Diabetes mellitus does not alter mortality or hospitalisation risk in patients with newly diagnosed heart failure with preserved ejection fraction: Time to rethink pathophysiological models of disease progression.

INTRODUCTION: Type 2 diabetes is a common and adverse prognostic co-morbidity for patients with heart failure with reduced ejection fraction (HFrEF). The effect of diabetes on long-term outcomes for heart failure with preserved ejection fraction (HFpEF) is less established. METHODS: Prospective cohort study of patients referred to a regional HF clinic with newly diagnosed with HFrEF and HFpEF according to the 2016 European Society of Cardiology guidelines. The association between diabetes, all-cause mortality and hospitalisation was quantified using Kaplan-Meier or Cox regression analysis. RESULTS: Between 1st May 2012 and 1st May 2013, of 960 unselected consecutive patients referred with suspected HF, 464 and 314 patients met the criteria for HFpEF and HFrEF respectively. Within HFpEF and HFrEF groups, patients with diabetes were more frequently male and in both groups patients with diabetes were more likely to be treated with ß-adrenoceptor antagonists and angiotensin converting enzyme inhibitors. After adjustment for age, sex, medical therapy and co-morbidities, diabetes was associated with increased mortality in individuals with HFrEF (HR 1.46 95% CI: 1.05-2.02; p = .023), but not in those with HFpEF (HR 1.26 95% CI 0.92-1.72; p = .146). CONCLUSION: In unselected patients with newly diagnosed HF, diabetes is not an adverse prognostic marker in patients with HFpEF, but is in HFrEF.

Studying Adipose Endothelial Cell/Adipocyte Cross-Talk in Human Subcutaneous Adipose Tissue.

Microvascular endothelial cells (MVECs) have many critical roles, including control of vascular tone, regulation of thrombosis, and angiogenesis. Significant heterogeneity in endothelial cell (EC) genotype and phenotype depends on their vascular bed and host disease state. The ability to isolate MVECs from tissue-specific vascular beds and individual patient groups offers the opportunity to directly compare MVEC function in different disease states. Here, using subcutaneous adipose tissue (SAT) taken at the time of insertion of cardiac implantable electronic devices (CIED), we describe a method for the isolation of a pure population of functional human subcutaneous adipose tissue MVEC (hSATMVEC) and an experimental model of hSATMVEC-adipocyte cross-talk. hSATMVEC were isolated following enzymatic digestion of SAT by incubation with anti-CD31 antibody-coated magnetic beads and passage through magnetic columns. hSATMVEC were grown and passaged on gelatin-coated plates. Experiments used cells at passages 2-4. Cells maintained classic features of EC morphology until at least passage 5. Flow cytometric assessment showed 99.5% purity of isolated hSATMVEC, defined as CD31+/CD144+/CD45-. Isolated hSATMVEC from controls had a population doubling time of approximately 57 h, and active proliferation was confirmed using a cell proliferation imaging kit. Isolated hSATMVEC function was assessed using their response to insulin stimulation and angiogenic tube-forming potential. We then established an hSATMVEC-subcutaneous adipocyte co-culture model to study cellular cross-talk and demonstrated a downstream effect of hSATMVEC on adipocyte function. hSATMVEC can be isolated from SAT taken at the time of CIED insertion and are of sufficient purity to both experimentally phenotype and study hSATMVEC-adipocyte cross-talk.

Sodium-glucose cotransporter 2 inhibitors influence skeletal muscle pathology in patients with heart failure and reduced ejection fraction.

AIMS: Patients with heart failure and reduced ejection fraction (HFrEF) exhibit skeletal muscle pathology, which contributes to symptoms and decreased quality of life. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) improve clinical outcomes in HFrEF but their mechanism of action remains poorly understood. We aimed, therefore, to determine whether SGLT2i influence skeletal muscle pathology in patients with HFrEF. METHODS AND RESULTS: Muscle biopsies from 28 male patients with HFrEF (New York Heart association class I-III) treated with SGLT2i (>12 months) or without SGLT2i were compared. Comprehensive analyses of muscle structure (immunohistochemistry), transcriptome (RNA sequencing), and metabolome (liquid chromatography-mass spectrometry) were performed, and serum inflammatory profiling (ELISA). Experiments in mice (n = 16) treated with SGLT2i were also performed. Myofiber atrophy was ~20% less in patients taking SGLT2i (p = 0.07). Transcriptomics and follow-up measures identified a unique signature in patients taking SGLT2i related to beneficial effects on atrophy, metabolism, and inflammation. Metabolomics identified influenced tryptophan metabolism in patients taking SGLT2i: kynurenic acid was 24% higher and kynurenine was 32% lower (p < 0.001). Serum profiling identified that SGLT2i treatment was associated with lower (p < 0.05) pro-inflammatory cytokines by 26-64% alongside downstream muscle interleukin (IL)-6-JAK/STAT3 signalling (p = 008 and 0.09). Serum IL-6 and muscle kynurenine were correlated (R = 0.65; p < 0.05). Muscle pathology was lower in mice treated with SGLT2i indicative of a conserved mammalian response to treatment. CONCLUSIONS: Treatment with SGLT2i influenced skeletal muscle pathology in patients with HFrEF and was associated with anti-atrophic, anti-inflammatory, and pro-metabolic effects. These changes may be regulated via IL-6-kynurenine signalling. Together, clinical improvements following SGLT2i treatment in patients with HFrEF may be partly explained by their positive effects on skeletal muscle pathology.

Outcomes following cardiac resynchronisation therapy in older people.

INTRODUCTION: Older patients may be less likely to receive cardiac resynchronisation therapy (CRT) for the management of heart failure. We aimed to describe the differences in clinical response, complications, and subsequent outcomes following CRT implantation compared to younger patients. METHODS: We conducted a retrospective cohort study of unselected, consecutive patients implanted with CRT devices between March 2008 and July 2017. We recorded complications, symptomatic and echocardiographic response, hospitalisation for heart failure, and all-cause mortality comparing patients aged <70, 70-79 and ≥ 80 years. RESULTS: Five hundred and seventy-four patients (median age 76 years [interquartile range 68-81], 73.3% male) received CRT. At baseline, patients aged ≥80 years had worse symptoms, were more likely to have co-morbidities, and less likely to be receiving comprehensive medical therapy, although left ventricular function was similar. Older patients were less likely to receive CRT-defibrillators compared to CRT-pacemakers. Complications were infrequent and not more common in older patients. Age was not a predictor of symptomatic or echocardiographic response to CRT (67.2%, 71.2% and 62.6% responders in patients aged <70, 70-79 and ≥ 80 years, respectively; P = 0.43), and time to first heart failure hospitalisation was similar across age groups (P = 0.28). Ten-year survival was lower for older patients (49.9%, 23.9% and 6.8% in patients aged <70, 70-79 and ≥ 80 years, respectively; P < 0.001). CONCLUSIONS: The benefits of CRT on symptoms and left ventricular function were not different in older patients despite a greater burden of co-morbidities and less optimal medical therapy. These findings support the use of CRT in an ageing population.

Association Between Type 2 Diabetes and Changes in Myocardial Structure, Contractile Function, Energetics, and Blood Flow Before and After Aortic Valve Replacement in Patients With Severe Aortic Stenosis.

BACKGROUND: Type 2 diabetes (T2D) is associated with an increased risk of left ventricular dysfunction after aortic valve replacement (AVR) in patients with severe aortic stenosis (AS). Persistent impairments in myocardial energetics and myocardial blood flow (MBF) may underpin this observation. Using phosphorus magnetic resonance spectroscopy and cardiovascular magnetic resonance, this study tested the hypothesis that patients with severe AS and T2D (AS-T2D) would have impaired myocardial energetics as reflected by the phosphocreatine to ATP ratio (PCr/ATP) and vasodilator stress MBF compared with patients with AS without T2D (AS-noT2D), and that these differences would persist after AVR. METHODS: Ninety-five patients with severe AS without coronary artery disease awaiting AVR (30 AS-T2D and 65 AS-noT2D) were recruited (mean, 71 years of age [95% CI, 69, 73]; 34 [37%] women). Thirty demographically matched healthy volunteers (HVs) and 30 patients with T2D without AS (T2D controls) were controls. One month before and 6 months after AVR, cardiac PCr/ATP, adenosine stress MBF, global longitudinal strain, NT-proBNP (N-terminal pro-B-type natriuretic peptide), and 6-minute walk distance were assessed in patients with AS. T2D controls underwent identical assessments at baseline and 6-month follow-up. HVs were assessed once and did not undergo 6-minute walk testing. RESULTS: Compared with HVs, patients with AS (AS-T2D and AS-noT2D combined) showed impairment in PCr/ATP (mean [95% CI]; HVs, 2.15 [1.89, 2.34]; AS, 1.66 [1.56, 1.75]; P<0.0001) and vasodilator stress MBF (HVs, 2.11 mL min g [1.89, 2.34]; AS, 1.54 mL min g [1.41, 1.66]; P<0.0001) before AVR. Before AVR, within the AS group, patients with AS-T2D had worse PCr/ATP (AS-noT2D, 1.74 [1.62, 1.86]; AS-T2D, 1.44 [1.32, 1.56]; P=0.002) and vasodilator stress MBF (AS-noT2D, 1.67 mL min g [1.5, 1.84]; AS-T2D, 1.25 mL min g [1.22, 1.38]; P=0.001) compared with patients with AS-noT2D. Before AVR, patients with AS-T2D also had worse PCr/ATP (AS-T2D, 1.44 [1.30, 1.60]; T2D controls, 1.66 [1.56, 1.75]; P=0.04) and vasodilator stress MBF (AS-T2D, 1.25 mL min g [1.10, 1.41]; T2D controls, 1.54 mL min g [1.41, 1.66]; P=0.001) compared with T2D controls at baseline. After AVR, PCr/ATP normalized in patients with AS-noT2D, whereas patients with AS-T2D showed no improvements (AS-noT2D, 2.11 [1.79, 2.43]; AS-T2D, 1.30 [1.07, 1.53]; P=0.0006). Vasodilator stress MBF improved in both AS groups after AVR, but this remained lower in patients with AS-T2D (AS-noT2D, 1.80 mL min g [1.59, 2.0]; AS-T2D, 1.48 mL min g [1.29, 1.66]; P=0.03). There were no longer differences in PCr/ATP (AS-T2D, 1.44 [1.30, 1.60]; T2D controls, 1.51 [1.34, 1.53]; P=0.12) or vasodilator stress MBF (AS-T2D, 1.48 mL min g [1.29, 1.66]; T2D controls, 1.60 mL min g [1.34, 1.86]; P=0.82) between patients with AS-T2D after AVR and T2D controls at follow-up. Whereas global longitudinal strain, 6-minute walk distance, and NT-proBNP all improved after AVR in patients with AS-noT2D, no improvement in these assessments was observed in patients with AS-T2D. CONCLUSIONS: Among patients with severe AS, those with T2D demonstrate persistent abnormalities in myocardial PCr/ATP, vasodilator stress MBF, and cardiac contractile function after AVR; AVR effectively normalizes myocardial PCr/ATP, vasodilator stress MBF, and cardiac contractile function in patients without T2D.

Relationship Among Diabetes, Obesity, and Cardiovascular Disease Phenotypes: A UK Biobank Cohort Study.

OBJECTIVE: Obesity and diabetes frequently coexist, yet their individual contributions to cardiovascular risk remain debated. We explored cardiovascular disease biomarkers, events, and mortality in the UK Biobank stratified by BMI and diabetes. RESEARCH DESIGN AND METHODS: A total of 451,355 participants were stratified by ethnicity-specific BMI categories (normal, overweight, obese) and diabetes status. We examined cardiovascular biomarkers including carotid intima-media thickness (CIMT), arterial stiffness, left ventricular ejection fraction (LVEF), and cardiac contractility index (CCI). Poisson regression models estimated adjusted incidence rate ratios (IRRs) for myocardial infarction, ischemic stroke, and cardiovascular death, with normal-weight nondiabetes as comparator. RESULTS: Five percent of participants had diabetes (10% normal weight, 34% overweight, and 55% obese vs. 34%, 43%, and 23%, respectively, without diabetes). In the nondiabetes group, overweight/obesity was associated with higher CIMT, arterial stiffness, and CCI and lower LVEF (P < 0.005); these relationships were diminished in the diabetes group. Within BMI classes, diabetes was associated with adverse cardiovascular biomarker phenotype (P < 0.005), particularly in the normal-weight group. After 5,323,190 person-years follow-up, incident myocardial infarction, ischemic stroke, and cardiovascular mortality rose across increasing BMI categories without diabetes (P < 0.005); this was comparable in the diabetes groups (P-interaction > 0.05). Normal-weight diabetes had comparable adjusted cardiovascular mortality to obese nondiabetes (IRR 1.22 [95% CI 0.96-1.56]; P = 0.1). CONCLUSIONS: Obesity and diabetes are additively associated with adverse cardiovascular biomarkers and mortality risk. While adiposity metrics are more strongly correlated with cardiovascular biomarkers than diabetes-oriented metrics, both correlate weakly, suggesting that other factors underpin the high cardiovascular risk of normal-weight diabetes.

Atrial secondary mitral regurgitation: prevalence, characteristics, management, and long-term outcomes.

BACKGROUND: The prevalence, clinical characteristics, management and long-term outcomes of patients with atrial secondary mitral regurgitation (ASMR) are not well described. METHODS: We performed a retrospective, observational study of consecutive patients with grade III/IV MR determined by transthoracic echocardiography. The aetiology of MR was grouped as being either primary (due to degenerative mitral valve disease), ventricular SMR (VSMR: due to left ventricular dilatation/dysfunction), ASMR (due to LA dilatation), or other. RESULTS: A total of 388 individuals were identified who had grade III/IV MR; of whom 37 (9.5%) had ASMR, 113 (29.1%) had VSMR, 193 had primary MR (49.7%), and 45 (11.6%) were classified as having other causes. Compared to MR of other subtypes, patients with ASMR were on average older (median age 82 [74-87] years, p < 0.001), were more likely to be female (67.6%, p = 0.004) and usually had atrial fibrillation (83.8%, p = 0.001). All-cause mortality was highest in patients with ASMR (p < 0.001), but similar to that in patients with VSMR once adjusted for age and sex (hazard ratio [HR] 0.81, 95% confidence interval [CI] 0.52-1.25). Hospitalisation for worsening heart failure was more commonly observed in those with ASMR or VSMR (p < 0.001) although was similar between these groups when age and sex were accounted for (HR 0.74, 95% CI 0.34-1.58). For patients with ASMR, the only variables associated with outcomes were age and co-morbidities. CONCLUSIONS: ASMR is a prevalent and distinct disease process associated with a poor prognosis, with much of this related to older age and co-morbidities.

Improving the management of left ventricular thrombus in a tertiary cardiology centre: a quality improvement project.

Left ventricular (LV) thrombus is an increasingly recognised complication following anterior myocardial infarction and non-ischaemic cardiomyopathy. Whilst vitamin K antagonists (VKA) remain the only approved therapeutic option to reduce the risk of systemic thromboembolism including stroke, the off-label use of direct oral anticoagulants (DOACs) is becoming an attractive alternative.We aimed to improve the diagnosis and management of LV thrombus at a tertiary cardiology centre using quality improvement methodology. Outcomes included increasing the use of DOACs from 25% to 70% over a period of 1 year and shorten length of time from diagnosis to repeat imaging to within 3-6 months as recommended by guidelines.During the first Plan-Do-Study-Action (PDSA) cycle, we identified 84 patients diagnosed with LV thrombus between 1 December 2012 and 30 June 2018. The majority (74%) were prescribed VKA. Repeat imaging occurred in 89% of patients, but only 55% using the same modality. The mean duration between diagnosis and repeat imaging was 233±251 days. There were no significant differences between VKA and DOAC in terms of thrombus resolution, systemic embolisation or clinically significant bleeding. We published trust-wide guidelines on the management of LV thrombus with recommendations supporting the use of DOACs and appropriate follow-up imaging. A second PDSA cycle undertaken between 1 October 2019 and 31 March 2020 identified a further 20 patients. DOAC use increased to 70% and 70% of patients underwent follow-up imaging following a mean duration of 140±61 days, although in only 36% using the same modality.Using quality improvement methodology, we confirmed safe and efficient use of DOAC in the setting of LV thrombus. We published trust guidelines supporting their use, which was associated with an increase in DOAC use and in earlier follow-up imaging in line with our recommendations.

Guideline-directed medical therapy is similarly effective in heart failure with mildly reduced ejection fraction.

AIMS: Current guidelines recommend that disease-modifying pharmacological therapies may be considered for patients who have heart failure with mildly reduced ejection fraction (HFmrEF). We aimed to describe the characteristics, outcomes, provision of pharmacological therapies and dose-related associations with mortality risk in HFmrEF. METHODS AND RESULTS: We explored data from two prospective observational studies, which permitted the examination of the effects of pharmacological therapies across a broad spectrum of left ventricular ejection fraction (LVEF). The combined dataset consisted of 2388 unique patients, with a mean age of 73.7 ± 13.2 years of whom 1525 (63.9%) were male. LVEF ranged from 5 to 71% (mean 37.2 ± 12.8%) and 1504 (63.0%) were categorised as having reduced ejection fraction (HFrEF), 421 (17.6%) as HFmrEF and 463 (19.4%) as preserved ejection fraction (HFpEF). Patients with HFmrEF more closely resembled HFrEF than HFpEF. Adjusted all-cause mortality risk was lower in HFmrEF (hazard ratio [HR] 0.86 (95% confidence interval [CI] 0.74-0.99); p = 0.040) and in HFpEF (HR 0.61 (95% CI 0.52-0.71); p < 0.001) compared to HFrEF. Adjusted all-cause mortality risk was lower in patients with HFrEF and HFmrEF who received the highest doses of beta-blockers or renin-angiotensin inhibitors. These associations were not evident in HFpEF. Once adjusted for relevant confounders, each mg equivalent of bisoprolol (HR 0.95 [95% CI 0.91-1.00]; p = 0.047) and ramipril (HR 0.95 [95%CI 0.90-1.00]; p = 0.044) was associated with incremental reductions in mortality risk in patients with HFmrEF. CONCLUSIONS: Pharmacological therapies were associated with lower mortality risk in HFmrEF, supporting guideline recommendations which extend the indications of these agents to all patients with LVEF < 50%. HFmrEF more closely resembles HFrEF in terms of clinical characteristics and outcomes. Pharmacological therapies are associated with lower mortality risk in HFmrEF and HFrEF, but not in HFpEF.

Clinical implications and risk factors for QRS prolongation over time in heart failure patients.

BACKGROUND: QRS prolongation is an established prognostic marker in heart failure (HF). In contrast, the role of QRS width progression over time has been incompletely explored. The current study investigates the role of QRS width progression over time on clinical status and identifies underlying predictors. METHODS: Datasets of ≥ 2 consecutive visits from 100 attendees to our HF clinic between April and August 2021 were analysed for changes in QRS complex duration. RESULTS: In total 240 datasets were stratified into tertiles based on change in QRS duration (mm/month) (1st tertile: - 1.65 [1.50] 'regression'; 2nd tertile 0.03 [0.19] 'stable', 3rd tertile 3.57 [10.11] 'progression'). The incidence of the combined endpoint HF hospitalisation and worsening of symptomatic heart failure was significantly higher in the group with QRS width progression (3rd tertile) compared with the stable group (2nd tertile; log-rank test: p = 0.013). These patients were characterised by higher plasma NT-pro-BNP levels (p = 0.008) and higher heart rate (p = 0.007). A spline-based prediction model identified patients at risk of QRS width progression when NT-pro-BNP and heartrate were > 837 pg/ml and > 83/bpm, respectively. These markers were independent of guideline-directed medical HF therapy. Patients beyond both thresholds had a 14-fold increased risk of QRS width progression compared to those with neither or either alone (HR: 14.2 [95% 6.9 - 53.6]; p < 0.0001, p for interaction = 0.016). CONCLUSIONS: This pilot study demonstrates that QRS width progression is associated with clinical deterioration of HF. NTproBNP plasma levels and heart rate indicate patients at risk QRS width progression, independently of HF therapy.

'Acute Heart Failure': Should We Abandon the Term Altogether?

PURPOSE OF REVIEW: The distinction between 'acute' and 'chronic' heart failure persists. Our review aims to explore whether reclassifying heart failure decompensation more accurately as an event within the natural history of chronic heart failure has the potential to improve outcomes. RECENT FINDINGS: Although hospitalisation for worsening heart failure confers a poor prognosis, much of this reflects chronic disease severity. Most patients survive hospitalisation with most deaths occurring in the post-discharge 'vulnerable phase'. Current evidence supports four classes of medications proven to reduce cardiovascular mortality for those who have heart failure with a reduced ejection fraction, with recent trials suggesting worsening heart failure events are opportunities to optimise these therapies. Abandoning the term 'acute heart failure' has the potential to give greater priority to initiating proven pharmacological and device therapies during decompensation episodes, in order to improve outcomes for those who are at the greatest risk.

Atrial fibrillation and risk of progressive heart failure in patients with preserved ejection fraction heart failure.

AIMS: Understanding of the pathophysiology of progressive heart failure (HF) in patients with heart failure with preserved ejection fraction (HFpEF) is incomplete. We sought to identify factors differentially associated with risk of progressive HF death and hospitalization in patients with HFpEF compared with patients with HF and reduced ejection fraction (HFrEF). METHODS AND RESULTS: Prospective cohort study of patients newly referred to secondary care with suspicion of HF, based on symptoms and signs of HF and elevated natriuretic peptides (NP), followed up for a minimum of 6 years. HFpEF and HFrEF were diagnosed according to the 2016 European Society of Cardiology guidelines. Of 960 patients referred, 467 had HFpEF (49%), 311 had HFrEF (32%), and 182 (19%) had neither. Atrial fibrillation (AF) was found in 37% of patients with HFpEF and 34% with HFrEF. During 6 years follow-up, 19% of HFrEF and 14% of HFpEF patients were hospitalized or died due to progressive HF, hazard ratio (HR) 0.67 (95% CI: 0.47-0.96; P = 0.028). AF was the only marker that was differentially associated with progressive HF death or hospitalization in patients with HFpEF HR 2.58 (95% CI: 1.59-4.21; P < 0.001) versus HFrEF HR 1.11 (95% CI: 0.65-1.89; P = 0.7). CONCLUSIONS: De novo patients diagnosed with HFrEF have greater risk of death or hospitalization due to progressive HF than patients with HFpEF. AF is associated with increased risk of progressive HF death or hospitalization in HFpEF but not HFrEF, raising the intriguing possibility that this may be a novel therapeutic target in this growing population.

Reduction of heart failure guideline-directed medication during hospitalization: prevalence, risk factors, and outcomes.

AIMS: Optimal management of heart failure with reduced ejection fraction (HFrEF) includes titration of guideline-directed medical therapy (GDMT) to the highest tolerated dose within the licensed range. During hospitalization, GDMT doses are often significantly altered, although it is unknown whether the cause of hospitalization influences this. METHODS AND RESULTS: We recruited 711 people with stable HFrEF from specialist heart failure clinics and prospectively assessed events occurring during first unplanned hospitalization. Dose changes of ACE inhibitors or angiotensin receptor blockers (ACEi/ARB), beta-blockers, mineralocorticoid receptor antagonists, and loop diuretics were recorded during 414 hospitalizations, categorized as due to decompensated heart failure, other cardiovascular causes, infection, or other non-cardiovascular causes. Most hospitalizations resulted in no change to GDMT. ACEi/ARB dose was reduced in 21% of hospitalizations and was more common during non-cardiovascular hospitalization (25.4% vs. 13.9%; P = 0.005). ACEi/ARB dose reduction was associated with older age and lower left ventricular ejection fraction at study recruitment, and poorer renal function, lower systolic blood pressure, higher serum potassium, and less frequent care from a cardiologist during admission. People experiencing ACEi/ARB reduction had worse age-adjusted survival after discharge, without differences in heart failure re-hospitalization. De-escalation of beta-blockers occurred in 8% of hospitalizations, most often due to other non-cardiovascular causes; this was not associated with post-discharge survival or re-hospitalization with heart failure. CONCLUSIONS: De-escalation of HFrEF GDMT is more common during non-cardiovascular hospitalization and for ACEi/ARB is associated with reduced survival. Post-discharge care plans should include robust plans to consider re-escalation of GDMT in these cases.

Surgical Techniques and Outcomes in Patients With Intra-Cardiac Abscesses Complicating Infective Endocarditis.

Background: An intra-cardiac abscess is a serious complication of both native (NV-IE) and prosthetic valve infective endocarditis (PV-IE). Despite being an accepted indication for surgery, controversies remain regarding the optimal timing and type of operation. We aimed to report the outcomes of patients managed for intra-cardiac abscesses over more than a decade. Methods: Patients aged ≥18 years managed for intra-cardiac abscess between 1 January 2005 and 31 December 2017 were identified from a prospectively collected IE database. The primary outcome was 30-day mortality in operated patients and secondary outcomes were freedom from re-infection, re-operation and long-term mortality comparing those patients with aortic root abscess who underwent aortic valve replacement (AVR) and those who received aortic root replacement (ARR). Results: Fifty-nine patients developed an intra-cardiac abscess, and their median age was 55 (43-71) years; among them, 44 (75%) were men, and 10 (17%) were persons who injected drugs. Infection with beta-haemolytic streptococci was associated with NV-IE (p = 0.009) and coagulase-negative staphylococci with PV-IE (p = 0.005). Forty-four (75%) underwent an operation, and among those with aortic root abscess, 27 underwent AVR and 12 ARR. Thirty-day mortality was associated with infection with S. aureus (p = 0.006) but not the type or timing of the operation. Survival in operated patients was 66% at 1 year and 59% at 5 years. In operated patients, none had a relapse, although six developed late recurrence. Freedom from infection, re-operation and long-term mortality were similar in patients undergoing AVR compared to ARR. Conclusion: Patients diagnosed with intra-cardiac abscess who were not operated on had very poor survival. In those who underwent an operation, either by AVR or ARR based upon patient factors, imaging and intra-operative findings outcomes were similar.

An enormous right atrial myxoma highlights the role of echocardiography in heart failure pathways: a case report.

BACKGROUND: Myxomata are rare, benign, primary tumours of the heart which can present with a variety of symptoms depending on size, location, and mobility. Here, we report a case of enormous right atrial myxoma, obliterating the right atrial and right ventricular cavities presenting with symptoms of heart failure. CASE SUMMARY: A 66-year-old Caucasian female presented to primary care with symptoms of right heart failure and was found to have elevated N-terminal pro B-type natriuretic peptide of 2829 ng/L (normal value <125 ng/L). The patient was referred for urgent evaluation to the integrated heart failure service at our institution. Echocardiography revealed an enormous mobile mass attached to the right atrial septum, extending into the right ventricle and inferior vena cava measuring 90 × 42 mm. The patient underwent urgent surgical resection. Perioperative transoesophageal echocardiography demonstrated severe tricuspid regurgitation, which was treated with tricuspid annuloplasty ring. The patient made an uneventful recovery and was discharged. Subsequent imaging showed a reduction in right ventricular dimensions and improved systolic function. DISCUSSION: This case serves to remind us of the critical role of echocardiography in the diagnosis and management of people with breathlessness and raised natriuretic peptides. Therapies for heart failure are guided by ejection fraction, therefore timely and accurate diagnosis is critical. Moreover, as in this case, echocardiography can also identify other features of critical relevance to patient care.