Discussion In patients presenting with multi-territory stroke, IE should be considered despite sterile blood cultures and absent inflammatory response. C. acnes is an increasingly recognized cause of PVE in this context, often requiring surgical intervention. A high index of suspicion and collaboration with an Endocarditis Team is therefore essential to diagnose and treat.

BACKGROUND Coronavirus disease-2019 (COVID-19) is thought to predispose patients to thrombotic disease. To date there are few reports of ST-segment elevation myocardial infarction (STEMI) caused by type 1 myocardial infarction in patients with COVID-19. OBJECTIVES The aim of this study was to describe the demographic, angiographic, and procedural characteristics alongside clinical outcomes of consecutive cases of COVID-19-positive patients with STEMI compared with COVID-19-negative patients. METHODS This was a single-center, observational study of 115 consecutive patients admitted with confirmed STEMS treated with primary percutaneous coronary intervention at Barts Heart Centre between March 1, 2020, and May 20, 2020. RESULTS Patients with STEMS presenting with concurrent COVID-19 infection had higher levels of troponin T and tower lymphocyte count, but elevated D-dimer and C-reactive protein. There were significantly higher rates of multivessel thrombosis, stent thrombosis, higher modified thrombus grade post first device with consequently higher use of glycoprotein Ilb/Illa inhibitors and thrombus aspiration. Myocardial blush grade and left ventricular function were significantly tower in patients with COVID-19 with STEMI. Higher doses of heparin to achieve therapeutic activated dotting times were also noted. Importantly, patients with STEMS presenting with COVID-19 infection had a longer in-patient admission and higher rates of intensive care admission. CONCLUSIONS In patients presenting with STEMS and concurrent COVID-19 infection, there is a strong signal toward higher thrombus burden and poorer outcomes. This supports the need for establishing COVID-19 status in all STEMS cases. Further work is required to understand the mechanism of increased thrombosis and the benefit of aggressive antithrombotic therapy in selected cases. (C) 2020 by the American College of Cardiology Foundation.

Infective endocarditis (ie, the infection of a native or prosthetic heart valve, the endocardium or implanted cardiac device1) is a clinical chameleon whose epidemiology and natural history are in constant evolution, reflecting the complex interaction between an ageing population, elusive microorganisms, evolving patterns of healthcare, available therapies and the application of aggressive surgery. Despite overall advances in treatment, there is no consistent signal of falling incidence and clinical outcomes remain poor. IE is uncommon with a generally accepted overall annual incidence of 3–10 cases per 100 000 people.1 However, recent data indicate that this incidence has increased significantly in England where IE admissions (primary ICD-10 diagnostic code I33) remained stable between 1998–1999 (26.6 cases/million) and 2009–2010 (26.9 cases/million) but rose dramatically (by 86%) to 50.0 cases/million in 2018–2019 (figure 1).2 While some of this increase may partly relate to recommendations by the National Institute for Health and Care Excellence in 2008 regarding the cessation of antibiotic prophylaxis in at-risk individuals undergoing selected dental and other invasive medical procedures,3 this association cannot be confirmed in the absence of microbiological data. Indeed, multiple contributory factors are likely, including (A) an ageing population, (B) increased use of both intra-cardiac (including permanent pacemakers, implantable cardioverter-defibrillators, surgical and transcatheter heart valves) and vascular devices (including those used for chronic haemodialysis), (C) epidemic levels of opioid addiction and associated injection drug use, (D) emergence of staphylococci and enterococci (neither of which are targeted by current antibiotic prophylaxis strategies) as more common causative organisms, and (E) greater clinical awareness of IE. Nevertheless, these findings are disturbing and contrast with reports of falling incidence in the USA4 and falling or more modest increases in Europe.5 European guidelines …

AIM:The mortality of patients with infective endocarditis (IE) is high. The management of patients with large vegetations is controversial. This study sought to investigate the association of vegetation size on outcomes including valve destruction, embolism and mortality. METHODS AND RESULTS:One hundred and forty-two (142) patients with definite IE and transoesophageal echocardiography (TEE) imaging available for analysis were identified and data retrospectively reviewed. Vegetation length, width and area were measured. Severe valve destruction was defined as the composite of one or more of severe valve regurgitation, abscess, pseudoaneurysm, perforation or fistula. Associations with 6-month mortality were identified by Cox regression analysis. Eighty (80) (56.3%) patients had evidence of valve destruction on TEE. Vegetation length ≥10 mm and vegetation area ≥50 mm2 were significantly associated with increased risk of valve destruction, (both odds ratio OR 1.21, p=0.03 and p=0.02 respectively). Thirty-nine (39) (72.2%) patients who had an embolic event, did so prior initiation of antibiotics. Six (6)-month mortality was 18.3%. In the surgically managed group, vegetation size was not associated with mortality. In the medically managed group, vegetation area (mm2) was associated with increased mortality (HR 1.01, p<0.01) along with age (HR 1.06, p=0.03). CONCLUSION:Vegetation length ≥10 mm or area ≥50 mm2 are associated with increased risk of valve destruction. Vegetation size may also predict mortality in medically managed but not surgically managed patients with IE. Further studies to evaluate whether surgery in patients with large vegetation size improves outcomes is warranted.

This issue of the Journal features a moving and powerful article1 about a son, who just happens to be a doctor, watching his father die from heart failure. Despite advanced disease, the possibility of mortality was not discussed, and the physicians adopted an overoptimistic position despite ample evidence to the contrary. To many of us, this is an all too familiar scenario. Despite the familiarity, the power of the piece is in its capacity to shock and make us reflect. Inevitably one is left wondering about international norms for training and provision of heart failure services. The decision to initiate end-of-life care in heart failure is undoubtedly challenging. Clinicians find it difficult to identify when a patient is entering the last few days of life. Indeed, identifying heart failure patients who are dying is prone with error. All heart failure clinicians will be aware of patients whom they diagnosed as imminently dying, only for them to live, perhaps for a very long time. Alternatively, sudden death can unexpectedly intervene in a patient with an apparently good prognosis, or the underlying condition can progress at a faster rate than predicted leading to shorter life spans than expected. Heart failure prognosis is often compared to the prognosis in cancer by clinicians. The attitude of the general public to heart failure prognosis has been little studied but it is clear that heart failure clinicians need to lead the debate, or the public will expect that we can do more than we can. My experience is that the public tend to view heart disease as curable and cancer as terminal, when, in reality, both diseases have a similar prognosis.2 This enhanced expectation can result in patients and relatives believing that the impossible can be done. As the current article shows, doctors are also not immune from this or at least from expressing unreasonable hope for a patient. Despite numerous attempts to produce a scoring system to identify patients in the terminal stage of heart failure, the systems we use are imperfect. They give a risk of death for a population based on characteristics which may be symptom, laboratory or treatment related but the output remains stubbornly population derived and not individualised. Since scoring systems measure population risk, they are prone to inaccuracy for an individual patient. Consider a 75-year-old man requiring 250 mg of intravenous furosemide, 5 mg of metolazone with a low sodium at 130 mEq/L and a normal haemoglobin on typical triple therapy (angiotensin-converting enzyme inhibitors, beta-blockers and mineralocorticoid receptor antagonists) for heart failure. Using the Seattle heart failure scoring system,3 he has a 25% risk of mortality at one year yet many of us would not be surprised if he did not die a few weeks after these observations. With such uncertainty, perhaps we need to think again about how we talk to patients about the diagnosis of heart failure and its implications. The diagnosis of heart failure does not leave a patient in a hopeless position. Established and novel drugs, pacemakers, defibrillators,4 and even new pumps have been developed that improve the quality of life and prognosis for patients, predominantly with systolic left ventricular dysfunction. Indeed, the mortality of heart failure, including the mortality of acute heart failure, has progressively fallen over the last few years.5 However, although these treatments prolong life, we are not yet at the stage where we can ‘cure’ heart failure. As the disease progresses, patients often become more and more disabled and eventually die. Additionally, there is a high risk of sudden cardiac death even in the presence of a defibrillator.6 As the author points out,1 advance notice of death assists families and patients in planning and managing symptoms. He asserts that we should use the principle of ‘plan for the worst and hope for the best’, which has been used in oncology settings. Using such a principle, the cardiologist would inform the patient about the risk of death, including the risk of sudden death at the time of diagnosis. This would allow open and frank discussions with patients about what their goals are and how we might assist them in achieving their goals. The parallel with cancer diagnosis and management remains appropriate. In the UK, psychological support services are recommended across the whole cancer pathway and should be offered to patients and carers,7 and the 2016 European Society of Cardiology guidance suggests psychologists to be part of the multidisciplinary team managing the heart failure programme.4 The same is true for palliative care services but few heart failure clinics have the necessary psychological and palliative care support that is seen in cancer clinics. In addition, there is a need for clinicians who manage heart failure to acknowledge that the disease is often terminal. We are often so caught up in new and established treatments that we neglect to talk about mortality. As the disease progresses, the struggle to save a patient's life overshadows everything that we do, and as a result end-of-life care may drop down the priority list. Perhaps this is where the parallel with cancer management is no longer appropriate. In heart failure there is often another treatment modality, another device, another procedure, another drug or a different programme that can be tried. On occasion, these last-gasp interventions are successful, at least for a while. More often, they are unsuccessful and deflect attention away from other therapies. We need to develop ways to assess what is important for the patient perhaps by structured interview8 or more simply by asking the patient in the clinic room. For example, patients may have personal goals that they wish to achieve before they die. At times, this will coincide with the emphasis on prolonging life (e.g. for a patient who wishes to see a grandchild born). At other times, prolonging life and achieving an ambition may require divergent paths. For example, a hospitalised patient may wish to attend a specific function or celebration outside of town. Whilst it might be possible to facilitate this, for example with a pre-discharge infusion of levosimendan,9 this might be potentially injurious to their length of life despite a marked improvement in their symptoms. Clearly this is a matter for the patient and doctor to discuss but the matter might not even come up if the entire focus is on prognosis. There is therefore an argument that it is time for us to change ‘our script’. Perhaps we should be talking about mortality much earlier on in the disease pathway.10 Since heart failure is rarely cured, perhaps we should be talking to patients about the likelihood of death at the time of diagnosis. As with the case highlighted in this edition of the Journal, we can then talk easily when patients deteriorate about what they want and when they want it. We should continue to talk to patients about their goals, aspirations and mortality throughout the disease course. Most of the time the therapies offered will be those that prolong life. Just occasionally though, the therapies offered will differ. Once patients start to have functional decline, severe symptoms, cachexia or are clinically just failing, then an urgent discussion on end-of-life care is necessary.4 Conflict of interest: none declared.

Heart failure continues to cost patients their lives and governments and individuals their money. In a recently published UK national audit the mortality of the disease, although falling slowly remains remarkably high with 8.9% of patients dying during admission and 26.7%, dying within 1 year of discharge. Additionally, the disease has a high morbidity with patients often being admitted multiple times within their remaining lifetimes. This results in a huge cost for disease treatment, treatment of complications (e.g. renal failure, falls caused by postural hypotension, asthmatic exacerbation caused by beta blockers, and depression) and treatment of co-morbidity that may be worsened by treatment or ignored if heart failure takes priority. Yet to our shame we understand little of what drives these poor outcomes, especially how we might improve the quality of life for these individuals and prevent second and subsequent admissions to hospital. Most of the research in heart failure has been driven by drug and device companies funding research into their products. This has produced startling results and the mortality for heart failure patients has improved over time. Many would argue that the era of rapid advancement of heart failure treatment is coming to an end, and we now need to concentrate on other factors, such as co-morbidity, to move treatment further forwards. The life of heart failure patients is blighted by admission to hospital, often when the disease is first diagnosed and then subsequently by a series of readmissions. Patients may not regain their full functional status after each admission and become progressively more disabled as a result. We therefore need to invest heavily in studies that aim to understand the reasons and risk factors behind readmission. Hitherto, we have had limited tools to understand multiple admissions, reflected in the poorly refined statistical techniques for analysing multiple events. For example, the Cox proportional hazards model calculates the risk of an event (such as admission or death) but ignores subsequent events. This is fine for terminal events such as death but is less useful when there are multiple events, often in series. In this issue of the journal, Braga et al. report on a study using a new method (at least to heart failure studies) to statistically analyse readmissions and assess the causes of them. In order to investigate the risk factors for multiple admissions, the authors used the Prentice–Williams–Peterson Model to stratify patients based on the number of recurrent events in the study. In this model, individuals are not considered at risk for the next event until the previous event has occurred and ended. This allowed the authors to analyse many more events than would be possible with the Cox proportional hazards method. Thus, within this study population of 8948 patients there would only have been 7562 events in a time to first event analysis. This would have ignored 75.6% (23 441) of the total of 31 003 admissions. The study population was drawn from the EFFECT study a randomized controlled investigation of the efficacy of scorecards produced from publicly available administrative data to improve the quality of care of patients with acute coronary syndromes and heart failure. Unfortunately, the underlying cardiac dysfunction was not well characterized in this patient population—in just 55% of the patients was there a measurement of LV dysfunction. The data for the EFFECT trial was abstracted by an experienced cardiac research nurse from the hospital notes. We are assured that the patients fulfilled the Framingham criteria for the diagnosis of heart failure. Such deficiencies in a study are to be expected when administrative data are used to define study cohorts, but this fact underlines the need for prospective studies to be performed in this area. A clear majority of hospital readmissions did not have a heart failure cause. Just 26.6% of the admissions were caused by heart failure exacerbations with a further 16.6% of admissions caused by other cardiac diseases. It is not clear from the paper whether some of the readmissions classified as non-cardiac were complications of treatment for heart failure (such as renal failure or hypotension). Age, diabetes, and COPD consistently increased the risk of the first and subsequent admissions. Cirrhotic liver disease and renal failure requiring dialysis increased the risk of admission by 30% while COPD and diabetes increased the rate by 20%. A final, but important observation was that the time between admissions fell sequentially: from 765 days between the 1st and 2nd admission to 226 days between the 4th and 5th admission. Thus, as time goes on patients are more

Infective endocarditis (IE) is associated with high mortality and morbidity. The aim of this study was to investigate the impact of timing of echocardiography on IE complications. We studied 151 consecutive patients with definite IE. Valve destruction was defined as ≥1 of severe regurgitation, cardiac abscess, or fistula. A definitive echocardiogram was the first echocardiogram (transthoracic (TTE) or Transesophageal (TEE)) which identified pathology consistent with IE and further echocardiography was not required for the diagnosis. TTE and TEE were performed within 4 days of admission in 62% and 15% patients respectively. Definitive echocardiography was achieved with TTE in 60% patients and required additional TEE in 40% patients. Significantly more in-patient embolic events occurred when definitive echocardiography was performed late (≥4 days) compared with early (<4 days) (40% vs 14%, p = 0.043). A significantly greater proportion of patients who underwent late definitive echocardiography (≥4 days) required valve surgery (73% vs 56%, p = 0.04). Time to definitive echocardiography (odds ratio [OR] 1.015, p = 0.011), male gender (OR 1.254, p = 0.005) and age (OR 0.992, p = 0.002) were predictors of severe valve destruction. Late definitive echocardiography (OR 1.166, p=0.035) was a predictor of in-patient embolism. In conclusion, time to definitive echocardiography is an important predictor of valve destruction, embolic events, and subsequent valve surgery. Pathways to reduce delays to echocardiography are required in patients with suspected IE.

Introduction Diagnosing infective endocarditis (IE) is challenging. The modified Duke’s criteria have shortcomings. European Society of Cardiology guidance (2015) suggests a potential role of18F-Fluorodeoxyglucose positron emission tomography (PET), based on class C evidence. There is a lack of data for native valve IE (NVE). Methods Dual centre retrospective study of all patients with suspected IE, from 01/2010. Patients were classified as confirmed/probable/rejected IE pre- and post-PET, with incremental benefit assessed versus actual diagnosis. This was defined by surgical specimen or Endocarditis Team (MDT) consensus at least three months following index admission. Results PET was undertaken in 71 patients from 2010 to date; 59 since the inception of the MDT in October 2015 (male=50; mean age 60.6 y (range 19–89)). At discharge, 27/39 (69%) had confirmed NVE and 21/32 (66%) confirmed prosthetic IE (PVE). 30/71 (42%) patients required surgical intervention with concomitant device extraction in 7. Whilst Staphylococcus was isolated in 30/71 (42%) patients, 22/71 (31%) were peripheral blood culture-negative. PET sensitivity, specificity, positive and negative predictive values were 72%, 100%, 67% and 100% respectively in NVE, and 84%, 54%, 70% and 73% in PVE. PET highlighted 12/71 (16.9%) patients as having an alternative non-cardiac source of infection. Receiver Operating Characteristic (ROC) curves showed incremental benefit of PET over Duke’s criteria alone (AUC 0.875 vs 0.750, p=0.003) in NVE, though no difference in PVE (AUC 0.682 vs 0.613, p=0.649) compared to discharge diagnosis. Conclusion PET has incremental value above modified Duke’s criteria in diagnosing IE, especially in NVE. PET has reduced specificity in PVE, likely related to post-surgical uptake.