Importance:Recurrent coronary events in patients with recent myocardial infarction remain a major clinical problem. Noninvasive measures of coronary atherosclerotic disease activity have the potential to identify individuals at greatest risk.Objective:To assess whether coronary atherosclerotic plaque activity as assessed by noninvasive imaging is associated with recurrent coronary events in patients with myocardial infarction.Design, Setting, and Participants:This prospective, longitudinal, international multicenter cohort study recruited participants aged 50 years or older with multivessel coronary artery disease and recent (within 21 days) myocardial infarction between September 2015 and February 2020, with a minimum 2 years' follow-up.Intervention:Coronary 18F-sodium fluoride positron emission tomography and coronary computed tomography angiography.Main Outcomes and Measures:Total coronary atherosclerotic plaque activity was assessed by 18F-sodium fluoride uptake. The primary end point was cardiac death or nonfatal myocardial infarction but was expanded during study conduct to include unscheduled coronary revascularization due to lower than anticipated primary event rates.Results:Among 2684 patients screened, 995 were eligible, 712 attended for imaging, and 704 completed an interpretable scan and comprised the study population. The mean (SD) age of participants was 63.8 (8.2) years, and most were male (601 [85%]). Total coronary atherosclerotic plaque activity was identified in 421 participants (60%). After a median follow-up of 4 years (IQR, 3-5 years), 141 participants (20%) experienced the primary end point: 9 had cardiac death, 49 had nonfatal myocardial infarction, and 83 had unscheduled coronary revascularizations. Increased coronary plaque activity was not associated with the primary end point (hazard ratio [HR], 1.25; 95% CI, 0.89-1.76; P = .20) or unscheduled revascularization (HR, 0.98; 95% CI, 0.64-1.49; P = .91) but was associated with the secondary end point of cardiac death or nonfatal myocardial infarction (47 of 421 patients with high plaque activity [11.2%] vs 19 of 283 with low plaque activity [6.7%]; HR, 1.82; 95% CI, 1.07-3.10; P = .03) and all-cause mortality (30 of 421 patients with high plaque activity [7.1%] vs 9 of 283 with low plaque activity [3.2%]; HR, 2.43; 95% CI, 1.15-5.12; P = .02). After adjustment for differences in baseline clinical characteristics, coronary angiography findings, and Global Registry of Acute Coronary Events score, high coronary plaque activity was associated with cardiac death or nonfatal myocardial infarction (HR, 1.76; 95% CI, 1.00-3.10; P = .05) but not with all-cause mortality (HR, 2.01; 95% CI, 0.90-4.49; P = .09).Conclusions and Relevance:In this cohort study of patients with recent myocardial infarction, coronary atherosclerotic plaque activity was not associated with the primary composite end point. The findings suggest that risk of cardiovascular death or myocardial infarction in patients with elevated plaque activity warrants further research to explore its incremental prognostic implications.

Background Uraemic cardiomyopathy is present in >70% of patients with end-stage renal disease (ESRD). Myocardial fibrosis is a hallmark of uraemic cardiomyopathy and is associated with an increased risk of heart failure and sudden cardiac death. Coronary microvascular dysfunction (CMD) is common in ESRD and is an adverse prognostic marker that may contribute to this increased mortality. In hypertrophic cardiomyopathy (HCM), a condition that shares phenotypical similarities with uraemic cardiomyopathy including hypertrophy, cellular disarray and fibrosis, a negative correlation exists between myocardial fibrosis and CMD, raising the possibility that fibrosis is the result of microvascular ischaemia. This study aimed to determine whether a similar relationship exists in ESRD. Methods 15 patients with ESRD underwent transthoracic echocardiography, coronary flow velocity reserve (CFVR) assessment by Doppler echocardiography and 3Tesla cardiac magnetic resonance imaging. Subjects with known coronary artery disease, moderate/severe valvular heart disease, diabetes and uncontrolled hypertension were excluded. Coronary microvascular dysfunction was defined using a cut-off value of CFVR<2. Myocardial fibrosis was assessed using native T1 times – with higher T1 values representing increased fibrosis. Basal septal, mid-septal and global native T1 times were calculated. T2 times, a marker of myocardial oedema, were also calculated. Results 5/15 (33%) subjects had CMD. Baseline data were similar between patients with and without CMD apart from higher calcium in the CMD group – table 1. There were no differences in echocardiographic parameters apart from global longitudinal strain which was lower in the CMD group (-17% ± 1 vs -20% ± 2, p=0.02). There were significant negative correlations between CFVR and basal septal (r= -0.7, p=0.003), mid-septal (r= -0.5, p=0.037) and global T1 times (r= -0.6, p=0.012) – figure 1. Basal septal T1 times were significantly elevated in subjects with CMD – median 1309ms (IQR 1301-1313) vs 1292ms (IQR 1281-1295), p=0.028. There was a trend towards increased mid-septal and global T1 times in the CMD group - figure 2 and table 2. There was no difference in T2 times between the groups. Conclusions This is the first study to show that, similar to HCM, increased myocardial fibrosis is associated with reduced CFVR in ESRD. Although causation cannot be demonstrated in this study, it raises the fascinating question of whether myocardial fibrosis is ‘the chicken or the egg’ in this inverse relationship. Further mechanistic studies are needed to confirm this association and to determine which is the primary pathology. It is likely that the interplay between myocardial fibrosis and CMD contributes to the significant cardiac mortality seen in ESRD. Conflict of Interest None to declare

Type of funding sources: Public Institution(s). Main funding source(s): BHF MRC Cardiac fibroblasts (cFbs) are responsible for deposition of extracellular matrix in the heart, providing support to the contracting myocardium and contributing to a myriad of physiological signalling processes. Prolonged and excessive activation of cFbs, via stimulation by transforming growth factor β (TGF-β), causes conversion of cFbs into myofibroblasts. Myofibroblasts are believed to cause pathological cardiac remodelling and to contribute to heart failure and arrhythmias. Reversion of myofibroblasts into cFbs has been demonstrated in rodent cells; it has yet to be explored in human cells. To characterise the effects of long-term 2D standard culture on the activation status of human cFbs. To identify the potential for human myofibroblasts to dedifferentiate back to cFbs. Primary human cFbs were cultured in Corning Costar flasks (Young’s modulus E = ∼3GPa) for up to 10 passages. Cells were subsequently plated onto dishes with a Young’s modulus of ∼3GPa, 25kPa and 2kPa in the presence or absence of TGF-β (10ng/ml) and/or TGF-β receptor I inhibitor SD208 (10nM) for up to 4 days. The proliferative capacity of the cells was assessed using the CyQUANT NF® assay. Cells were assessed for mRNA and protein expression of myofibroblast activation markers α-smooth muscle actin (α-SMA) and collagen-1 by qPCR and western blotting. The localised distribution of α-SMA was assessed by confocal microscopy. Human cardiac fibroblasts robustly expressed α-SMA. Proliferation was significantly decreased at 2kPa compared to higher Young’s moduli (mean percentage change over 2 days: 2kPa = 115.1, 25kPa = 191.4, 3GPa = 205.9, p < 0.0001). qPCR analysis revealed no significant changes in expression of myofibroblast gene markers α-SMA and collagen 1 at either ∼3GPa, 25kPa or 2kPa Young’s Moduli in the presence or absence of TGF-β treatment (median fold change (interquartile range [IQR]) versus control: TGF-β(α-SMA, 3GPa) = 1.226 (0.820); TGF-β(Collagen 1, 3GPa) = 1.636 (1.403); TGF-β(α-SMA, 25kPa) = 1.069 (7.030); TGF-β(Collagen 1, 25kPa) = 1.103 (0.411); TGF-β(α-SMA, 2kPa) = 0.800 (5.021); TGF-β(Collagen 1, 2kPa) = 1.629 (7.092); n = 2-3). These data was confirmed by western blotting (median relative protein expression (IQR) versus control: TGF-β(α-SMA, 3GPa) = 1.012 (0.500); TGF-β(Collagen 1, 3GPa) = 1.008 (1.466); TGF-β(α-SMA, 25kPa) = 1.321 (2.282); TGF-β(Collagen 1, 25kPa) = 0.944 (1.125); TGF-β(α-SMA, 2kPa) = 1.142 (0.705); TGF-β(Collagen 1, 2kPa) = 0.283 (1.127), p > 0.05; n = 2-3). TGF-β or SD208 treatment did not affect α-SMA expression when assessed by confocal microscopy. Long-term culture of human cFbs in 2D format leads to a robust and persistent activation of myofibroblasts that is unresponsive to TGF-ß activation or inhibition. Ongoing work is focussed on investigating whether human myofibroblast de-differentiation is possible.

Abstract Background National Institute of Clinical Excellence (NICE) guidelines recommend consideration of Chest X-rays (CXRs) in patients presenting with chest pain to exclude non-cardiac causes of chest pains. However, patients with ST-segment elevation myocardial infarction (STEMI) have a clear diagnosis, rendering the rationale for routine CXRs in this cohort of patients unclear. However, this remains a common practice across the health service. Methods We performed a retrospective study use of CXRs in consecutive patients admitted with STEMI undergoing primary percutaneous coronary intervention in a single UK tertiary cardiac center. We aimed to investigate if CXRs added clinical and diagnostic value by comparing routine vs. clinically indicated use. Results A total of 122 patients (Mean Age 63±12, 87% Male) were admitted with STEMI during the study period and 114/122 (93.4%) patients received at least one CXR during their in-patient stay. All but 2/114 were portable thus resource-intensive. Of these, 75/114 (65.8%) were routine while 39/114 (34.2%) were clinically indicated. Although CXRs were performed in almost all the patients, only 56/114 (49.1%) of patients had the findings of CXRs documented in the clinical records. The diagnostic efficacy for CXR abnormalities was significantly higher in the clinically indicated CXR group (76.9%) rather than the routine CXR group (2.7%) (p=<0.001). The therapeutic efficacy was 53.8% for clinically indicated CXRs, whereas the routine CXRs had a therapeutic efficacy of 1.3% (p=<0.001). There was a significant association between CXR findings and whether the CXR requested was routine or not (χ2(1)=70.07, p<0.001) and also management changes (χ2(1)=45.43, p<0.001). Conclusions Routine CXR in patient admitted with STEMI are often unnecessary and may add very little clinical value. On the other hand, selective post-procedural CXRs have a significantly higher diagnostic and therapeutic yield. Our study questions the rationale behind routine CXRs in the care of patients with STEMIs. Funding Acknowledgement Type of funding sources: None. Table 1

Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): (1) University Hospitals Birmingham Charity (2) Metchley Park Medical Society Introduction Coronary microvascular dysfunction (CMD) is common among patients with end-stage renal disease (ESRD) and confers poor prognosis. Coronary flow velocity reserve (CFVR) is a marker of coronary microvascular function and can be reliably measured using Doppler echocardiography. Reduced CFVR in ESRD has been attributed to factors such as hypertension and left ventricular hypertrophy (LVH). Anaemia is prevalent in ESRD but the association between haemoglobin and CFVR in ESRD has not been studied. Purpose To assess if CFVR is related to haemoglobin among patients with ESRD. Methods 22 subjects with ESRD and awaiting kidney transplant (8 pre-dialysis and 14 on peritoneal dialysis) were studied with adenosine myocardial contrast echocardiography, Doppler CFVR assessment and serum multiplex immunoassay analysis. Individuals with diabetes, uncontrolled hypertension or ischaemic heart disease were excluded. Results 7/22 (32%) of subjects had CMD (defined as CFVR <2). Age (47 years ± 15 vs 55 ± 10, p = 0.177), estimated glomerular filtration rate [7ml/min/1.73m² (5-11) vs 9 (7-10), p = 0.837], systolic blood pressure (129mmHg ± 25 vs 137 ± 20, p = 0.398) and left ventricular mass index (98g/m² ± 31 vs 98 ± 28, p = 0.936) did not significantly differ between subjects with or without CMD. There were no significant differences in other demographic, haemodynamic, laboratory or echocardiographic variables between the two groups. A panel of biomarkers of inflammation, myocardial stretch, cardiac fibrosis and LVH studied by multiplex immunoassay also did not show any significant differences between the two groups. No subjects had wall motion abnormalities or perfusion defects on myocardial contrast echocardiography. CFVR was significantly lower in subjects with CMD (1.6 ± 0.2 vs 3.2 ± 0.9, p < 0.001). Subjects with CMD had significantly lower haemoglobin than subjects without CMD (102g/L ± 12 vs 117g/L ± 11, p = 0.008). There was a moderate positive correlation between haemoglobin and CFVR (r = 0.65, p = 0.001) – figure 1. In a stepwise multiple regression model with CFVR as the dependent variable and age, haemoglobin, systolic blood pressure, left ventricular mass index and estimated glomerular filtration rate as independent variables, only haemoglobin was an independent predictor of CFVR (β=0.051 95%CI 0.023-0.079, p = 0.001). Conclusions Among our cohort of ESRD patients awaiting kidney transplant, there was a high prevalence of CMD despite well controlled blood pressure and no significant LVH. Subjects with CMD had significantly lower haemoglobin than subjects without CMD. Reduced haemoglobin causes impaired oxygen carrying capacity to the myocardium, which may lead to microvascular ischaemia and adverse microvascular remodelling, causing CMD. Thus, anaemia may be a potentially correctible driver of CMD in ESRD. This association needs to be confirmed in larger studies. Abstract Figure 1

Type of funding sources: None. Left ventricular systolic dysfunction (LVSD) is a common consequence of myocardial infarction (MI). Data from historic series identified LVSD in up to 60% of patients post-MI. However, in modern practice, with high-sensitivity cardiac biomarkers leading to early detection of MI and widespread use of early revascularization, the prevalence of LVSD in the acute phase of MI and its impact on subsequent clinical heart failure remains unknown. To ascertain the prevalence of LVSD on pre-discharge echocardiography and its impact on subsequent clinical heart failure after type 1 MI treated with percutaneous coronary intervention (PCI) in a UK tertiary cardiac centre. A retrospective electronic patient records review of consecutive patients with type 1 MI treated with PCI between January 2016 - December 2017. Patients treated conservatively or with surgical revascularization were excluded. 1000 consecutive patients were identified and 948/1000 who had an inpatient echocardiogram prior to discharge were included in this analysis – 413 ST elevation MI (STEMI) and 535 non-ST elevation (NSTEMI). Median door to balloon time for STEMI was 42 minutes (IQR 28-79). Median time from symptom onset to intervention for NSTEMI was 3 days (IQR 1-6). LVSD was defined as left ventricular ejection fraction (LVEF) <50% on transthoracic echocardiogram carried out during the hospital episode. LVSD was significantly more prevalent in patients with STEMI compared to NSTEMI (37.4% vs 17.3%, p < 0.001). Median LVEF was significantly lower in the STEMI population (55%, IQR 45-60) compared to patients with NSTEMI (60%, IQR 54-65), p < 0.001. However, rates of clinical heart failure at index presentation with MI did not vary significantly between STEMI and NSTEMI patients (6.1% vs 4.9%, p = 0.414). In stepwise multivariate regression models: age, peak troponin and previous coronary artery bypass grafting were predictors of LVEF, whereas LVEF and previous MI were predictors of clinical heart failure Patients with LVSD on pre-discharge echocardiography had significantly higher rates of 30-day readmission with heart failure (2.9% vs 0.7%, p = 0.017), 30-day all-cause mortality (6.1% vs 2%, p = 0.001), 30-day cardiac mortality (5.7% vs 1%, p < 0.001) and 2-year all-cause mortality (5.7% vs 1.6%, p = 0.001). However, at 2-years, there was no difference in hospital readmission with heart failure (0.8% vs 0.3%, p = 0.276). There were no significant differences between STEMI and NSTEMI patients for these endpoints. Early revascularisation with PCI has led to a reduction in the prevalence of early LVSD post-MI compared to historical data. However, the presence of LVSD remains a powerful predictor of adverse clinical outcomes. Despite lower rates of LVSD on pre-discharge echocardiography in patients with NSTEMI compared with STEMI, the incidence of subsequent clinical heart failure is similar. This however may be underestimated due to survival bias.

Previous studies of the incidence and severity of mitral regurgitation (MR) following acute myocardial infarction (MI) were limited by the study population (ST-elevation MI only), by diagnostic methods (lack of multiparametric quantification), or by the time-frame of study (late assessment post-MI). The true incidence of ischaemic MR (IMR) immediately following type 1 MI [non-ST-elevation (NSTEMI) and ST-elevation (STEMI)] patients in the modern era of universal early revascularisation remains unclear. Since even mild IMR confers a poor prognosis, factors which promote or protect against the development of MR require further evaluation. To determine the incidence, clinical and angiographic characteristics of patients with IMR following type 1 MI treated with PCI. This was a single-centre study of 1000 consecutive, prospectively recruited patients admitted to the Queen Elizabeth Hospital Birmingham with type 1 MI who underwent PCI. Early inpatient transthoracic echocardiography (TTE) was performed by accredited echocardiographers using standard multiparametric quantification. MR was observed in 294/1000 patients (29.4%) post-MI, graded as mild (76%), moderate (21%) and severe (3%). Median time from symptom onset to PCI was 1 day (IQR 0–4) and to TTE 2 days (IQR 1–3). Compared to patients without MR (MR-), those with MR (MR+) were older (73±12 years vs 66±13 years; p<0.001), male (75% vs 64%; p<0.001) and more likely to have a history of hypertension (HTN) (63% vs 55%; p=0.0117), heart failure (HF) (3.4% vs 1.1%; p=0.0140) and previous MI (28% vs 20%; p<0.005). MR+ patients more frequently presented with HF (8.5% vs 4.2%; p=0.0075), lower LV ejection fraction (LVEF) (50±14% vs 55±11%; p<0.001) and higher peak high sensitivity troponin T (765ng/L, IQR 170–3032 vs 400ng/L, IQR 51–1966; p<0.0001). MR+ patients were more likely to have severe disease in the left circumflex (LCx) (50% vs 33%; p<0.0001) or right coronary artery (RCA) (51% vs 43%; p=0.0135). Incidence of severe disease in the left main stem and left anterior descending artery (LAD) did not significantly differ between the two groups. Incidence of MR was equal (29%) amongst STEMI (126/431) and NSTEMI (168/569) patients. While the time to revascularisation did not affect the prevalence of MR following STEMI (linear regression analysis of door-to-balloon time in MR+ and MR- patients p=0.843), NSTEMI patients were more likely to develop MR if revascularisation was delayed (linear regression analysis of symptom onset to PCI time MR+ vs MR- p=0.061). Almost 1/3 of patients with type 1 MI undergoing revascularisation have MR evident on pre-discharge TTE. Factors promoting MR include older age, male sex, HTN, HF, larger non-LAD territory infarct, and depressed LVEF. The incidence of MR following STEMIs and NSTEMIs is equal. Earlier revascularisation is unlikely to reduce MR in STEMI patients but may improve MR prevalence following NSTEMI. Type of funding source: None

Abstract Introduction Echocardiography is essential for the management of patients with atrial fibrillation (AF), but current methods are time consuming and lack any evidence of reproducibility. Purpose To compare conventional averaging of consecutive beats with an index beat approach, where systolic and diastolic measurements are taken once after two prior beats with a similar RR interval (not more than 60 ms difference). Methods Transthoracic echocardiography was performed using a standardized and blinded protocol in patients enrolled into the RAte control Therapy Evaluation in permanent AF randomised controlled trial (RATE-AF; NCT02391337). AF was confirmed in all patients with a preceding 12-lead ECG. A minimum of 30-beat loops were recorded. Left ventricular function was determined using the recommended averaging of 5 and 10 beats and using the index beat method, with observers blinded to clinical details. Complete loops were used to calculate the within-beat coefficient of variation (CV) and intraclass correlation coefficient (ICC) for Simpson's biplane left ventricular ejection fraction (LVEF), global longitudinal strain (GLS) and filling pressure (E/e'). Results 160 patients (median age 75 years (IQR 69–82); 46% female) were included, with median heart rate 100 beats/min (IQR 86–112). For LVEF, the index beat had the lowest CV of 32% compared to 51% for 5 consecutive beats and 53% for 10 consecutive beats (p<0.001). The index beat also had the lowest CV for GLS (26% versus 43% and 42%; p<0.001) and E/e' (25% versus 41% and 41%; p<0.001; see Figure for ICC comparison). Intra-operator reproducibility, assessed by the same operator from two different recordings in 50 patients, was superior for the index beat with GLS bias −0.5 and narrow limits of agreement (−3.6 to 2.6), compared to −1.0 for 10 consecutive beats (−4.0 to 2.0). For inter-operator variability, assessed in 18 random patients, the index beat also showed the smallest bias with narrow confidence intervals (CI). Using a single index beat did not impact on the validity of LVEF, GLS or E/e' measurement when correlated with natriuretic peptides. Index beat analysis substantially shortened analysis time; 35 seconds (95% CI 35 to 39 seconds) for measuring E/e' with the index beat versus 98 seconds (95% CI 92 to 104 seconds) for 10 consecutive beats (see Figure). Conclusion Index beat determination of left ventricular function improves reproducibility, saves time and does not compromise validity compared to conventional quantification in patients with heart failure and AF. After independent validation, the index beat method should be adopted into routine clinical practice. Comparison for measurement of E/e' Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Institute of Health Research UK

Abstract Background Ischaemic mitral regurgitation (IMR) confers a poor prognosis. Transcatheter intervention may improve survival but benefit is likely to depend on severity of IMR relative to LV remodelling following myocardial infarction (MI). In theory, those with “discordant” IMR (significant regurgitant volume without severe LV dilatation or impairment), are expected to benefit most from mitral intervention. While subcategorization may help to inform treatment, there are no data on post-MI patients in this respect. Purpose To determine the incidence of discordant & concordant IMR categorised on echocardiography post-MI and impact on outcomes. Methods 1000 consecutive patients admitted to our hospital with myocardial infarction who underwent coronary angioplasty were included. Early inpatient TTE was performed by accredited echocardiographers using standard multiparametric quantification. Using TTE parameters, 4 subgroups were identified (figure) according to the degree of MR relative to LV remodelling. Thresholds were based on European guidelines (± 2SD from normal) and median value among survivors for vena contracta (VC): – LVEF: 52% (♂), 54% (♀) – Indexed LV end diastolic volume (LVEDVi): 74ml/m2 (♂), 61ml/m2 (♀) – Effective regurgitant orifice area (EROA) ≥0.2cm2 – Regurgitant volume (RVol) ≥30ml – VC ≥0.5cm Results MR was seen in 294/1000 patients (29.4%) with a severity of mild (76%), moderate (21%) and severe (3%). Concordant and discordant IMR were each seen in 16/294 (5%) of IMR patients post-MI. After a mean follow up of 3.2 years, IMR patients had a 3% rate of heart failure (HF) within 1 year and 19% mortality. Non-survivors had significantly worse IMR (PISA 0.65±0.25cm vs 0.54±0.19cm; p=0.033; VC 0.63±0.25cm vs 0.49±0.18cm; p=0.014), worse LV function (LVEF 44±17% vs 51±13%; p<0.001), larger LV (LVEDVi 67±23ml/m2 vs 60±22ml/m2; p=0.032) and larger indexed LA volume (LAVi) (44±22ml vs 35±15ml; p<0.001). Those with concordant IMR had the worst survival (50%) although almost 1 in 5 of those with discordant MR died within the follow up period (19%). Using multivariable Cox regression, significant predictors of mortality included LVEF (p<0.001; HR 0.96, 0.94–0.98) and LAVi (p<0.001; HR 1.02, 1.01–1.03) but not LVEDVi. Conclusion 1) Significant predictors of mortality in IMR include LA dilatation and decline in LVEF, but not LV dilatation. 2) Although discordant severe IMR is uncommon following MI, mortality if left untreated remains high. Attention should be paid to early selection of this cohort for intervention. Funding Acknowledgement Type of funding source: None

Abstract Background National Institute of Clinical Excellence guideline (NICE, CG95) recommends CTCA as a 1st line diagnostic test for evaluation of ambulatory patients with suspected stable angina based on its high sensitivity and low cost. This has led to increasing demand for CTCA across the National Health Service (NHS) in order to comply with the NICE recommendation. Purpose We studied the utility and effectiveness of CTCA in the evaluation of ambulatory patients with suspected stable angina attending rapid access chest pain clinic (RACPC) in a large tertiary hospital in the UK. Methods The study included consecutive patients attending RACPC over a pre-specified period of 6-months who were suspected of having stable angina and hence, referred for CTCA. The data were collected on demographics, CTCA results including incidental finding and downstream investigations. All patients had a minimum of 12-months follow up for clinical outcomes. Results A total of 170 patients were referred for CTCA (mean age = 56.8 years, male = 53.5%) out of the 388 consecutive patients who were reviewed in the RACPC during the 6-month period. CTCA was non-diagnostic in 48/170 (28.2%) cases (Breathing artefact 35%, Severe Coronary Calcification 31%, Elevated heart rate/Ectopy 30%) while 63/170 (37.1%) of patients had incidental extra-cardiac findings. Amongst patients with incidental findings, 17/63 (27.0%) underwent further investigations. A total of 54/170 (31.7%) of patients were recommended to have downstream cardiac investigations such as a stress test (DSE/MRI/MPS) (23/170, 15.8%) while 31/170 (18.2%) were referred for invasive coronary angiography. Revascularisation procedures (PCI n=7.6%, CABG n=4.7%) were required in 21/170 (12.4%) patients. Based on 2017 NHS tariffs, overall average cost-per-patient with the initial CTCA approach was £122.11 excluding downstream investigations and £548.43 including the cost of downstream cardiac investigations. Incidental Findings after CTCA Conclusions Our study suggests that a CTCA based approach is associated with non-diagnostic information in at least 1:4 patients and incidental extracardiac findings in 1:3 patients. Further downstream cardiac investigations are required in around 1:3 patients after a CTCA carried out for evaluation suspected stable angina. The NICE recommendation is based on the low initial cost of CTCA and high sensitivity, however, taking in to account the additional cost of downstream investigations, the average cost per patient of this approach is significantly (4.5 times) higher. Acknowledgement/Funding None

A 30 year old asymptomatic male with stage 3 chronic kidney disease (CKD) secondary to Focal Segmental Glomerulosclerosis was found to have features of CKD associated cardiomyopathy including left ventricular hypertrophy (LVH) and focal sub-endocardial scarring on cardiac magnetic resonance imaging. There was also a significantly raised CT coronary calcium score and evidence of non-flow limiting coronary artery disease (CAD) on a CT coronary angiogram. Early stage CKD is a major risk factor for cardiovascular risk causing myocardial hypertrophy and fibrosis and coronary artery atheroma. Cardiovascular risk begins to increase from an eGFR of around 75ml/min/1.73m2. The pathophysiology of cardiovascular disease in CKD is under investigation but to date, treatment options are limited. Blood pressure control and statins have the strongest supportive evidence.

Background The role of glycoprotein IIb/IIIa inhibitors (GPI) in primary PCI (PPCI) remains uncertain. We aim to compare patient outcomes between routine and selective GPI usage strategies. Methods All consecutive PPCIs in England between January 2009 and April 2015 were prospectively recorded in the BCIS database. The cohort was divided into routine and selective GPI usage groups based on the responsible consultant’s (RC) strategy. The primary endpoint was all-cause mortality, which was compared using Cox regression analyses. Results We assessed 110327 PPCIs. Routine compared to selective GPI usage (defined as GPI used in ≥75% and≤25% PPCIs performed by RC, respectively) was associated with significantly decreased Kaplan-Meier estimated rates for all-cause mortality at one year of 9.7% vs 11.0% (p Conclusion A strategy of routine GPI usage in patients undergoing PPCI was associated with lower all-cause mortality as compared to selective GPI usage.

OBJECTIVE:Variability in the measurement of left ventricular (LV) parameters in cardiovascular imaging has typically been assessed over a short time interval, but clinicians most commonly compare results from studies performed a year apart. To account for variation in technical, procedural and biological factors over this time frame, we quantified the within-subject changes in LV volumes, LV mass (LVM) and LV ejection fraction (EF) in a well-defined cohort of healthy adults at 12 months. METHODS:Cardiac MR (CMR) was performed in 42 healthy control subjects at baseline and at 1 year (1.5 T Magnetom® Avanto; Siemens Healthcare, Erlangen, Germany). Analysis of steady-state free precession images was performed manually offline (Argus software; Siemens Healthcare) for assessment of LV volumes, LVM and EF by a single blinded observer. A random subset of 10 participants also underwent repeat imaging within 7 days to determine short-term interstudy reproducibility. RESULTS:There were no significant changes in any LV parameter on repeat CMR at 12 months. The short-term interstudy biases were not significantly different from the long-term changes observed at 1 year. The smallest detectable change (SDC) for LVEF, end-diastolic volume, end-systolic volume and LVM that could be recognized with 95% confidence were 6%, 13 ml, 7 ml and 6 g, respectively. CONCLUSION:The variability in CMR-derived LV measures arising from technical, procedural and biological factors remains minimal at 12 months. Thus, for patients undergoing repeat annual assessment by CMR, even small differences in LV function, size and LVM (which are greater than the SDC) may be attributed to disease-related factors. ADVANCES IN KNOWLEDGE:The reproducibility and reliability of CMR data at 12 months is excellent allowing clinicians to be confident that even small changes in LV structure and function over this time frame are real.

Background: Poor quality cardiopulmonary resuscitation (CPR) predicts adverse outcome. During invasive cardiac procedures automated-CPR (A-CPR) may help maintain effective resuscitation. The use of A-CPR following in-hospital cardiac arrest (IHCA) remains poorly described.Aims & methods: Firstly, we aimed to assess the efficiency of healthcare staff using A-CPR in a cardiac arrest scenario at baseline, following re-training and over time (Scenario-based training). Secondly, we studied our clinical experience of A-CPR at our institution over a 2-year period, with particular emphasis on the details of invasive cardiac procedures performed, problems encountered, resuscitation rates and in-hospital outcome (AutoPulse-CPR Registry).Results: Scenario-based training: Forty healthcare professionals were assessed. At baseline, time-to-position device was slow (mean 59 (+/- 24) s (range 15-96 s)), with the majority (57%) unable to mode-switch. Following re-training time-to-position reduced (28 (+/- 9) s, p < 0.01 vs baseline) with 95% able to mode-switch. This improvement was maintained over time. AutoPulse-CPR Registry: 285 patients suffered IHCA, 25 received A-CPR. Survival to hospital discharge following conventional CPR was 28/260 (11%) and 7/25 (28%) following A-CPR. A-CPR supported invasive procedures in 9 patients, 2 of whom had A-CPR dependant circulation during transfer to the catheter lab.Conclusion: A-CPR may provide excellent haemodynamic support and facilitate simultaneous invasive cardiac procedures. A significant learning curve exists when integrating A-CPR into clinical practice. Further studies are required to better define the role and effectiveness of A-CPR following IHCA. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

Introduction Feature-tracking (FT) analysis offers a novel, fast and practicable method to calculate strain from routinely acquired steady state free precession (SSFP) images without the need to perform additional tagged sequences. There is no validation of this technique, however, against a reference standard myocardial tagging analysis for any strain parameter other than mid-left ventricular whole slice circumferential strain. In an adult study of patients with dilated cardiomyopathy (DCM) and healthy controls, we sought to validate the FT method (TomTec Imaging systems, Munich) against spatial modulation of magnetisation (SPAMM) tissue tagging analysis (Cardiac Image Modelling Package (CIMTag2D), University of Auckland) for the computation of long axis function. Methods We compared measures of global longitudinal strain from the horizontal long axis view using the two techniques in 45 patients (mean age 44±14 years, male 63%). Normal healthy adults (n=35) were identified from an ongoing prospective, observational research study examining the effects of living kidney donation on cardiovascular structure and function (NCT01028703). Consecutive DCM patients (n=10) were identified after undergoing myocardial tagging for clinically indicated scans. Retrospective off-line analysis was performed on matched tagged and SSFP slices by two independent blinded observers (WEM and RJT). After manually drawing endocardial borders in the end-diastolic frame for each image, the FT software automatically propagated the contour and followed its features (brightness gradient at the tissue-cavity interface, dishomogeneties of the tissue, spatial coherence) throughout the remainder of the cardiac cycle to compute longitudinal strain parameters. Results Longitudinal strain (Ell). Peak systolic FT-Ell (−18.1±5.0%) correlated most strongly with CIMTag-Ell values derived from the subendocardium (−16.7±4.8%) with a Pearson9s correlation coefficient of 0.70 (p<0.001; figure 1A). A Bland Altman plot (figure 1B) showed good agreement with only a small systematic overestimation from FT (mean difference 1.3±3.8%, p=0.03). Whilst in DCM patients peak systolic global Ell values were not significantly different between the two techniques (−9.7±4.5% vs −8.8±3.9%, p=0.44), among healthy controls there was a small but significant difference in Ell values between FT and tagging image analysis (−19.5±3.5% vs −18.0±3.5%, p=0.04; figure 2). Longitudinal strain rate (SR) There was good agreement between the two techniques for peak systolic global longitudinal SR values but with a small tendency towards higher FT values as compared with tagging (mean difference 0.09±0.26 1/s, p=0.04; r=0.64, p<0.001). The weakest correlation between the two techniques was for early diastolic global longitudinal SR but even this relationship was still highly significant (mean difference 0.09±0.26 1/s; r=0.42, p=0.007). Reproducibility testing Intraobserver and interobserver variability for FT-Ell analysis was small (−0.49±1.83% and 0.22±1.13%, respectively). Timed analysis The average time taken for post-processing strain analysis using FT software was significantly less than that required for CIMTag (5.9±0.8 min vs 23.2±3.5 min, p<0.0001). Conclusions FT based assessment of longitudinal strain correlated highly with values derived from tagged images in a population with a wide range of left ventricular function. Furthermore, FT can be performed without the need for additional imaging and lengthy post-processing times.

Patients with chronic kidney disease (CKD) and renal transplant recipients (RTR) have increased cardiovascular risk. The value of measuring central pulse pressure (cPP) over brachial pulse pressure (pPP) is not known. Central PP was measured in 597 patients (364 CKD: 233 RTR). In multivariate analysis, age and female gender positively correlated with cPP; heart rate and estimated glomerular filtration rate negatively correlated with cPP. Associations for age, heart rate and gender persisted after additional adjustment for pPP and aortic wave reflection. This model accounted for 91% of the variability in cPP, with pPP alone accounting for 74%. Results were similar when both patient groups were analysed separately. A subset of patients with CKD had aortic pulse wave velocity (PWV) and left ventricular mass index (LVMI) measured. There were no differences in the univariate correlations between PWV (r = 0.368 vs 0.315; P = 0.4) or LVMI (r = 0.125 vs 0.163; P = 0.7); nor in the multivariate models created for PWV (P = 0.1) or LVMI (P = 0.1) when either cPP or pPP were used. This study demonstrates that in these patients most of the variability in cPP can be explained by pPP. Additionally, cPP does not appear to provide additional information beyond pPP in determining PWV and LVMI.

Raised serum uric acid levels are associated with increased cardiovascular risk in many patient groups, including those with chronic kidney disease. Mineralocorticoid receptor antagonists are showing great promise as a means of lowering cardiovascular risk in patients with chronic kidney disease; yet their actions on serum uric acid are not known. The present study examined the actions of the mineralocorticoid receptor antagonist spironolactone on serum uric acid in patients with early chronic kidney disease.