Explore the vast range of titles available.

Objectives Assess the impact of end-stage renal disease (chronic kidney disease stage 5 (CKD5)) on cardiovascular outcomes in patients with Fabry disease on enzyme replacement therapy. Background Fabry disease, an X-linked lysosomal storage disease, causes hypertrophic cardiomyopathy and cardiovascular dysfunction. Methods Cardiac and renal function of 25 male patients with Fabry disease were analysed at 0, 1, 2, 5, 7 and 10 years after initiation of treatment. Patients were grouped at baseline into those with CKD5 (n=10) and those without (n=15). ECG and echocardiography were performed 6 and 12 monthly, respectively, while renal function was measured yearly. Results After 10 years of treatment, cardiac and renal function in non-CKD5 patients remained unchanged. In contrast, CKD5 was associated with worse baseline cardiac parameters and progressive LV hypertrophy. LV mass index grew by 35.4±31.8 g/m2.7 in CKD5 versus 5.7±7.9 g/m2.7, p=0.044 in non-CKD5, predominantly due to increased interventricular septal wall thickness (7.7±5.5 mm vs 1.3±1.7 mm, p=0.003). Cardiovascular events, including sudden death, arrhythmia and pacing device insertion, occurred in 100% patients with CKD5 (21 events) and 26% non-CKD5 patients (7 events), p<0.0001. Additionally, estimated LV filling pressure (E/Ea) was significantly higher in patients having cardiovascular events (21.1±7.7 vs 12.5±4.5, p=0.008) irrespective of renal function. Conclusions End-stage renal disease was the strongest indicator of cardiovascular disease progression in Fabry disease. Enzyme replacement initiated prior to CKD5 was associated with stability in cardiac and renal disease while patients with CKD5 showed ongoing deterioration. Additionally, E/Ea ≥15 may predict risk of cardiac events.

Background Fabry disease (FD) is a treatable X-linked condition leading to progressive cardiac disease, arrhythmia and premature death. We aimed to increase awareness of the arrhythmogenicity of Fabry cardiomyopathy, by comparing device usage in patients with Fabry cardiomyopathy and sarcomeric HCM. All Fabry patients with an implantable cardioverter defibrillator (ICD) implanted in the UK over a 17 year period were included. A comparator group of HCM patients, with primary prevention ICD implantation, were captured from a regional registry database. Results Indications for ICD in FD varied with 72% implanted for primary prevention based on multiple potential risk factors. In FD and HCM primary prevention devices, arrhythmia occurred more frequently in FD over shorter follow-up (HR 4.2, p  < 0.001). VT requiring therapy was more common in FD (HR 4.5, p  = 0.002). Immediate shock therapy for sustained VT was also more common (HR 2.5, p  < 0.001). There was a greater burden of AF needing anticoagulation and NSVT in FD (AF: HR 6.2, p  = 0.004, NSVT: HR 3.1, p  < 0.001). Conclusion This study demonstrates arrhythmia burden and ICD usage in FD is high, suggesting that Fabry cardiomyopathy may be more ‘arrhythmogenic’ than previously thought. Existing risk models cannot be mutually applicable and further research is needed to provide clarity in managing Fabry patients with cardiac involvement.

Aims The clinical reliability of echocardiographic surrogate markers of left ventricular filling pressures (LVFPs) across different cardiovascular pathologies remains unanswered. The main objective was to evaluate the evidence of how effectively different echocardiographic indices estimate true LVFP. Methods and results Design: this is a systematic review and meta‐analysis. Data source: Scopus, PubMed and Embase. Eligibility criteria for selecting studies were those that used echocardiography to predict or estimate pulmonary capillary wedge pressure or left ventricular end‐diastolic pressures. Twenty‐seven studies met criteria. Only eight studies (30%) reported both correlation coefficient and bias between non‐invasive and invasively measured LVFPs. The majority of studies (74%) recorded invasive pulmonary capillary wedge pressure as a surrogate for left ventricular end‐diastolic pressures. The pooled correlation coefficient overall was r = 0.69 [95% confidence interval (CI) 0.63–0.75, P < 0.01]. Evaluation by cohort demonstrated varying association: heart failure with preserved ejection fraction (11 studies, n = 575, r = 0.59, 95% CI 0.53–0.64) and heart failure with reduced ejection fraction (8 studies, n = 381, r = 0.67, 95% CI 0.61–0.72). Conclusions Echocardiographic indices show moderate pooled association to invasively measured LVFP; however, this varies widely with disease state. In heart failure with preserved ejection fraction, no single echocardiography‐based metric offers a reliable estimate. In heart failure with reduced ejection fraction, mitral inflow‐derived indices (E/e′, E/A, E/Vp, and EDcT) have reasonable clinical applicability. While an integrated approach of several echocardiographic metrics provides the most promise for estimating LVFP reliably, such strategies need further validation in larger, patient‐specific studies.

IntroductionHeart failure (HF) incidence is increasing in older adults with high hospitalisation and mortality rates. Treatment is complicated by side effects and comorbidities. We investigated the clinical characteristics of octogenarians presenting to the HF clinic.MethodsData were collected on octogenarians (80–89 years) referred to the HF clinic in two periods. The data included demographics, HF phenotype, comorbidities, symptoms and treatment. We investigate the temporal changes in clinical characteristics using χ2 test. We aimed to determine the clinical characteristics which were associated with optimisation of HF pharmacological intervention in the clinic, conducting multivariate regression analysis. Statistical significance is determined at p<0.05.ResultsData were collected in April 2012 to January 2014 and in June 2021 to December 2022. In this cross-sectional study of temporal data, 571 octogenarians were referred to the clinic in the latter period, in whom the prevalence of HF was 68.48% (391 patients). HF with preserved ejection fraction (HFpEF) was the most common phenotype and increased significantly compared with the first period (46.3% and 29.2%, p<0.001). Frailty, chronic kidney disease and ischaemic heart disease increased significantly versus the first period (p<0.001). During the second period, and following the consultation, of the patients with HF with reduced ejection fraction (HFrEF), 86.4% and 82.7% were on a beta blocker and on an ACE inhibitor/angiotensin receptor blocker/angiotensin receptor-neprilysin inhibitor, respectively. Clinical characteristics associated with further optimisations of HF pharmacological therapy in the HF clinic were: New York Heart Association (NYHA) functional class III and the presence of HFrEF phenotypeConclusionsWith a prevalence of HF at 68% among the octogenarians referred to the HF clinic, HFpEF incidence is rising. The decision to optimise HF pharmacological treatment in octogenarians is driven by NYHA functional class III and the presence of HFrEF phenotype.

ObjectivesWe aim to assess the association of cardiovascular medications with outcomes of patients referred to the diagnostic heart failure (HF) clinic with symptoms or signs of possible HF, raised N-terminal pro-brain-type natriuretic peptide (NT-proBNP) but no evidence of HF on transthoracic echocardiography (TTE).MethodsData were collected prospectively into the Sheffield HEArt Failure (SHEAF) registry between April 2012 and January 2020. The inclusion criteria were symptoms or signs suggestive of HF, NT-proBNP >400 pg/mL, but no evidence of HF on TTE. Cox proportional-hazards regression model was used to investigate the association between the survival time of patients and different cardiovascular medications. The outcome was defined as all-cause mortality.ResultsFrom the SHEAF registry, we identified 1766 patients with raised NT-proBNP with no evidence of HF on TTE. Survival was higher among the younger patients, and among those with hypertension or atrial fibrillation (AF). Mortality was increased with male gender, valvular heart disease and chronic kidney disease. Using univariate Cox proportional-hazards regression, the only cardiac therapeutic agent independently associated with all-cause mortality was beta-blocker (HR 0.86; 95% CI: 0.77 to 0.97; p=0.02). The use of beta-blockers was significantly higher in patients with AF (63% vs 39%, p<0.01) and hypertension (51% vs 42%, p<0.01). However, using multivariate Cox proportional-hazards regression to adjust for all variables associated with mortality, the influence of beta-blockers became non-significant (HR 0.96; 95% CI: 0.85 to 1.1, p=0.49).ConclusionWhen all variables associated with mortality are considered, none of the cardiovascular agents are associated with the improved survival of patients with suspected HF, raised NT-proBNP but no HF on echocardiography.

ObjectivesTo characterise and risk-stratify patients presenting to a heart failure (HF) clinic according to the National Institute for health and Care Excellence (NICE) algorithm.MethodsThis is an observational study of prospectively collected data in the Sheffield HEArt Failure registry of consecutive patients with suspected HF between April 2012 and January 2020. Outcome was defined as all-cause mortality.Results6144 patients were enrolled: 71% had HF and 29% had no HF. Patients with N-terminal pro-brain-type natriuretic peptide (NT-proBNP) >2000 pg/mL were more likely to have HF than those with NT-proBNP of 400–2000 pg/mL (92% vs 64%, respectively). Frequency of HF phenotypes include: HF with preserved ejection fraction (HFpEF) (33%), HF with reduced ejection fraction (HFrEF) (29%), HF due to valvular heart disease (4%), HF due to pulmonary hypertension (5%) and HF due to right ventricular systolic dysfunction (1%). There were 1485 (24%) deaths over a maximum follow-up of 6 years. The death rate was higher in HF versus no HF (11.49 vs 7.29 per 100 patient-years follow-up, p<0.0001). Patients with HF and an NT-proBNP >2000 pg/mL had lower survival than those with NT-proBNP 400–2000 pg/mL (3.8 years vs 5 years, p<0.0001). Propensity matched survival curves were comparable between HFpEF and HFrEF (p=0.88).ConclusionOur findings support the use by NICE’s HF diagnostic algorithm of tiered triage of patients with suspected HF based on their NT-proBNP levels. The two pathways yielded distinctive groups of patients with varied diagnoses and prognosis. HFpEF is the most frequent diagnosis, with its challenges of poor prognosis and paucity of therapeutic options.

IntroductionThe Charlson comorbidity index (CCI) is a validated 10-year mortality risk score. It has been validated in patients with cardiovascular disease showing a high comorbidity score correlates with increased mortality.1 2 We applied and validated this risk score retrospectively to our implantable cardiac defibrillator (ICD) therapy cohort to determine its utility in aiding decision making for ICD therapy in comorbid patients.MethodsAll consecutive ICD implants (April 2018- March 2019) at our tertiary centre were reviewed retrospectively and CCI calculated using device implantation documentation, GP records and blood results at time of implant. Patients were followed up until November 2022 and all cause mortality data recorded during this period (median follow up 1428 days +/- 331 days). Comparison was made for calculated CCIs between surviving and deceased patients with sub group analysis of primary or secondary prevention indication, arrhythmic presentation and underlying pathological aetiology. Data was analysed using Microsoft Excel3 and Chi squared and Log rank analysis was performed on the data using an online Kaplan-Meier survival analysis tool.4 Results118 ICDs were implanted between April 2018-March 2019, 24 patients (20.3%) died in the follow up period. Median age at implant was 63.4 years +/- 12.8 years with predominant Male sex (80.5%). The majority had ischaemic aetiology (55.9%) with equal distribution between primary and secondary prevention indications (48.3% & 50.8%). Deceased patients had a higher median CCI compared to surviving patients 5.9 (+/- 1.9) vs 4 (+/- 2.2). A CCI >5 was associated with increased mortality (38.4%) compared to a CCI ≤5 (13.1%) (p<0.001). Similar findings were seen across the sub group analysis. A total of 66.6% of deceased patients received no ICD therapies prior to death, with 29.1% receiving multiple appropriate therapies.ConclusionIn our cohort, a CCI >5 was associated with significantly increased all cause mortality, independent of aetiology, arrhythmic presentation and device indication.ReferencesCharlson ME, Pompei P, Ales KL, MacKenzie CR. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. J Chronic Dis. 1987;40(5):373–83. doi: 10.1016/0021–9681(87)90171–8. PMID: 3558716.Radovanovic D, Seifert B, Urban P, Eberli FR, Rickli H, Bertel O, Puhan MA, Erne P; AMIS Plus Investigators. Validity of Charlson Comorbidity Index in patients hospitalised with acute coronary syndrome. Insights from the nationwide AMIS Plus registry 2002–2012. Heart 2014 Feb;100(4):288–94. doi: 10.1136/heartjnl-2013–304588. Epub 2013 Nov 1. PMID: 24186563.Radovanovic D, Seifert B, Urban P, Eberli FR, Rickli H, Bertel O, Puhan MA, Erne P; AMIS Plus Investigators. Validity of Charlson Comorbidity Index in patients hospitalised with acute coronary syndrome. Insights from the nationwide AMIS Plus registry 2002–2012. Heart 2014 Feb;100(4):288–94. doi: 10.1136/heartjnl-2013–304588. Epub 2013 Nov 1. PMID: 24186563.Microsoft Excel, Microsoft Inc, Redmond, WA, USAKaplan Meier Survival Analysis (internet); Statistics Kingdom 2017 (cited November 2023). Available from https://www.statskingdom.com/kaplan-meier.htmlConflict of InterestNilAbstract 116 Figure 1

Requiring no statistical or mathematical background, this work shows how the rules of risk can work to protect and enhance investor value. It explains why \"unreason\" is the more evil twin brother of greed, describes what leads people to make disastrous investment decisions, and illustrates how high intelligence can trick you into catastrophic losses. With exercises and references at the end of each chapter, the book also presents notable lessons learned to keep your investments safe.

Aims Clinical outcomes for patients suspected of having heart failure (HF) who do not meet the diagnostic criteria of any type of HF by echocardiography remain unknown. The aim of this study was to investigate the clinical predictors of all‐cause mortality in patients with suspected HF, a raised N‐terminal pro‐b‐type natriuretic peptide (NTproBNP) and who do not meet the diagnostic criteria of any type of HF by echocardiography. Methods and results Relevant data were taken from the Sheffield HEArt Failure (SHEAF) registry (222349P4). The inclusion criteria were presence of symptoms raising suspicion of HF, NTproBNP > 400 pg/mL, and preserved left ventricular function. Exclusion criteria were any type of HF by echocardiography. The outcome was defined as all‐cause mortality. Cox proportional‐hazards regression model was used to investigate the association between the survival time of patients and clinical variables; 1031 patients were identified with NTproBNP > 400 pg/mL but who did not have echocardiographic evidence of HF. All‐cause mortality was 21.5% (222 deaths) over the mean follow‐up (FU) period of 6 ± 2 years. NTproBNP was similar in patients who were alive or dead (P = 0.96). However, age (HR 1, P < 0.01), chronic kidney disease (CKD, HR 1.2, P < 0.01), chronic pulmonary obstructive disease (COPD, HR 1.6, P < 0.01), dementia (HR 5.9, P < 0.01), male gender (HR 1.4, P < 0.01), first‐degree atrioventricular block (HR 2.1, P < 0.01), left axis deviation (HR 1.6, P = 0.04), and diabetes (HR 1.4, P = 0.03) were associated with all‐cause mortality. In multivariate regression, age, gender, CKD stage, COPD, and dementia were independently associated with mortality. In patients with NTproBNP > 627 pg/mL, NYHA class predicted death (II, 19.6%; III, 27.4%; IV, 66.7%; P < 0.01). Conclusions Patients with no HF on echocardiography but raised NTproBNP suffer excess mortality particularly in the presence of certain clinical variables. Age, male gender, worsening CKD stage, presence of COPD, and dementia are independently associated with all‐cause mortality in these patients. An NTproBNP > 627 pg/mL coupled with NYHA class could identify patients at greatest risk of death.

Background: State Health Departments (SHDs) have systematically studied the validity of healthcare-associated infection (HAI) surveillance data submitted by healthcare facilities in their jurisdictions to the Centers for Disease Control and Prevention’s (CDC’s) National Healthcare Safety Network (NHSN) for central-line–associated bloodstream infections (CLABSIs), catheter-associated urinary tract infections (CAUTIs), surgical site infections following colon and abdominal hysterectomy procedures (SSI COLO and HYST), methicillin-resistant Staphylococcus aureus and Clostridioides difficile laboratory identified (MRSA and CDI LabID respectively) events. These studies are a key source of information about data quality and completeness serving as an impetus and a guide for improving the caliber of NHSN’s HAI data. Methods: We contacted SHD HAI coordinators in all states for an inventory of HAI validation studies. We used data from these studies to calculate pooled mean sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for HAI case determinations. HAI case reporting “error rates” were computed as the proportion of mismatches (underreport and overreport) among the medical records reviewed by SHDs and reasons for misclassification were categorized. Results: SHD validation studies varied by HAI type (range, 4 studies for MRSA LabID and 23 for CLABSI). Pooled mean sensitivity of HAI reporting ranged from 73.1% (COLO SSI) to 92.7% (CDI LabID). Pooled mean specificity and PPV exceeded 90% for all HAIs. LabID event validations demonstrated the lowest NPV (58.8% for MRSA and 55.1% for CDI). Error rates of HAI reporting to NHSN ranged from 2.5% (HYST SSI) to 13.6% (MRSA LabID). Common errors identified during CLABSI and CAUTI validations were incorrect application of general NHSN and CLABSI- and CAUTI-specific definitions. Incorrect secondary BSI attribution was the most frequently identified reason by CLABSI SHD validations (64.7%). Of all operative procedure-associated misclassifications, inconsistent surveillance practices (66.6%), incorrect NHSN operative procedure category assignment (55.5%), and misapplication of general organ-space and/or site-specific infection criteria (44.4%) were identified as the most common shortcomings. Among MRSA and CDI LabID validations, missed case finding due to failure to review candidate events and gaps in understanding the 14-day reporting rule of LabID protocol were identified as predominant reasons for inaccurate reporting. Conclusions: SHD HAI data validations identified specific targets for additional surveillance training, especially CLABSI determinations and application of the protocol rules for MDRO/CDI LabID case determinations. Further work is also needed to assure that data sources in addition to wound cultures are used for SSI determinations and that postdischarge SSI surveillance is more vigorous and comprehensive. Funding: None Disclosures: None