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Aims Implantable device‐based sensor measurements including heart sounds, markers of ventilation, and thoracic impedance have been shown to predict heart failure (HF) hospitalizations. We sought to assess how these parameters changed prior to COVID‐19 (Cov‐19) and how these compared with those presenting with decompensated HF or pneumonia. Methods and results This retrospective analysis explores patterns of changes in daily measurements by implantable sensors in 10 patients with Cov‐19 and compares these findings with those observed prior to HF (n = 88) and pneumonia (n = 12) hospitalizations from the MultiSENSE, PREEMPT‐HF, and MANAGE‐HF trials. The earliest sensor changes prior to Cov‐19 were observed in respiratory rate (6 days) and temperature (5 days). There was a three‐fold to four‐fold greater increase in respiratory rate, rapid shallow breathing index, and night heart rate compared with those presenting with HF or pneumonia. Furthermore, activity levels fell more in those presenting with Cov‐19, a change that was often sustained for some time. In contrast, there were no significant changes in 1st or 3rd heart sound (S1 and S3) amplitude in those presenting with Cov‐19 or pneumonia compared with the known changes that occur in HF decompensation. Conclusions Multi‐sensor device diagnostics may provide early detection of Cov‐19, distinguishable from worsening HF by an extreme and fast rise in respiratory rate along with no changes in S3.

Aims The SMART (Strategic MAnagement to optimize response to cardiac Resynchronization Therapy) Registry was designed to assess real‐world outcomes for patients receiving a cardiac resynchronization therapy defibrillator (CRT‐D) and to better understand which programming and optimization techniques are used and how effective they are. Methods and results The SMART Registry is a global, multicentre, prospective, observational, post‐market CRT‐D registry with a planned enrolment of 2000 subjects from a maximum of 200 sites in Europe, North America, and Asia‐Pacific region. Each subject will be followed up for a minimum of 12 months. The primary endpoint of CRT response rate at 12 months is defined by a clinical composite score of all‐cause mortality, heart failure events, New York Heart Association Class, and quality of life as assessed by a patient global assessment instrument. A subgroup composed of the first 103 consecutive European subjects implanted with an NG4 device will have left ventricular multisite pacing feature enabled at any time during the initial 12 months of follow‐up. The primary endpoint for this sub‐analysis will be the NG4 PG‐related complication‐free rate at 36 months. Conclusions The SMART Registry achieved its recruitment target in August 2019, with 2014 patients enrolled. The baseline demographics demonstrated that patients were generally older, with greater co‐morbidity, and on more contemporary medical therapy than in the key CRT trials. The results of the SMART Registry will determine which programming and optimization techniques are effective in this real‐world population.

Aims This study aims to characterize the range of implantable device‐based sensor values including heart sounds, markers of ventilation, thoracic impedance, activity, and heart rate for patients with heart failure (HF) when patients were deemed to be in clinically stable periods against the time course of acute decompensation and recovery from HF events. Methods and results The MultiSENSE trial followed 900 patients implanted with a COGNIS CRT‐D for up to 1 year. Chronic, ambulatory diagnostic sensor data were collected and evaluated during clinically stable periods (CSP: unchanged NYHA classification, no adverse events, and weight change ≤2.27 kg), and in the timeframe leading up to and following HF events (HF admissions or unscheduled visits with intravenous HF treatment). Physiologic sensor data from 1667 CSPs occurring in 676 patients were compared with those data leading up to and following 192 HF events in 106 patients. Overall, the mean age was 66.6 years, and the population were predominantly male (73%). Patients were primarily in NYHA II (67%), with a mean LVEF of 29.6% and median NT‐proBNP of 754.5 pg/mL. Sensor values during CSP were poorer in patients who had HF events during the study period than those without HF events, including first heart sound (S1: 2.18 ± 0.84 mG vs. 2.62 ± 0.95 mG, P = 0.002), third heart sound (S3: 1.13 ± 0.36 mG vs. 0.91 ± 0.30 mG, P

This chapter discusses the ‘classical causes’ of heart failure. Heart failure is the common endpoint of a diverse range of cardiovascular and non-cardiovascular conditions. The list of potential causes of this syndrome continues to expand as the knowledge of the pathophysiology of heart failure increases. In western societies, coronary heart disease and hypertension are the commonest causes of heart failure. However, valvular heart disease, arrhythmias, and alcohol are also frequently implicated. The prevalence of heart failure secondary to coronary heart disease has increased in recent years, due in part to improved survival following acute myocardial infarction. The chapter then highlights the importance of establishing an aetiology of heart failure. Establishing the aetiology of heart failure is important, but it is often challenging for the clinician. Several causes of heart failure frequently coexist and determining the primary aetiology can be difficult: one cause may obviously dominate, but frequently patients may have multiple contributing aetiologies.

Aims None of the existing studies on adherence have directly measured levels of all medications (or their metabolites) in patients with heart failure (HF). Methods and results We used liquid chromatography–tandem mass spectrometry to measure the presence of prescribed drugs (diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, and mineralocorticoid receptor antagonists) in the urine of patients reviewed 4–6 weeks after hospitalization with HF. Patients were unaware that adherence was being assessed. Of the 341 patients studied, 281 (82.4%) were adherent, i.e. had all prescribed drugs of interest detectable in their urine. Conversely, 60 patients (17.6%) were partially or completely non-adherent. Notably, 24 of the 60 were non-adherent to only diuretic therapy and only seven out of all 341 patients studied (2.1%) were completely non-adherent to all prescribed HF drugs. There were no major differences in baseline characteristics between adherent and non-adherent patients. Conclusion Non-adherence, assessed using a single spot urine measurement of drug levels, was confirmed in one of five patients evaluated 4–6 weeks after hospitalization with HF.

Objectives To compare the relationship between the third heart sound (S3) measured by implantable cardiac devices (devS3) and auscultation (ausS3) and evaluate their prognostic power for predicting heart failure events (HFEs). Methods In the MultiSENSE study, devS3 was measured daily with continuous values while ausS3 was assessed at study visits with discrete grades. They were compared between patients with and without HFEs at baseline and against each other directly. Cox proportional hazard models were developed between follow-up visits (FUs) and over the whole study. Simulations were performed on devS3 to match limitations of auscultation. Results Nine hundred patients were studied, of whom 106 patients experienced 192 HFEs. Two S3 sensing modalities correlated with each other but at baseline only devS3 differentiated patients with or without HFEs (p Conclusions S3 measured from implantable cardiac devices has stronger prognostic power to predict episodes of future HF events than that of auscultation.

These are the clinical practice guidelines from the European Society of Cardiology for the diagnosis and treatment of acute and chronic heart failure, from 2021.

ObjectiveHeart failure is a prothrombotic state, and it has been hypothesised that thrombosis and embolism cause non-fatal and fatal events in heart failure and reduced ejection fraction (HFrEF). We sought to determine the effect of anticoagulant therapy on clinical outcomes in patients with HFrEF who are in sinus rhythm.MethodsWe conducted an updated systematic review and meta-analysis to examine the effect of anticoagulation therapy in patients with HFrEF in sinus rhythm. Our analysis compared patients randomised to anticoagulant therapy with those randomised to antiplatelet therapy, placebo or control, and examined the endpoints of all-cause mortality, (re)hospitalisation for worsening heart failure, non-fatal myocardial infarction, non-fatal stroke of any aetiology and major haemorrhage.ResultsFive trials were identified that met the prespecified search criteria. Compared with control therapy, anticoagulant treatment did not reduce all-cause mortality (risk ratio [RR] 0.99, 95% CI 0.90 to 1.08), (re)hospitalisation for heart failure (RR 0.97, 95% CI 0.82 to 1.13) or non-fatal myocardial infarction (RR 0.92, 95% CI 0.75 to 1.13). Anticoagulation did reduce the rate of non-fatal stroke (RR 0.63, 95% CI 0.49 to 0.81, p=0.001), but this was offset by an increase in the incidence of major haemorrhage (RR 1.88, 95% CI 1.49 to 2.38, p=0.001).ConclusionsOur meta-analysis provides evidence to oppose the hypothesis that thrombosis or embolism plays an important role in the morbidity and mortality associated with HFrEF, with the exception of stroke-related morbidity.

Funding Acknowledgements Type of funding sources: None. Background The insertable cardiac monitor (ICM) is an essential tool for the ambulatory diagnosis of arrhythmias. However, definitive diagnoses still rely on time-consuming, manual adjudication of electrograms (EGMs) transmitted to the patient care network. This EGM review burden may be minimized by automatically selecting a subset of EGMs for fast review without delaying the diagnosis. Purpose Develop EGM selection strategies to reduce the EGM review burden without delaying diagnoses. Methods A retrospective analysis of 1,000 randomly selected Abbott Confirm Rx devices with 90+ days of remote transmission history was performed, regardless of transmission frequency, and all EGMs were adjudicated as either true or false positive (TP, FP). Up to 3 EGMs per day per arrhythmia type were prioritized for review based on ventricular rate and episode duration, with rules specific to each arrhythmia type: atrial fibrillation (AF), tachycardia, bradycardia, and pause. The resulting reduction in EGM review burden and TP days (patient-days with at least 1 TP EGM), as well as any diagnostic delay from the first transmitted TP, were calculated relative to reviewing all transmitted EGMs. Results In this population and transmission period, at least one AF, tachycardia, bradycardia, and pause EGM was transmitted by 424, 343, 190, and 325 unique devices, respectively, with a total of 35,723, 12,239, 19,752, and 28,002 EGMs, and a total of 6,163, 1,572, 1,438, and 646 TP days. For these patients with ≥1 EGM, the median [IQR] EGM transmission rate was 2.6 [0.7, 11.6], 1.1 [0.4, 4.7], 2.1 [0.6, 10.7], and 3.4 [0.6, 29.9] EGMs/patient/month, respectively. The optimal EGM selection strategy reduced this EGM review burden by 43%, 67%, 76%, and 50%, while only missing 3.4%, 2.2%, 0.3%, and 0.2% of TP days, respectively. Ultimately, 97%, 99%, 99%, and 99% of devices with a TP AF, tachycardia, bradycardia, or pause EGM exhibited no diagnostic delay vs. reviewing all transmitted EGMs. Conclusion EGM prioritization rules for selecting up to 3 episodes/day significantly reduced EGM burden across all patients, not just "frequent fliers," with no delay-to-diagnosis in >97% of patients who exhibited a true arrhythmia. Implementing these rules on the patient care network may improve clinical workflow and ICM patient management. Abstract Figure.

Aims: We investigated which patients with heart failure (HF) should receive specialist palliative care (SPC) by first creating a definition of need for SPC in patients hospitalised with HF using patient‐reported outcome measures (PROMs) and then testing this definition using the outcome of days alive and out of hospital (DAOH). We also evaluated which baseline variables predicted need for SPC and whether those with this need received SPC. Methods and results: PROMs assessing quality of life (QoL), symptoms, and mood were administered at baseline and every 4 months. SPC need was defined as persistently severe impairment of any PROM without improvement (or severe impairment immediately preceding death). We then tested whether need for SPC, so defined, was reflected in DAOH, a measure which combines length of stay, days of hospital re‐admission, and days lost due to death. Of 272 patients recruited, 74 (27%) met the definition of SPC needs. These patients lived one third fewer DAOH than those without SPC need (and less than a quarter of QoL‐adjusted DAOH). A Kansas City Cardiomyopathy Questionnaire (KCCQ) summary score of

Aim The aim of this study was to evaluate the haemodynamic correlates of heart sound (HS) parameters such as third HS (S3), first HS (S1), and HS-based systolic time intervals (HSTIs) from an implantable cardiac device. Methods and results Two unique animal models (10 swine with myocardial ischaemia and 11 canines with pulmonary oedema) were used to evaluate haemodynamic correlates of S1, S3, and HSTIs, namely, HS-based pre-ejection period (HSPEP), HS-based ejection time (HSET), and the ratio HSPEP/HSET during acute haemodynamic perturbations. The HS was measured using implanted cardiac resynchronization therapy defibrillator devices simultaneously with haemodynamic references such as left atrial (LA) pressure and left ventricular (LV) pressure. In the ischaemia model, S1 amplitude (r = 0.76 ± 0.038; P = 0.002), HSPEP (r = −0.56 ± 0.07; P = 0.002), and HSPEP/HSET (r = −0.42 ± 0.1; P = 0.002) were significantly correlated with LV dP/dtmax. In contrast, HSET was poorly correlated with LV dP/dtmax (r = 0.14 ± 0.14; P = 0.23). In the oedema model, a physiological delayed response was observed in S3 amplitude after acute haemodynamic perturbations. After adjusting for the delay, S3 amplitude significantly correlated with LA pressure in individual animals (r = 0.71 ± 0.07; max: 0.92; min: 0.17) as well as in aggregate (r = 0.62; P 25 mmHg, with a sensitivity = 58% and specificity = 90%. Conclusions The HS parameters such as S1, S3, and HSTIs measured using implantable devices significantly correlated with haemodynamic changes in acute animal models, suggesting potential utility for remote heart failure patient monitoring.

Background Estimated plasma volume (ePV) can be calculated from haematocrit and body weight, and has been shown to correlate with PV measured using 125Iodine labelled human serum albumin. Comparing a patient's ePV to ideal PV (iPV), an estimate of a patient's relative congestion, called PV status (PVS), is possible. Higher PVS is associated with increased mortality in patients with heart failure (HF), and has been proposed as a simple, cheap, and non-invasive way of assessing congestion. Purpose Whether PVS is associated with invasively measured markers of congestion is unknown. We calculated PVS in patients with HF who had right heart catheterisation (RHC), and assessed any correlation between PVS and invasive measures of congestion. Methods We calculated PVS in consecutive patients who had RHC performed as part of transplant assessment. iPV was calculated as: iPV = c × weight (kg) where c=39 in males and c=40 in females. ePV was calculated using subjects' haematocrit and weight as follows: ePV = (1 − haematocrit) × [a + (b × weight in kg)], where haematocrit is a fraction, a=1530 in males and a=864 in females, and b=41 in males and b=47.9 in females. PVS was calculated as: PVS = PVS = (ePV − iPV) /iPV × 100%. Correlation between PVS and invasive wedge pressure, mean right atrial (RA) pressure, and NTproBNP were made using Pearson correlation. Results PV indices and RHC data were available for 61 patients, 43 (71%) were male. Median age was 55 [IQR 48, 58] years. 20 (33%), 24 (39%), and 15 (25%) were NYHA association class II, III, and IV respectively. The median NTproBNP was 1390 [IQR 512, 3612] pg/ml and median ejection fraction was 29 [IQR 20, 35] %. The median PVS was −5.9% (IQR −12.5, −1.6]. Median wedge and mean-RA pressures were 14 [7, 21] and 4 [1, 8] mmHg, respectively. Correlation between mean RA pressure and PVS is shown in the figure. There was no correlation between PVS and mean RA pressure (r=0.12, p=0.34) or wedge pressure (r=0.01, p=0.92). There was a weak correlation between NTproBNP and PVS (r=0.31, p=0.01) Correlation mean RA pressure and PVS Conclusion PVS did not correlate with the invasive measures of congestion, mean RA and wedge pressure, but was weakly correlated with NTproBNP. Although there were limited number of patients in this study, we question the conclusion that PVS is a marker of congestion, and whether it can be used clinically for this purpose.

ObjectivesUltra-small superparamagnetic particles of iron oxide (USPIO)-enhanced MRI can detect cellular inflammation within tissues and may help non-invasively identify cardiac transplant rejection. Here, we aimed to determine the normal reference values for USPIO-enhanced MRI in patients with a prior cardiac transplant and examine whether USPIO-enhanced MRI could detect myocardial inflammation in patients with transplant rejection.MethodsTen volunteers and 11 patients with cardiac transplant underwent T2, T2* and late gadolinium enhancement 1.5T MRI, with further T2* imaging at 24 hours after USPIO (ferumoxytol, 4 mg/kg) infusion, at baseline and 3 months.ResultsTen patients with clinically stable cardiac transplantation were retained for analysis. Myocardial T2 values were higher in patients with cardiac transplant versus healthy volunteers (53.8±5.2 vs 48.6±1.9 ms, respectively; p=0.003). There were no differences in the magnitude of USPIO-induced change in R2* in patients with transplantation (change in R2*, 26.6±7.3 vs 22.0±10.4 s-1 in healthy volunteers; p=0.28). After 3 months, patients with transplantation (n=5) had unaltered T2 values (52.7±2.8 vs 52.12±3.4 ms; p=0.80) and changes in R2* following USPIO (29.42±8.14 vs 25.8±7.8 s-1; p=0.43).ConclusionStable patients with cardiac transplantation have increased myocardial T2 values, consistent with resting myocardial oedema or fibrosis. In contrast, USPIO-enhanced MRI is normal and stable over time suggesting the absence of chronic macrophage-driven cellular inflammation. It remains to be determined whether USPIO-enhanced MRI may be able to identify acute cardiac transplant rejection.Trial registration numberNCT02319278349 (https://clinicaltrials.gov/ct2/show/NCT02319278) Registered 03.12.2014 EUDraCT 2013-002336-24.

Aims: In recent years there has been an increase in the number of biomarkers in heart failure ( HF ). The clinical role for these novel biomarkers in combination is not clear. Methods and results: The following novel biomarkers were measured from 628 patients recently hospitalized with decompensated HF; mid-regional pro-adrenomedullin ( MR-proADM ), mid-regional pro-atrial natriuretic peptide ( MR-proANP ), copeptin, high-sensitivity cardiac troponin T ( hs-cTnT ), ST2, galectin-3, cystatin C, combined free light chains ( cFLC ) and high sensitivity C-reactive protein ( hsCRP ). The incremental prognostic value of these novel biomarkers was evaluated within an extensive model containing established predictors of mortality. During a mean ( SD ) follow-up of 3.2 ( 1.5 ) years, 290 ( 46% ) patients died. Elevated concentrations of all novel biomarkers were associated with an increased unadjusted risk of mortality but only two-thirds were independent predictors following multivariable analysis. Using dichotomized cut-points from receiver operating characteristic analysis, MR-proADM, hs-cTnT, cFLC, hsCRP, and ST2 remained independent predictors of mortality. Further dichotomization into low ( 0–2 elevated biomarkers ) or high ( at least three of the five biomarkers elevated ) risk groups provided greatest incremental prognostic value ( hazard ratio 2.20, 95% confidence interval 1.37–3.54; P = 0.001 ) and improved the performance of the model ( C-statistic 0.730 from 0.721, net reclassification index 32.5% ). Conclusion: The novel biomarkers included in this study added little, if any, incremental prognostic value on their own to a model containing established predictors of mortality. However, following dichotomization, five of the novel biomarkers provided incremental prognostic value. There was a clear gradient in the risk of death with increasing numbers of elevated novel biomarkers, with the presence of at least three identifying patients at greatest risk of mortality.

Background N-terminal pro-B-type natriuretic peptide (NT-proBNP), a non-active fragment of the prohormone proBNP, is produced by the heart and released in response to volume or pressure overload. NT-proBNP has proven to be a valuable biomarker in the diagnosis and prognosis of heart failure (HF), and NT-proBNP concentrations rise with worsening HF. HeartLogic, a multi-sensor composite index and alert algorithm, aggregates multiple physiologic trends associated with HF status, and proactively provides alerts for worsening HF with high sensitivity and low alert burden. Objective To compare NT-proBNP concentrations during periods IN or OUT of an active HeartLogic alert. Methods The MultiSENSE study enrolled 900 HF patients with an implanted COGNIS CRT-D, and followed them up to 1 year. Device software was modified to permit collection of chronic trends HeartLogic leveraged (heart sounds, heart rate, thoracic impedance, respiration and activity). Clinicians were blinded to individual sensors and results of HeartLogic during the study. Optional NT-proBNP tests were conducted when clinically needed (e.g., patients hospitalized with HF symptoms). HeartLogic index of the day before each of the NT-proBNP test dates was extracted. Based on HeartLogic alert state (i.e., IN alert vs OUT of alert), NT-proBNP concentrations were divided into two groups and compared using a one-way ANOVA. Results Of a total of 855 valid NT-proBNP tests in 741 patients with valid associated HeartLogic index, 180 NT-proBNP concentrations were measured in 150 patients while the HeartLogic alert state was IN alert, and 675 were measured in 616 patients while HeartLogic was OUT of alert. Figure 1 shows when HeartLogic was IN alert, the NT-proBNP concentrations (6957.9±10398.0 pg/ml) were significantly higher than those when HeartLogic was OUT of alert (1675.5±4403.1 pg/ml) (p Conclusion HF patients’ NT-proBNP concentrations were significantly elevated when HeartLogic was IN alert status, consistent with the HeartLogic algorithm capturing clinical worsening of HF status.

Heart failure (HF) is a clinical syndrome characterized by reduced exercise tolerance, dyspnoea and peripheral oedema, which is confirmed with imaging evidence of ventricular dysfunction and, if available, cardiac biomarkers. HF is one of the major cardiovascular causes of morbidity and mortality worldwide. It has a prevalence of 1–2%, rising with age to >10% in those over 70 years old. Pharmacological and device-based therapy for HF with reduced ejection fraction (HFrEF) has dramatically improved over the last 30 years, resulting in significantly better outcomes for patients, in terms of improvements in quality of life, and reduction in morbidity and mortality. However, some patients remain highly symptomatic despite these measures and for a select few, advanced therapies (e.g. mechanical circulatory support devices and cardiac transplantation) might be suitable. This article provides an overview of contemporary management of patients with HFrEF.

Purpose of Review:\ud Treatment with a defibrillator can reduce the risk of sudden death by terminating ventricular arrhythmias. The identification of patient groups in whom this function reduces overall mortality is challenging. In this review, we summarise the evidence for who benefits from a defibrillator.\ud \ud Recent Findings:\ud Recent evidence suggests that contemporary pharmacologic and non-defibrillator device therapies are altering the potential risks and benefits of a defibrillator.\ud \ud Summary:\ud Who benefits from a defibrillator is determined by both the risk of sudden death and the competing risk of other, non-sudden causes of death. The balance of these risks is changing, which calls into question whether historic evidence for the use of defibrillators remains robust in the modern era.

Acute heart failure syndromes consist of a spectrum of clinical presentations due to an impairment of some aspect of the cardiac function. They represent a final common pathway for a vast array of pathologies and may be either a de novo presentation or, more commonly, a decompensation of pre-existing chronic heart failure. Despite being one of the most common medical presentations, there are no definitively proven prognosis-modifying treatments. The mainstay of current therapy is oxygen and intravenous diuretics. However, within this spectrum of presentations, there is a crucial dichotomy which governs the ultimate treatment approach, i.e. the presence, or absence, of cardiogenic shock. Patients without cardiogenic shock may receive vasodilators, whilst shocked patients should be considered for treatment with inotropic therapy or mechanical circulatory support, when appropriate and where available.

After reading this article the reader should be familiar with: Current guidelines for implantable cardioverter defibrillator (ICD) use post myocardial infarction (MI) and ischaemic cardiomyopathy. Primary prevention ICD guidelines. Secondary prevention ICD guidelines. Non-sustained ventricular tachycardia in patients post MI and the use of ICDs. Programming ICDs.

A systematic search of Medline, EMBASE and CINAHL electronic databases was performed. Original research articles reporting all-cause mortality following surgery in patients with aortic regurgitation and severe left ventricular systolic dysfunction (LVSD) were identified. Nine of the 10 eligible studies were observational, single-center, retrospective analyses. Survival ranged from 86 to 100% at 30 days; 81 to 100% at 1 year and 68 to 84% at 5 years. Three studies described an improvement in mean left ventricular ejection fraction (LVEF) following aortic valve replacement (AVR) of 5-14%; a fourth study reported an increase in mean left ventricular ejection fraction (LVEF) of 9% in patients undergoing isolated AVR but not when AVR was combined with coronary artery bypass graft and/or mitral valve surgery. Three studies demonstrated improvements in functional New York Heart Association (NYHA) class following AVR. Additional studies are needed to clarify the benefits of AVR in patients with more extreme degrees of left ventricular systolic dysfunction (LVSD) and the potential roles of cardiac transplantation and transaortic valve implantation.

Peripartum cardiomyopathy (PPCM) is a rare condition with a diverse spectrum of potential outcomes, ranging from frequent complete recovery to fulminant heart failure and death. The pathogenesis of PPCM is not well understood, and relatively little is known about its incidence and prevalence. PPCM is often under-recognised in the clinical setting. Early investigation and diagnosis with subsequent expert management may improve outcomes. The development of registries will allow this condition to be better characterised and may help answer crucial questions regarding its optimal medical and surgical management. This paper reviews the potential approaches to improve outcomes in patients with PPCM.

Aims To investigate the relationship between angina pectoris and fatal and non-fatal clinical outcomes in heart failure with reduced and preserved ejection fraction (HF-REF and HF-PEF, respectively). Methods and results Of 7599 patients in the CHARM program, 5408 had ischaemic heart disease; 3855 had HF-REF (ejection fraction ≤45%) and 1553 had HF-PEF. These patients were separated into three groups: no history of angina, previous angina, and current angina. Three coronary outcomes were examined: fatal or non-fatal myocardial infarction (MI); MI or hospitalization for unstable angina (UA); and MI, UA or coronary revascularization. The composite heart failure outcome of cardiovascular death or heart failure hospitalization (HFH) was also analysed, along with its components and all-cause mortality. New York Heart Association functional class was worse in both HF-REF and HF-PEF patients with current angina compared with patients without angina (P

Aim: Angina pectoris is common in patients with heart failure and reduced ejection fraction (HF-REF) but its relationship with outcomes has not been well defined. This relationship was investigated further in a retrospective analysis of the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA). Methods and results: Four thousand, eight hundred and seventy-eight patients were divided into three categories: no history of angina and no chest pain at baseline (Group A; n = 1240), past history of angina but no chest pain at baseline (Group B; n = 1353) and both a history of angina and chest pain at baseline (Group C; n = 2285). Outcomes were examined using Kaplan–Meier and Cox regression survival analysis. Compared with Group A, Group C had a higher risk of non-fatal myocardial infarction or unstable angina (HR: 2.36, 1.54–3.61; P < 0.001), this composite plus coronary revascularization (HR: 2.54, 1.76–3.68; P < 0.001), as well as HF hospitalization (HR: 1.35, 1.13–1.63; P = 0.001), over a median follow-up period of 33 months. There was no difference in cardiovascular or all-cause mortality. Group B had a smaller increase in risk of coronary events but not of heart failure hospitalization. Conclusion: Patients with HF-REF and ongoing angina are at an increased risk of acute coronary syndrome and HF hospitalization. Whether these patients would benefit from more aggressive medical therapy or percutaneous revascularization is not known and merits further investigation.

Background: Care of heart failure (HF) patients results in a high burden on healthcare resources, and estimating prognosis is becoming increasingly important to triage resources wisely. Natriuretic peptides are recommended prognosticators in chronic HF. Our objective was to evaluate whether a multisensor HF index and alert algorithm (HeartLogic) replaces or augments current HF risk stratification. Methods and Results: MultiSENSE (Multisensor Chronic Evaluation in Ambulatory Heart Failure Patients) enrolled 900 patients with cardiac resynchronization therapy defibrillators enabled for collection of heart sounds, respiration, thoracic impedance, heart rate, and activity data. The HeartLogic algorithm automatically calculated a daily HF index and identified periods IN or OUT of an active alert state relative to a configurable threshold. Patients experienced 192 independently adjudicated HF events (average rate, 0.20/patient-year [pt-yr]) during 1 year of follow-up. HF event rates while IN alert was 10-fold higher than OUT of alert (0.80 versus 0.08 events/pt-yr). Combined with NT-proBNP (N-terminal pro-B-type natriuretic peptide) at enrollment (relative to 1000 pg/mL threshold, event rate was 0.42 [HIGH] versus 0.07 [LOW] events/pt-yr), substratification found the lowest risk group (LOW NT-proBNP and OUT of alert) experienced 0.02 events/pt-yr, whereas the highest risk group (HIGH NT-proBNP and IN alert) was associated with a 50-fold increased risk of an HF event (1.00 events/pt-yr) relative to the lowest risk group. Conclusions: Dynamic assessment using implantable device sensors within HeartLogic by itself or in conjunction with NT-proBNP measurements can identify time-intervals when patients are at significantly increased risk of worsening HF and potentially better triage resources to this vulnerable patient population. Clinical Trial Registration: https://www.clinicaltrials.gov . Unique identifier: NCT01128166.

ObjectiveThe recent Danish Study to Assess the Efficacy of ICDs in Patients with Non-ischemic Systolic Heart Failure on Mortality (DANISH) trial suggested that implantable cardioverter defibrillators (ICDs) do not reduce overall mortality in patients with non-ischaemic cardiomyopathy (NICM), despite reducing sudden cardiac death. We performed an updated meta-analysis to examine the impact of ICD therapy on mortality in NICM patients.MethodsA systematic search for studies that examined the effect of ICDs on outcomes in NICM was performed. Our analysis compared patients randomised to an ICD with those randomised to no ICD, and examined the endpoint of overall mortality.ResultsSix primary prevention trials and two secondary prevention trials were identified that met the pre-specified search criteria. Using a fixed-effects model, analysis of primary prevention trials revealed a reduction in overall mortality with ICD therapy (RR 0.76, 95% CI 0.65 to 0.91).ConclusionsAlthough our updated meta-analysis demonstrates a survival benefit of ICD therapy, the effect is substantively weakened by the inclusion of the DANISH trial—which is both the largest and most recent of the analysed trials—indicating that the residual pooled benefit of ICDs may reflect the risk of sudden death in older trials which included patients treated sub-optimally by contemporary standards. As such, these data must be interpreted cautiously. The results of the DANISH trial emphasise that there is no ‘one size fits all’ indication for primary prevention ICDs in NICM patients, and clinicians must consider age and comorbidity on an individual basis when determining whether a defibrillator is appropriate.

Heart failure (HF) is a clinical syndrome characterized by dyspnoea, fatigue and fluid retention accompanied by objective evidence of cardiac dysfunction. The syndrome affects around 2% of the general population, affecting men more commonly than women (under the age of 80), with incidence and prevalence rising steeply with age. HF causes substantial morbidity and reduced life expectancy, and coronary artery disease accounts for two-thirds of cases in developed countries. Investigation is important to ascertain the diagnosis, identify the aetiology (which might be reversible) and give some indication of prognosis. Currently, more than 40% of people die within 18 months of a new diagnosis of HF. Treatment has been revolutionized by large randomized-controlled clinical trials studying the effects of antagonism of the renin–angiotensin–aldosterone and sympathetic nervous systems, and, more recently, the effects of device therapy. Cardiac transplantation remains an option for patients who are severely symptomatic (and at high risk) despite optimal medical and appropriate device therapy.

Cardiac transplantation can be a life-saving treatment for selected patients with heart failure. However, despite advances in immunosuppressive therapy, acute allograft rejection remains a significant cause of morbidity and mortality. The current ‘gold standard’ for rejection surveillance is endomyocardial biopsy, which aims to identify episodes of rejection prior to development of clinical manifestations. This is an invasive technique with a risk of false-positive and false-negative results. Consequently, a wide variety of noninvasive alternatives have been investigated for their potential role as biomarkers of rejection. This article reviews the evidence behind proposed alternatives such as imaging techniques, electrophysiological parameters and peripheral blood markers, and highlights the potential future role for biomarkers in cardiac transplantation as an adjunct to biopsy.

Heart failure is a complex multifaceted syndrome occurring as a result of impaired cardiac function. Understanding the neurohormonal, inflammatory and molecular pathways involved in the pathophysiology of this syndrome has led to the development of effective and widely used pharmacological treatments. Despite this, mortality and hospitalization rates associated with this condition remain high. The natural course of this illness is usually progressive, often leading inexorably to end stage heart failure, for which orthotopic heart transplant is a treatment option but one with limited resource. In the past decade, mechanical circulatory support has emerged as a potential therapy for certain patients with advanced heart failure. This article reviews the published data regarding biomarkers in the setting of mechanical circulatory support, and highlights areas of ongoing work and potential future areas of interest.

Aim: Our understanding of heart failure in younger patients is limited. The Meta-analysis Global Group in Chronic Heart Failure (MAGGIC) database, which consisted of 24 prospective observational studies and 7 randomized trials, was used to investigate the clinical characteristics, treatment, and outcomes of younger patients. Methods and Results: Patients were stratified into six age categories: < 40 (n = 876), 40–49 (n = 2638), 50–59 (n = 6894), 60–69 (n = 12 071), 70–79 (n = 13 368), and ≥80 years (n = 6079). Of 41 926 patients, 2.1, 8.4, and 24.8% were younger than 40, 50, and 60 years of age, respectively. Comparing young ( < 40 years) against elderly (≥80 years), younger patients were more likely to be male (71 vs. 48%) and have idiopathic cardiomyopathy (63 vs. 7%). Younger patients reported better New York Heart Association functional class despite more severe left ventricular dysfunction (median ejection fraction: 31 vs. 42%, all P < 0.0001). Comorbidities such as hypertension, myocardial infarction, and atrial fibrillation were much less common in the young. Younger patients received more disease-modifying pharmacological therapy than their older counterparts. Across the younger age groups ( < 40, 40–49, and 50–59 years), mortality rates were low: 1 year 6.7, 6.6, and 7.5%, respectively; 2 year 11.7, 11.5, 13.0%; and 3 years 16.5, 16.2, 18.2%. Furthermore, 1-, 2-, and 3-year mortality rates increased sharply beyond 60 years and were greatest in the elderly (≥80 years): 28.2, 44.5, and 57.2%, respectively. Conclusion: Younger patients with heart failure have different clinical characteristics including different aetiologies, more severe left ventricular dysfunction, and less severe symptoms. Three-year mortality rates are lower for all age groups under 60 years compared with older patients.

We review the journey to myocardial and neurologic recovery of a 42-year-old mother with severe acute cardiogenic shock and multiorgan failure after extensive subarachnoid hemorrhage, who was salvaged successfully using a CentriMag short-term biventricular assist device.

It is well established that organized care of heart failure patients, including specialist management by cardiologists, improves patient outcomes. In response to this, other national training bodies (the UK and the USA) have developed heart failure subspecialty curricula within their Cardiology Training Curricula. In addition, European Society of Cardiology (ESC) subspecialty curricula exist for Interventional Cardiology and Heart Rhythm Management. The purpose of this heart failure curriculum is to provide a framework which can be used as a blueprint for training across Europe. This blueprint mirrors other ESC curricula. Each section has three components: the knowledge required, the skills which are necessary, and the professionalism (attitudes and behaviours) which should be attained. The programme is designed to last 2 years. The first year is devoted to the specialist heart failure module. The second year allows completion of the optional modules of advanced imaging, device therapy for implanters, cardiac transplantation, and mechanical circulatory support. The second year can also be devoted to continuation of specialist heart failure training and/or research for those not wishing to continue with the advanced modules.

Non-ischaemic cardiomyopathy (NICM) is a common cause of heart failure. If no cause is identified it is termed idiopathic dilated cardiomyopathy (IDCM). Guideline-recommended therapy can improve left ventricular systolic function (LVSF). Although criteria for defining myocardial recovery exist, its

Although peripartum cardiomyopathy (PPCM) is associated with mortality and morbidity, improvement in cardiac function – termed myocardial recovery – can occur. No study has systematically reviewed myocardial recovery in PPCM and its independent predictors. A systematic review was performed of

Vitamin K antagonists, such as warfarin, have a narrow therapeutic window; patients on these therapies therefore require regular international normalized ratio (INR) monitoring to maintain optimal dosing. This involves periodic checks and laboratory testing using venepuncture, which are often perceived as a burden. This study aimed to determine the accuracy and precision of the LumiraDx INR Test, a new point-of-care in vitro diagnostic platform, in an anticoagulation clinic setting. In this observational, cross-sectional study, precision of the LumiraDx INR Test was assessed using paired replicate samples (n = 366) and 3 test strip lots. Accuracy was determined by comparing capillary blood INR, ascertained by the LumiraDx INR Test, with venous plasma INR, measured by the laboratory reference instrument, the IL ACL ELITE Pro. Furthermore, INR was assessed across a range of hematocrit (25%-55%). In addition, feedback was collected from health-care professionals via a self-completed questionnaire. This trial was registered at ClinicalTrials.gov (NCT03682419). The precision (% coefficient of variation) of the LumiraDx INR Test was

Aims Microvolt T-wave alternans (MTWA) testing identifies beat-to-beat fluctuations in T-wave morphology, which have been linked to ventricular arrhythmias. However, clinical studies have produced conflicting results and data in heart failure (HF) have been limited. The aim of this study was to determine the prevalence and incremental prognostic value of spectral MTWA testing in an unselected cohort of patients recently hospitalized with HF. Methods and results Consecutive admissions with confirmed HF were recruited, and survivors were invited to attend 1 month post-discharge for MTWA testing. A total of 648 of 1003 enrolled patients returned for MTWA testing (58% male, mean age 71 years). Forty-nine per cent were ineligible due to AF, pacemaker dependency, or inability to exercise. Of the 330 MTWA test results, 30% were positive, 24% negative, and 46% indeterminate. Overall, 268 deaths occurred during a median follow-up of 3.1 (interquartile range 1.9–3.9) years. Of the ineligible patients, 48% died vs. 35% of eligible patients (P < 0.001). Of those patients with positive, negative, and indeterminate tests, 27, 35, and 40%, respectively, died (P = 0.12). Even when analysed as non-negative (positive/indeterminate) vs. negative, there was still no between-group difference in mortality (P = 0.95). MTWA results categorized as positive, negative, or indeterminate showed no incremental prognostic value in a multivariable model, which included BNP. Paradoxically, when compared in a binary fashion with a non-negative result, a negative test was an independent predictor of death, as was ineligibility for MTWA testing. Conclusion Spectral MTWA testing was not widely applicable and failed to predict mortality, and so cannot be endorsed as a risk stratification tool in HF.

A 61-year old gentleman with a past medical history of type-2 diabetes mellitus presented to hospital with breathlessness and ankle swelling for 1 week. He reported no chest pain. Resting electrocardiogram revealed sinus rhythm with non-specific ST segment changes, and his high sensitivity troponin T was elevated. An echocardiogram demonstrated severe left ventricular systolic dysfunction. Coronary angiography revealed severe multi-vessel coronary artery disease. …

Patients with left ventricular assist devices (LVADs) are at high risk of sustained ventricular arrhythmias, but these may be remarkably well tolerated and the association with sudden death is unclear. Many patients who receive an LVAD already have an implantable cardioverter defibrillator (ICD). While it is standard practice to reactivate a previously implanted ICD in an LVAD recipient, this should include discussion of the revised risks and benefits of ICD therapy following LVAD implantation. In particular, patients should be warned that they might receive a significant number of ICD shocks that may not be life saving. When ICDs are reactivated, device programming should minimize the risk of repeated shocks for non-sustained or well-tolerated ventricular arrhythmias. Implantation of a primary prevention ICD after implantation of an LVAD is not supported by current evidence, poses potential risks, and should be the subject of a clinical trial before it becomes standard practice.

Implantable cardioverter defibrillators (ICDs) reduce mortality in selected patients with chronic heart failure but prognostic benefit is likely to attenuate with progression to end-stage heart failure. The incidence of multiple futile ICD shocks before death is uncertain. Only individual patients, supported by their healthcare professionals, can decide when ICD therapy becomes futile in end-stage heart failure. Despite consensus that ICD deactivation should be routinely discussed, this rarely occurs in clinical practice for many reasons including uncertainty about when to initiate these discussions and reluctance to confront death and dying. Patient and carer opinions about end-stage heart failure and ICD deactivation may not meet professional expectations. Future research should focus on these opinions and examine interventions that bridge the gap between best practice and the reality of current clinical practice.

Patients with advanced heart failure have a dismal prognosis and poor quality of life. Heart transplantation provides an effective treatment for a subset of these patients. This article provides cardiologists with up-to-date information about referral for transplantation, the role of left ventricular assist devices prior to transplant, patient selection, waiting-list management and donor heart availability. Timing is of central importance; patients should be referred before complications (eg, cardiorenal syndrome or secondary pulmonary hypertension) have developed that will increase the risk of, or potentially contraindicate, transplantation. Issues related to heart failure aetiology, comorbidity and adherence to medical treatment are reviewed. Finally, the positive role that cardiologists can play in promoting and facilitating organ donation is discussed.

Background The third heart sound (S3) is regarded as one of the earliest signs of heart failure (HF) and is typically assessed via auscultation clinically. The embedded accelerometer sensor in implantable devices can pick up the mechanical vibration caused by S3. We compared the device-measured S3 amplitude (devS3) to auscultated S3 volume grades (audS3). Methods In the MultiSENSE study, ambulatory HF patients implanted with a CRT-D were enrolled and followed up for 1 year. DevS3 amplitude was trended daily. Clinicians were asked to auscultate for S3 intensity on a graded scale (None/Low/Moderate/Loud) at baseline and each regular follow-up. Clinicians were blinded to the devS3 data at the time of assessment. We compared devS3 on the day of assessment in patients with different level of audS3 intensity. ANOVA test was used to compare the mean S3 amplitudes among groups and unpaired t-tests for between-group comparison. Conclusion This demonstrates that device-measured S3 amplitude reflects auscultated S3 heart sound volume grades. Since device-measured S3 is an objective measure on a continuous scale as opposed to auscultation which is subjectively categorized, it could avoid inter-observer auscultation variability and enables monitoring of this clinical variables in ambulatory HF patients. Result A total of 5211 auscultation reports were obtained from the 900 patients in the study. AudS3 intensity was None in 4709, Low in 391, Moderate in 108, and Loud in 3 reports (moderate and loud were combined for this analysis). Figure represents the devS3 amplitude (mean ± standard error) on the day of the follow-up as a function of the audS3 grades reported, the mean devS3 values for None, Low, and Moderate/Loud audS3 was 0.96 ± 0.01 mG, 1.02 ± 0.02 mG, and 1.27± 0.06 mG respectively. Both ANOVA test and unpaired tests between groups were significant and remained significant after adjusting for repeated measures.

Heart failure (HF) is a clinical syndrome characterized by dyspnoea, fatigue and fluid retention accompanied by objective evidence of cardiac dysfunction. The syndrome affects around 2% of the general population, affecting men more commonly than women (under the age of 80), with incidence and prevalence rising steeply with age. HF causes substantial morbidity and reduced life expectancy, and coronary artery disease accounts for two-thirds of cases in developed countries. Investigation is important to ascertain the diagnosis, identify the aetiology (which might be reversible) and give some indication of prognosis. Currently, more than 40% of people die within 18 months of a new diagnosis of HF. Treatment has been revolutionized by large randomized-controlled clinical trials studying the effects of antagonism of the renin–angiotensin–aldosterone and sympathetic nervous systems, and, more recently, the effects of device therapy. Cardiac transplantation remains an option for patients who are severely symptomatic (and at high risk) despite optimal medical and appropriate device therapy.

Background A multisensor algorithm has been demonstrated to predict heart failure (HF) events in patients with implanted devices with high sensitivity and low false positive rate. However, it is not known how the individual sensors change from hospital admission to discharge and whether it can be indicative of readmissions or death within 30 days. Methods The MultiSENSE study followed 900 HF patients with CRT-D for up to 1 year. Devices were modified to enable the collection of first (S1) and third (S3) heart sounds, thoracic impedance (TI), respiratory rate (RR), rapid shallow breathing index (RSBI), night heart rate (nHR), and activity. All hospitalizations were adjudicated by an independent committee. Hospitalizations with HF as a primary cause (HFH) were identified. HFH with an admission outside of the customized data collection were excluded due to lack of sensor data. Each HFH was classified as unresolved if it was followed by all-cause hospitalization or death within 30 days of discharge; otherwise, it was classified as resolved. For each type of HFH, daily sensor values on the day before admission and the day before discharge were compared with a pairwise t-test. The changes in each sensor were compared between the resolved and the unresolved group via t-test. Significant difference in comparisons was defined as that with p Results Out of 149 HFHs, 109 were determined as resolved and 40 as unresolved. Additional HFHs were excluded if sensor data at admission or discharge was not available (see Figure). Admission-to-discharge differences for resolved HFHs showed improvement in S3, S1, TI, and RR; no change in RSBI and nHR, and reduction in activity. Admission-to-discharge differences for unresolved HFHs showed improvement in TI; no change in S3, S1, RR, nHR; worsening in RSBI, and reduction in activity. Changes in RSBI were significantly different between the two groups of HFHs. Conclusions Worsening in RSBI during hospitalization identified a group of patients with either early HF readmissions or death.