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Introduction A large number of important clinical trials in cardiology were published or presented at major international conferences during 2019. This paper aims to offer a concise overview of these significant advances and to put them into clinical context. Methods Trials presented at the major international cardiology meetings during 2019 were reviewed including The American College of Cardiology (ACC), Euro PCR, The European Society of Cardiology (ESC), Transcatheter Cardiovascular Therapeutics (TCT), and the American Heart Association (AHA). In addition to this a literature search identified several other publications eligible for inclusion based on their relevance to clinical cardiology, their potential impact on clinical practice and on future guidelines. Results A total of 70 trials met the inclusion criteria. New interventional and structural data include trials examining use of drug-coated balloons in patients with acute myocardial infarction (MI), interventions following shockable cardiac arrest, mechanical circulatory support in cardiogenic shock complicating MI, intervention in stable coronary artery disease, surgical or percutaneous revascularisation strategies in left main coronary artery disease, revascularisation strategy in ST elevation MI, transcatheter aortic valve replacement in low-risk patients, and percutaneous mitral or tricuspid valve interventions. Preventative cardiology data included the use of sodium–glucose cotransporter 2 (SGLT2) inhibitors (dapagliflozin), proprotein convertase subtilisin–kexin type 9 (PCSK9) inhibitors (evolocumab), bempedoic acid, and novel approaches to the management of hypertension. Antiplatelet data included trials evaluating both the optimal length of course and combination of antiplatelet agents and regimes including combination antithrombotic therapies for patients with atrial fibrillation. Heart failure data included trials of sacubitril–valsartan in heart failure with preserved ejection fraction and the use of SGLT2 inhibitors in patients with heart failure but without diabetes. Electrophysiology data included trials examining alcohol in atrial fibrillation and the use of wearable fitness devices for identifying atrial fibrillation. Conclusion This article presents key clinical trials completed during 2019 and should be valuable to clinicians and researchers working in cardiology.

Background: Improvements in drug-eluting stent design have led to a reduced frequency of repeat revascularisation and new biodegradable polymer coatings may allow a shorter duration of dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI). Aims: The Improved Drug-Eluting stent for All-comers Left Main (IDEAL-LM) study aims to investigate long-term clinical outcomes after implantation of a biodegradable polymer platinum-chromium everolimus-eluting stent (BP-PtCr-EES) followed by 4 months DAPT compared to a durable polymer cobalt-chromium everolimus-eluting stent (DP-CoCr-EES) followed by 12 months DAPT in patients undergoing PCI of unprotected left main coronary artery (LMCA) disease. Methods: This is a multicentre randomised clinical trial study in patients with an indication for coronary artery revascularisation who have been accepted for PCI for LMCA disease after Heart Team consultation. Patients were randomly assigned in a 1:1 ratio to receive either the BP-PtCr-EES or the DP-CoCr-EES. The primary endpoint was a non-inferiority comparison of the rate of major adverse cardiovascular events (MACE), defined as all-cause death, myocardial infarction, or ischaemia-driven target vessel revascularisation at 2 years. Results: Between December 2014 and October 2016, 818 patients (410 BP-PtCr-EES and 408 DP-CoCr-EES) were enrolled at 29 centres in Europe. At 2 years, the primary endpoint of MACE occurred in 59 patients (14.6%) in the BP-PtCr-EES group and 45 patients (11.4%) in the DP-CoCr-EES group; 1-sided upper 95% confidence interval (CI) 7.18%; p=0.04 for non-inferiority; p=0.17 for superiority. The secondary endpoint event of BARC 3 or 5 bleeding occurred in 11 patients (2.7%) in the BP-PtCr-EES group and 2 patients (0.5%) in the DP-CoCr-EES group (p=0.02). Conclusions: In patients undergoing PCI of LMCA disease, after two years of follow-up, the use of a BP-PtCr-EES with 4 months of DAPT was non-inferior to a DP-CoCr-EES with 12 months of DAPT with respect to the composite endpoint of all-cause death, myocardial infarction or ischaemia-driven target vessel revascularisation.

Over the course of 2021, numerous key clinical trials with valuable contributions to clinical cardiology were published or presented at major international conferences. This review seeks to summarise these trials and reflect on their clinical context.The authors reviewed clinical trials presented at major cardiology conferences during 2021 including the American College of Cardiology (ACC), European Association for Percutaneous Cardiovascular Interventions (EuroPCR), European Society of Cardiology (ESC), Transcatheter Cardiovascular Therapeutics (TCT), American Heart Association (AHA), European Heart Rhythm Association (EHRA), Society for Cardiovascular Angiography and Interventions (SCAI), TVT-The Heart Summit (TVT) and Cardiovascular Research Technologies (CRT). Trials with a broad relevance to the cardiology community and those with potential to change current practice were included.A total of 150 key cardiology clinical trials were identified for inclusion. Interventional cardiology data included trials evaluating the use of new generation novel stent technology and new intravascular physiology strategies such as quantitative flow ratio (QFR) to guide revascularisation in stable and unstable coronary artery disease. New trials in acute coronary syndromes focused on shock, out of hospital cardiac arrest (OOHCA), the impact of COVID-19 on ST-elevation myocardial infarction (STEMI) networks and optimal duration/type of antiplatelet treatment. Structural intervention trials included latest data on transcatheter aortic valve replacement (TAVR) and mitral, tricuspid and pulmonary valve interventions. Heart failure data included trials with sodium-glucose cotransporter 2 (SGLT2) inhibitors, sacubitril/valsartan and novel drugs such as mavacamten for hypertrophic cardiomyopathy (HCM). Prevention trials included new data on proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. In electrophysiology, new data regarding atrial fibrillation (AF) screening and new evidence for rhythm vs. rate control strategies were evaluated.This article presents a summary of key clinical cardiology trials published and presented during the past year and should be of interest to both practising clinicians and researchers.

Background There is little evidence on how the occurrence of a bleed in individuals on vitamin K antagonists (VKAs) impacts the risk of subsequent bleeds, and thromboembolic and ischemic events. Such information would help to inform treatment decisions following bleeds. Objective To estimate the impact of bleeding events on the risk of subsequent bleeds, venous thromboembolism (VTE), stroke, and myocardial infarction (MI) among patients initiating VKA treatment for new-onset nonvalvular atrial fibrillation (NVAF). Methods We conducted an observational cohort study using a linked Clinical Practice Research Datalink—Hospital Episode Statistics dataset. Among a cohort of individuals with NVAF, the risk of clinically relevant bleeding, VTE, stroke, and MI was compared between the period prior to the first bleed and the periods following each subsequent bleed. The rate and cost of general practitioner (GP) consultations, prescriptions, and hospitalizations were also compared across these periods. Results The risk of clinically relevant bleeding events was observed to be elevated at least twofold in all periods following the first bleeding event. The risk of VTE, stroke, and MI was not found to differ according to the number of clinically relevant bleeding events. The rate and cost of GP consultations, GP prescriptions, and hospitalizations were increased in all periods relative to the period prior to the first bleed. Conclusions The doubling in the risk of bleeding following the first bleed, taken alongside the stable risk of MI, VTE, and stroke, suggests that the risk–benefit balance for VKA treatment should be reconsidered following the first clinically relevant bleed.

Background/introduction Chronic kidney disease (CKD) is a risk factor for contrast induced acute kidney injury (CI-AKI). Contrast angiography in CKD patients is a common procedure. Creatinine is a delayed marker of CI-AKI and delays diagnosis which results in significant morbidity and mortality. Aim Early diagnosis of CI-AKI requires validated novel biomarkers. Design A prospective observation study of 301 consecutive CKD patients undergoing coronary angiography was performed. Methods Samples for plasma neutrophil gelatinase-associated lipocalin (NGAL), serum liver fatty acid-binding protein (L-FABP), serum kidney injury marker 1, serum interleukin 18 and serum creatinine were taken at 0, 1, 2, 4, 6 and 48 h post-contrast. Urinary NGAL and urinary cystatin C were collected at 0, 6 and 48 h. Incidence of major adverse clinical events (MACE) was recorded at 1 year. CI-AKI was defined as an absolute delta rise in creatinine of ≥26.5 µmol/l or a 50% relative rise from baseline at 48 h following contrast. Results CI-AKI occurred in 28 (9.3%) patients. Plasma NGAL was most predictive of CI-AKI at 6 h. L-FABP performed best at 4 h. A combination of Mehran score > 10, 4 h L-FABP and 6 h NGAL improved specificity to 96.7%. MACE was statistically higher at 1 year in CI-AKI patients (25.0 vs. 6.2% in non-CI-AKI patients). Discussion/conclusion Mehran risk score, 4 h serum L-FAPB and 6 h plasma NGAL performed best at early CI-AKI prediction. CI-AKI patients were four times more likely to develop MACE and had a trebling of mortality risk at 1 year.

Background Thin stent struts may be associated with reduced vessel injury and use of biodegradable polymers may further improve long term outcomes. However, data with earlier stents has been inconsistent; thus further studies with newer devices are needed. Purpose To evaluate the efficacy and safety of a new ultra-thin (65um) strut cobalt chromium sirolimus-eluting stent with a hybrid design (closed cell at ends and open cells in middle to reduce edge injury and optimise conformability) in all-comers patients undergoing percutaneous coronary intervention (PCI). Methods We enrolled 752 patients from 14 sites undergoing PCI into a prospective, non-randomised, multi-centre, open-label, observational registry. Inclusion of patients with complex anatomy (long stent lengths, bifurcations and chronic total occlusions) was encouraged. Clinical follow-up was scheduled at 1, 9, 12 and 24 months. The primary endpoint was incidence of major adverse cardiac events (MACE) - cardiac death, non-fatal myocardial infarction (MI), or target vessel revascularization (TVR) - at 9 months. Results Mean patient age was 64.7±12.2 years, 20.7% had diabetes, 58.8% had dyslipidaemia, 40.4% had multi-vessel disease, 22% had previous PCI, 4.7% had previous coronary-artery bypass graft, and 19.6% had a clinical history of previous MI. Mean lesion length was 25.7±17.3 mm. The primary endpoint of cumulative MACE up to 9 months (from 624 patients reaching 9 months follow-up) occurred in 12 patients (1.92%), including 6 (0.96%) cardiac death, 5 (0.80%) MI and 6 (0.96%) clinically indicated TVR. Definite stent thrombosis was reported in 3 patients (0.48%) and probable stent thrombosis in 2 patients (0.32%). Conclusions Use of an ultra-thin strut biodegradable polymer sirolimus-eluting stent in all-comers patients undergoing PCI was associated with good clinical efficacy and safety. Acknowledgement/Funding Meril Life

Aims Thinner stent struts may improve deliverability, conformability and reduce vessel injury. We report the first clinical outcomes of the thinner strut (84–88um) cobalt chromium biolimus eluting stent from the Biomatrix Alpha registry and compare these with objective performance criteria from the stainless steel BioMatrix Flex arm of the Leaders study. Methods A total of 1257 patients were studied: 400 patients from 12 centres receiving ≥1 Biomatrix Alpha stent were prospectively enrolled into the Biomatrix Alpha registry and then underwent a pre-specified comparison with 857 patients who received a Biomatrix Flex stent in the Leaders study. The primary endpoint was major adverse cardiac events (MACE) defined as the composite of cardiac death, myocardial infarction (MI) or clinically driven target vessel revascularization (TVR) at 9 months. Assuming a 9.2% event rate with BioMatrix Flex, a one-sided type I error (α) of 0.05, and a 4% non-inferiority margin, a sample size of 400 in the Biomatrix alpha registry had >80% power to conclude non-inferiority. Results Baseline characteristics in the Alpha registry were typical of an all-comers population with a mean age of 64.7±11.3, diabetes 19%, current smoking 21%, dyslipidemia 57%, hypertension 57%, total stent length per lesion 25.49±13.45, mean stents per procedure 1.59±0.88 and overlapping stents in 13.4%. Observed MACE at 9 months with Alpha was 3.94% (upper limit 5.98%) vs. 9.28% MACE rate with Flex stents in Leaders, which met pre-specified criteria for non-inferiority (p While both Alpha and Leaders enrolled all-comers, Alpha included longer total stent length per lesion (25.49 vs 23.85mm, p Conclusion The thinner strut (84–88um) cobalt chromium Biomatrix Alpha stent demonstrated low MACE rates at 9 months which were non-inferior to MACE outcomes with the stainless steel Biomatrix Flex in the Leaders study. The robustness of this finding was further confirmed by a propensity score analysis. Acknowledgement/Funding Biosensors

Background/Introduction Contrast induced acute kidney injury (CI-AKI), defined as a delta rise in creatinine of >26.5 µmol/L or a 50% relative rise within 48 hours following iodinated contrast, is associated with considerable mortality risk. Our previous study of 301 consecutive Chronic Kidney Disease (CKD) patients undergoing contrast coronary angiography/percutaneous coronary intervention (PCI) highlighted a CI-AKI rate of 9.3% at index procedure. Few studies have looked at long term prognosis, adverse events and mortality following CI-AKI. Objective Our objective was to assess the 5 year mortality rate following contrast coronary angiography and to evaluate independent risk factors and presence of index CI-AKI on 5 year mortality. Methods A prospective cohort study in a single cardiology centre in the UK was carried out from 2011–2013, the results of which have been previously published. In total 2,519 patients were screened, 321 (12.7%) of which had CKD, which was defined as a Glomerular Filtration Rate (GFR) of Results At 5 years follow up data was available for 292 (97%) of the original 301 patients. Type 2 diabetes, contrast volume, Mehran risk score, lower glomerular filtration rate (GFR) and use of intravenous fluids at index procedure were independently associated with five year mortality, p Conclusions This study highlights that index CI-AKI is an independent risk factor for 5 year mortality and MACE. Several risk factors act independently as surrogate markers of CI-AKI prior to administration of iodinated contrast, many of which are incorporated in the Mehran CI-AKI risk score. Furthermore, these are associated with adverse incidents and mortality at five years following index contrast procedure. A combination approach of these findings, including novel biomarkers as previously demonstrated, will help to reduce risk and identify early CI-AKI to facilitate timely therapeutic intervention. Table 1 highlights the 5 year mortality and MACE data in patients with and without baseline CI-AKI, showing a significantly higher proportion of patients with baseline CI-AKI developing mortality or MACE following index contrast. Table 2 illustrates predictability of index biomarker results for 5 year mortality, showing a statistically significant prediction across all biomarkers.

Introduction Contrast induced acute kidney injury (CI-AKI), currently defined as a delta rise in serum creatinine of ≥26.5 µmol/litre or a relative rise of ≥50% from baseline measured at 48 hours following administration of iodinated contrast media, is reported to complicate almost 20% of studies in high-risk individuals1. As previously presented, we implemented a formalised protocol for the management of chronic kidney disease (CKD) patients in our cardiac catheterisation laboratory2–3. This included clear pre and post-hydration guidance, use of the Mehran score to identify high-risk patients, ensuring nephrotoxic medications were withheld and use of advice sheets for patients and GPs. With this we achieved an 8.9% reduction in the rates of CI-AKI for patients with CKD. This study highlights a five-year re-audit of CI-AKI rates. Methods During the period between August 2018 and February 2019, a total of 2025 patients underwent contrast angiography ± percutaneous coronary intervention (PCI) at our institution. Of these, 266 (11.1%) had CKD. All patients with an estimated glomerular filtration rate (eGFR) ≤60 mls/min/m2 presenting for coronary angiography at our laboratory were included. Data were obtained from lab reporting systems and from the Northern Ireland electronic care record. Demographics, risk factors and renal function before and at 48 hours post angiogram were recorded. Mehran scores were calculated for each patient and pre/post procedure intravenous fluids prescribed if appropriate. CI-AKI was defined as a delta rise in serum creatinine of ≥26.5 µmol/litre or relative rise of ≥50%. Case report forms were used to record blood results. Patients were telephoned at 48 hours and advised to restart withheld nephrotoxic medications if appropriate or, if necessary, given AKI advice with repeat blood sampling a further 48 hours later. Data were non-parametric on Shapiro-Wilk testing therefore Mann-Whitney U test (p Results Of the 266 patients identified, 22 (8.3%) developed CI-AKI 48 hours post-contrast. Using the previous definition of CI-AKI at the time of our initial study in 2014 (creatinine rise ≥25%), 11 patients (4.1%) developed CI-AKI which remains well below the published literature rate of 10–15%. Average Mehran scores were significantly higher in those patients that went on to develop CI-AKI compared with those that did not (14 vs. 10, p Conclusion/Implications Our comprehensive protocol for the peri-angiography management of CKD patients has achieved a significant reduction in the rates of CI-AKI at our institution, which has been sustained over a five-year period. There is a statistically significant correlation between higher Mehran score and development of CI-AKI, indicating the value of this tool as a surrogate marker for high-risk patients.

Introduction Contrast induced acute kidney injury (CI-AKI), defined as a delta rise in creatinine of >26.5 umol/L or a 50% relative rise within 48 hours following iodinated contrast, is associated with considerable mortality risk. Our previous study of 301 patients undergoing contrast coronary angiography/percutaneous coronary intervention (PCI) highlighted a CI-AKI rate of 9.3% at index procedure. Few studies have looked at long term prognosis, adverse events and mortality following CI-AKI. Our objective is to assess the 5 year mortality rate following contrast coronary angiography and to evaluate independent risk factors and presence of index CI-AKI on 5 year mortality. Methods A prospective cohort study in a single cardiology centre in the UK was carried out from 2011–2013, the results of which have been previously published.1 In total 2,519 patients were screened, 321 (12.7%) of which had CKD, in total 301 (93.7%) patients were recruited. Written consent was obtained from all patients. Patient demographics, CI-AKI risk factors, CKD stage and contrast dose at initial contrast angiography were recorded. A Mehran risk score was calculated for each patient. Samples for plasma NGAL, serum L-FABP, serum KIM-1, serum IL-18 and serum creatinine were previously collected pre and post contrast angiography and statistically analysed to assess prediction of CI-AKI as previously described.1 At 5 years following index contrast procedure we analysed for MACE and mortality by accessing up to date electronic medical records. Patient consent was granted to access medical notes. Statistical analysis was performed to assess the predicative ability of CI-AKI risk factors and Mehran risk score on 5 year mortality risk. Results At 5 years follow up data was available for 292 (97%) of the original 301 patients. Type 2 diabetes, contrast volume, Mehran risk score, lower glomerular filtration rate (GFR) and use of intravenous fluids at index procedure were independently associated with five year mortality, p At 5 year follow up 76 (26.0%) of the total cohort of patient had died. Out of the 28 patients who developed CI-AKI at index contrast procedure 17 (60.7%) of the 28 patients had died at 5 years versus 58 (22.0%) of the 264 non CI-AKI patients (p Conclusion This study highlights that index CI-AKI is an independent risk factor for 5 year mortality and MACE. Several risk factors act independently as surrogate markers of CI-AKI prior to administration of iodinated contrast, many of which are incorporated in the Mehran CI-AKI risk score. Furthermore, these are associated with adverse incidents and mortality at five years following index contrast procedure. A combination approach of these findings, including novel biomarkers as previously demonstrated, will help to reduce risk and early identify CI-AKI to facilitate timely therapeutic intervention. Reference Connolly M, Kinnin M, McEneaney D, Menown I, Kurth M, Lamont J, et al. Prediction of contrast induced acute kidney injury using novel biomarkers following contrast coronary angiography. Quarterly Journal of Medicine - An International Journal of Medicine 2018:103–110. Conflict of Interest n/a

Background Previous studies have shown that in acute heart failure, elevated heart rate (HR) on acute admission or on discharge is associated with increased short-medium term mortality and morbidity. In chronic heart failure, elevated HR is also associated with adverse outcome. The purpose of this study was (a) to evaluate heart rates in recently stabilised patients at the time of first outpatient review, 1–2 months following heart failure admission and (b) to assess if elevated heart rate at this time point continued to predict adverse outcome over long term follow up. Methods All patient records presenting to the heart failure service in our Centre between July 2011 and June 2013 were assessed. Inclusion criteria were patients with left ventricular ejection fraction ≤40% on echo, outpatient attendance ≤8 weeks post discharge, in sinus rhythm, and in whom resting HR was recorded. Patients in atrial fibrillation at presentation were excluded. Elevated HR was defined as ≥70 beats per minute (bpm). The incidence of readmission for heart failure, acute coronary syndrome (ACS), and death was determined from clinical records with a minimum follow up of three years. Fisher’s Exact Test and Student’s t-test were used to determine statistical significance. Results Of 235 patients presenting to the heart failure service between July 2011 and June 2013, 87 (37%) met inclusion criteria. Over half were >70 years of age, 57% were male, and 69% had an ischaemic cardiomyopathy. Mean HR was 69 bpm. Patients were followed for up to 5 years (mean 3.4 years, range 3.2–5 years). Readmission for heart failure occurred in 10 patients, ACS in 7 patients and death in 23 patients. Those with HR≥70 bpm compared to those with HR Conclusions In this study of recently stabilised patients managed by a single heart failure team, in consistent fashion and according to a standardised protocol, those with elevated HR≥70 were less likely to reach mean life expectancy and had a trend to premature death.

Background/introduction Type 4a myocardial infarction (MI) occurs when myocardial injury is combined with either symptoms suggestive of myocardial ischaemia, new left bundle branch block, angiographic loss of patency of a major artery or imaging suggestive of new loss of myocardium. Myocardial injury is defined as a rise of >5 x 99th upper reference limit (URL) of 14 ng/l (i.e. >70 ng/l) for highly sensitive troponin T (hsTnT) at 6 h if hsTnT was normal at baseline or >20% rise from 0 to 6 h if hsTnT was >14 ng/l at baseline. Aim To assess the prognostic value of biomarkers of myocardial injury following elective percutaneous coronary intervention (PCI). Design A cohort of 209 patients were included of whom 144 (68.9%) were male, mean age was 68.8 years, 28 (13.4%) were smokers, 31 (14.8%) were diabetic, 199 (95.2%) had hypercholesterolaemia and 138 (66.0%) had hypertension. Methods We evaluated hsTnT, heart-type fatty acid-binding protein (H-FABP), troponin I (TnI), creatine kinase MB type (CKMB), myoglobin, glycogen phosphorylase BB (GPBB) and carbonic anhydrase III (CA III) at 0, 4, 6 and 24 h following elective PCI. Patients were followed up at 1 year to assess for major adverse clinical events (MACE). Results Myocardial injury was observed in 37 (17.7%) patients. Median hsTnT/H-FABP at 4 h were most predictive. MACE was noted in 6 (2.9%) patients, 3 had type 4a MI post PCI, P = 0.036. Discussion/conclusions Median 4 h hsTnT/H-FABP were most predictive of myocardial injury following PCI. H-FABP and hsTnT were predictive of MACE.

The aim of this study was to compare the performance of drug-coated stents (DCS) versus bare-metal stents (BMS) in patients who are candidates for long-term oral anticoagulation (OAC) after percutaneous coronary interventions.The randomized controlled LEADERS FREE (A Randomized Clinical Evaluation of the BioFreedom™ Stent) trial demonstrated the superior safety and efficacy of a polymer-free biolimus A9 DCS compared with a similar BMS used with 1 month of dual antiplatelet therapy in 2,466 patients at high bleeding risk.The 2 stents were compared in a pre-specified analysis of the 879 LEADERS FREE patients (35.6%) scheduled to remain on OAC after percutaneous coronary intervention. The primary safety endpoint was a composite of cardiac death, myocardial infarction, and stent thrombosis. The primary efficacy endpoint was the incidence of clinically driven target lesion revascularization.Baseline characteristics of 448 DCS and 431 BMS recipients were similar, 78.8% had histories of atrial fibrillation, and 21% presented with acute coronary syndromes. Four hundred patients in the DCS group and 376 in the BMS group were discharged on OAC after percutaneous coronary intervention. At 2 years, for the DCS and BMS recipients, respectively, the incidence of clinically driven target lesion revascularization was 7.5% versus 11.2% (hazard ratio: 0.63; 95% confidence interval: 0.40 to 1.01; p = 0.0514), the safety endpoint was reached by 14.4% and 15.0% (p = NS), and the rates of major bleeding events (Bleeding Academic Research Consortium 3 to 5) were 10.7% and 12.9% (p = NS).The efficacy advantage of DCS over BMS up to 2 years appears confirmed in patients on long-term OAC. Despite the very short course of dual antiplatelet therapy, both the DCS and BMS groups experienced similarly high rates of major bleeding. (A Randomized Clinical Evaluation of the BioFreedom™ Stent [Leaders Free]; NCT01623180).

To define the size of the left mainstem coronary artery (LMS) in the Northern Irish population and investigate the clinical feasibility, safety, and efficacy of post dilation beyond nominal diameter of current generation Drug eluting stent (DES) when treating the LMS.There is no prospective data examining the need, feasibility, and safety of over-expansion of current generation DES beyond nominal diameter.Patients with flow-limiting coronary atheroma requiring IVUS assessment of the LMS were recruited. Standardized measurements of the distal LMS were made. Subsequently, patients requiring post dilation of current generation DES within the LMS were entered into a PCI registry.Overall, 125 patients were recruited into the initial study. Mean cross-sectional area (CSA) of the distal LMS was 22.6 mm(2) (SD ± 5.4 mm(2) ). Mean maximal vessel diameter was 5.7 mm (SD ± 0.7 mm). Increasing plaque burden was associated with reduced CSA (P 0.001). In 31 consecutive patients undergoing IVUS guided PCI of the LMS with 5.5 and 6.0 mm balloon catheters, mean maximal stent diameters were5.0 mm with the Biomatrix Flex 9 crown and Promus Element Large vessel platforms. No intraprocedural complications occurred. Mean follow up was 13.4 months. Clinical restenosis rate was 3.2%, with 2 deaths unrelated to index procedure.The majority of patients with angiographic coronary atheroma have a mean LMS diameter of4 mm indicating the requirement for post dilation beyond nominal diameter all of current generation DES in almost all patients when treating the LMS. This is achievable with current DES platforms with no intraprocedural complication. Clinical follow up indicates excellent short-term efficacy.

Objectives To investigate the outcomes of a cohort of acute and elective percutaneous coronary intervention (PCI) patients who were discharged home 6 hours postprocedure. Background Contemporary PCI is safe with a low rate of acute complications. It is well established as a day procedure in elective cases; however, data are lacking in acute cases. Methods We describe a prospective observational audit of routine clinical practice in the 3 PCI centers in Northern Ireland. Patients were selected for same-day discharge after 6 hours of post-PCI observation. Both elective and acute coronary syndrome (ACS) cases were included. Criteria for same-day discharge were based on the technical result of the procedure rather than lesion complexity or clinical presentation. Radial access was preferred but not mandatory. Patients were contacted directly to assess for 30-day major adverse cardiovascular events (MACE). Reported events were corroborated with the general practitioner or hospital notes. Results A total of 1,059 patients were selected for same-day discharge with 30-day follow-up available for all cases. Of these, 766 (72.3%) were elective and 293 (27.7%) were ACS patients. Radial access was almost universal (98%). A total of 1,224 lesions were stented, of which 432 (40.8%) were high risk (highest risk lesion in each case by AHA/ACC classification). MACE rate at 30 days was 0.85% with a sub-acute stent thrombosis rate of 0.4%. There were no MACE events from discharge to 24 hours. Conclusions Selected acute and elective patients with a range of lesion complexity and risk can be discharged safely home early after PCI.

Background Data from large epidemiological studies suggest that elevated heart rate is independently associated with cardiovascular and all-cause mortality in patients with hypertension and in those with established cardiovascular disease. Clinical trial findings also suggest that the favorable effects of beta-blockers and other heart rate–lowering agents in patients with acute myocardial infarction and congestive heart failure may be, at least in part, due to their heart rate–lowering effects. Contemporary clinical outcome prediction models such as the Global Registry of Acute Coronary Events (GRACE) score include admission heart rate as an independent risk factor. Aims This article critically reviews the key epidemiology concerning heart rate and cardiovascular risk, potential mechanisms through which an elevated resting heart rate may be disadvantageous and evaluates clinical trial outcomes associated with pharmacological reduction in resting heart rate. Conclusions Prospective randomised data from patients with significant coronary heart disease or heart failure suggest that intervention to reduce heart rate in those with a resting heart rate >70 bpm may reduce cardiovascular risk. Given the established observational data and randomised trial evidence, it now appears appropriate to include reduction of elevated resting heart rate by lifestyle +/− pharmacological therapy as part of a secondary prevention strategy in patients with cardiovascular disease.

The small but absolute increase in late and very late stent thrombosis associated with drug-eluting stent technology may in part be related to the permanent, durable polymers currently employed with these stent platforms. Research has recently focused on two strategies to combat this problem; bioabsorbable polymers and polymer-free stents. This article critically reviews the key clinical trials and recent conference updates surrounding these two approaches and future directions for technology development.

Early identification of acute coronary syndrome (ACS) is important to guide therapy at a time when it is most likely to be of value. In addition, predicting future risk helps identify those most likely to benefit from ongoing therapy. Cardiac troponin T (cTnT) is useful for both purposes although cannot reliably rule out ACS until 12 hours after pain onset and does not fully define future risk. In this review article we summarize our previously published research, which assessed the value of myocyte injury, vascular inflammation, hemostatic, and neurohormonal markers in the early diagnosis of ACS and risk stratification of patients with ACS. In addition to cTnT, we measured heart fatty acid binding protein (H-FABP), glycogen phosphorylase-BB, high-sensitivity C-reactive protein, myeloperoxidase, matrix metalloproteinase 9, pregnancy-associated plasma protein-A, D-dimer, soluble CD40 ligand, and N-terminal pro-brain natriuretic peptide (NT-proBNP). Of the 664 patients enrolled, 415 met inclusion criteria for the early diagnosis of acute myocardial infarction (MI) analysis; 555 were included in the risk stratification analysis and were followed for 1 year from admission. In patients presenting

Aims To determine whether the low-molecular weight heparin enoxaparin remains favourable when compared with unfractionated heparin (UFH) among patients with acute coronary syndromes (ACS) when incorporating efficacy and safety of these adjunctive therapies using a net clinical endpoint. Methods and results We performed a meta-analysis of randomized trials of enoxaparin vs. UFH in ST-elevation-MI (STEMI) or non-ST-elevation-ACS (NSTEACS) ( n = 49 088 patients in 12 trials). The net clinical endpoint was defined as death, MI, or major bleeding by 30 days. Death or myocardial infarction (MI) was significantly reduced with enoxaparin when compared with UFH (9.8 vs. 11.4%, OR 0.84, P < 0.001). The net clinical endpoint occurred less frequently with enoxaparin than UFH (12.5 vs. 13.5%, OR 0.90, P = 0.051). Major bleeding was higher with enoxaparin (4.3 vs. 3.4%, OR 1.25, P = 0.019). Among STEMI trials, the net clinical endpoint was significantly lower with enoxaparin (OR 0.84, P = 0.015), but there was no difference in NSTEACS trials (OR 0.97). Conclusions When compared with UFH, enoxaparin was associated with superior efficacy as adjunctive antithrombin therapy among >49 000 patients across the ACS spectrum. Although bleeding was increased with enoxaparin, this increase was offset by a reduction in death or MI. The net clinical benefit in favour of enoxaparin was evident among the STEMI population and was neutral among the NSTEACS population.

Aims To evaluate clinical outcomes in patients receiving the next-generation, paclitaxel-eluting, platinum-chromium TAXUS Element stent in a real-world setting. The PERSEUS Workhorse and Small Vessel studies showed positive results with the TAXUS Element stent in a clinical trial setting. Methods and results TE-PROVE was a prospective, open-label, multicentre, "all-comers" study which enrolled 1,014 patients at 37 European sites. Follow-up was at 30 days, six months and one year, and will continue annually up to five years. The primary endpoint was overall and stent-related target vessel failure (TVF), defined as cardiac death, target vessel-related myocardial infarction (MI) and target vessel revascularisation (TVR) at one year post implantation. Secondary endpoints included the components of TVF, all-cause mortality, and ARC definite/probable stent thrombosis. Follow-up was available in 97.3% (987/1,014) of patients. Patients were 75.0% male (760/1,014), mean age was 65.1±10.8 years, 25.5% had medically treated diabetes (259/1,014), and 10.7% (109/1,014) were treated for STEMI. At baseline, mean lesion length among 1,299 treated lesions was 19.8±12.0 mm and mean reference vessel diameter was 3.1±0.5 mm. At one year, the rate of TVF (primary endpoint) was 6.0% (59/987) overall; 3.7% (37/987) of TVF events were stent-related. Cardiac death was 0.7% (7/987), target vessel-related MI was 1.1% (11/987), and TVR was 4.7% (46/987). All-cause death occurred in 1.2% (12/987) of patients and ARC definite/probable ST was 0.5% (5/987). Conclusions The primary endpoint results from the TE-PROVE registry demonstrate good performance and safety for the TAXUS Element paclitaxel-eluting stent at one year in everyday clinical practice. Clinical trial registration information NCT01242696.

Background: Published literature was systematically reviewed to determine the diagnostic accuracy of new protein markers of acute coronary syndromes (ACS) in symptomatic outpatients at low risk of ACS and related complications comparable to patients evaluated in emergency department chest pain units.Methods: Studies were identified by a MEDLINE® (1966 to May week 3, 2005) search. Abstracts were reviewed for relevance, and manuscripts were included by the independent consensus of 2 observers based on explicit criteria restricting the analysis to studies relevant to screening ambulatory patients with symptoms suggesting ACS. Publication bias was identified by a modified funnel plot analysis [study size (y) vs the inverse of the negative likelihood ratio (x)]. Results of individual markers were reported separately. When 3 or more eligible studies were identified, data were aggregated by use of the summary ROC (SROC) curve.Results: Twenty-two protein markers in 10 unique populations met the inclusion criteria. Data required for SROC analysis (true- and false-positive rates) were available for 17 markers, in 9 unique populations, from publications and personal communications. Of these, only C-reactive protein was published in more than 2 populations to allow aggregation (6 studies total). C-Reactive protein demonstrated poor diagnostic performance on SROC curve analysis, with an area under the curve of 0.61 and a pooled diagnostic odds ratio of 1.81 (95% confidence interval, 1.06–3.07).Conclusion: Published evidence is not sufficient to support the routine use of new protein markers in screening for ACS in the emergency department setting.

To assess the safety and efficacy of Biolimus A9-eluting stents (BES, BioMatrix™ and BioMatrix Flex™) in routine clinical practice.The LEADERS randomized trial has documented equivalent efficacy and superior safety of the BES when compared to a first generation Sirolimus-eluting Cypher(TM) stent.5,472 patients from 57 centers, treated with BES, were enrolled in an international multicenter registry and followed clinically up to 2 years.Mean patient age was 63.2 ± 11 years, 24% of patients had diabetes, and 49.8% presented with an acute coronary syndrome. 99.3% of patients were discharged on dual antiplatelet therapy (DAPT), 83.3% remained on DAPT at 1 year and 30.6% at 2 years. The incidence of the composite primary end point [major adverse cardiac events (MACE) at 12 months] was 4.5% [cardiac death 0.9%, myocardial infarction 1.7%, clinically indicated target vessel revascularization (ci-TVR) 2.8%]. MACE incidence was 6.8% at 24 months (cardiac death 1.5%, myocardial infarction 2.4%, ci-TVR 4.3%). At 12 months, 32 patients (0.6%) had suffered at least one definite or probable stent thrombosis (ST), and 91 patients (1.7%) a major bleed (MB). Nine patients with ST (27.3%) and 7 patients with a MB (7.7%) died during the first year after the index procedure. Between 12 and 24 months after implantation, there were 18 (0.4%) additional MB and 8 (0.2%) additional ST.This large international cohort documents a low 12 and 24 months MACE incidence and a very low ST incidence in an unselected patient population undergoing BES implantation. The results are in keeping with those of the randomized controlled LEADERS trial. Even though ST with this stent was a rare event, it was still associated with significant mortality. MB remains a problem, and warrants improved tailoring of DAPT in recipients of drug eluting stents.

Aims Abciximab has previously been shown to enhance thrombolysis and improve myocardial perfusion when combined with reduced doses of alteplase. The purpose of the reteplase phase of TIMI 14 was to evaluate the effects of abciximab when used in combination with a reduced dose of reteplase for ST-elevation myocardial infarction. Methods and Results Patients (n=299) with ST-elevation myocardial infarction were treated with aspirin and randomized to a control arm with standard dose reteplase (10+10 U given 30 min apart) or abciximab (bolus of 0.25 mg. kg(-1)and 12-h infusion of 0.125 microg. kg(-1). min(-1)) in combination with reduced doses of reteplase (5+5 U or 10+5 U). Control patients received standard weight-adjusted heparin (bolus of 70 U. kg(-1); infusion of 15 U. kg(-1). h(-1)), while each of the combination arms with abciximab and reduced dose reteplase received either low dose heparin (bolus of 60 U. kg(-1); infusion of 7 U. kg(-1). h(-1)) or very low dose heparin (bolus of 30 U. kg(-1); infusion of 4 U. kg(-1). h(-1)). The rate of TIMI 3 flow at 90 min was 70% for patients treated with 10+10 U of reteplase alone (n=87), 73% for those treated with 5+5 U of reteplase with abciximab (n=88), and 77% for those treated with 10+5 U of reteplase with abciximab (n=75). Complete (>/=70%) ST resolution at 90 min was seen in 56% of patients receiving a reduced dose of reteplase in combination with abciximab compared with 48% of patients receiving reteplase alone. Conclusions Reduced doses of reteplase when administered in combination with abciximab were associated with higher TIMI 3 flow rates than reported previously for reduced doses of reteplase without abciximab and were at least as high as for full dose reteplase alone

Introduction Heart-type Fatty Acid-Binding Protein (H-FABP) may be useful for early diagnosis of ACS 1,2 and has been associated with increased cardiovascular events. Type 4 a procedural myocardial infarction (MI) may occur after percutaneous coronary intervention (PCI). 3 Little is known about the use of early biomarkers as predictors of cardiovascular events following elective PCI. Methods We prospectively evaluated highly sensitive troponin T (hsTnT), H-FABP, troponin I (TnI), creatine kinase MB type (CKMB), myoglobin, glycogen phosphorylase BB (GPBB) and carbonic anhydrase 3 (CA3) at 0, 4, 6 and 24 hours following elective PCI. Baseline demographic and cardiac risk factors were recorded. The primary endpoint was type 4 a MI, diagnosed as a rise of >5 × 99th upper reference limit (URL) of 14 ng/dl (i.e., rise of >70 ng/dl) at 6 hours if hsTnT was normal at baseline or >20% from 0 to 6 hours if hsTnT was >14 ng/dl at baseline. 3 Patients were followed up at 1 year to assess for major adverse clinical events (MACE); MI, target vessel revascularisation, heart failure, stroke and death. Results We enrolled 241 patients of whom 32 were excluded due to withdrawal of consent or PCI being cancelled after angiography. A cohort of 209 patients was included in analysis, of whom 144 (68.9%) were male, mean age was 68.8 years, 28 (13.4%) were smokers, 31 (14.8%) were diabetic, 199 (95.2%) had hypercholesterolaemia and 138 (66.0%) had hypertension. Type 4 a MI was observed in 37 (17.7%) patients. Comparing those with and without type 4 a MI, there was no statistical difference in risk factors (p > 0.05) except for age (p = 0.015). Median troponin at 6 hours was 90.24 ng/dl (95% CI: 76.56–186.41) versus 14.43 ng/dl (95% CI: 16.37–21.26) in the type 4 a/non type 4 a groups respectively, p ≤ 0.001, Figure 1. Median H-FABP at 4 hours was most predictive of type 4 a MI (followed by CKMB and myoglobin) with levels of 6.23 ng/l (95% CI: 4.38–18.96), versus 2.05 ng/l (95% CI: 2.23–2.74), p ≤ 0.001, AUC 0.91, Table 1, Figure 2. Results for TnI, CKMB, myoglobin, GBPP and CA3 are shown in Table 1. Multivariate logistic regression (stepwise elimination) showed H-FABP to be most predictive of type 4 a MI, p 6.32 ng/ml) for type 4 a MI was 51.5%, specificity 96.1%, positive predictive value (PPV) 73.9%, negative predictive value (NPV) 90.3%, odds ratio (OR) 26.39, relative risk (RR) 7.62. MACE was noted in 6 (2.9%) patients (three MI, two death and one stroke), 3 of which had type 4 a MI at index PCI, p = 0.036. Table 2 compares median change in H-FABP and hsTnT from 0–6 hours in patients who developed MACE at 1 year with CA3 performing best, p = 0.02. Conclusions/implications Median 4 hour H-FABP was most predictive of a 6 hour hsTnT rise as a consequence of type 4 a MI in elective PCI, followed by CKMB and myoglobin. H-FABP, hsTnT and CA3 were predictive of MACE at 1 year. References McCann CJ, Glover BM, Menown IB, Moore MJ, McEneny J, Owens CG, Smith B, Sharpe PC, Young IS, Adgey JA. Novel biomarkers in early diagnosis of acute myocardial infarction compared with cardiac troponin T. Eur Heart J 2008;29(23):2843–50 Body R, Carley S, Burrows G, Pemberton P, Mackway-Jones K. Combining heart fatty acid binding protein and high sensitivity troponin in the emergency department. 14th International Conference on Emergency Medicine. Acad Emerg Med 2012;19(6):748–9 Thygesen K, Alpert J, Jaffe A, Simoons M, Chaitman R, White H. Third universal definition of myocardial infarction. ESC/ACCF/AHA/WHF expert consensus document. J Am Coll Cardiol 2012;60(16):1581–98

Introduction Chronic Kidney Disease (CKD) is a risk factor for contrast induced nephropathy (CIN), defined as an increase in serum creatinine of >25% from baseline or a delta rise of >26.5 µmol/L within 48 h. Early diagnosis of CIN requires validated novel biomarkers. Methods A prospective observation study of 301 consecutive CKD patients undergoing elective invasive coronary angiography was performed. Low-osmolar contrast was standard. Demographics and Mehran risk score were recorded. Samples for plasma neutrophil gelatinase-associated lipocalin (NGAL), serum liver fatty acid-binding protein (L-FABP), serum kidney injury marker 1 (KIM-1), serum interleukin 18 (IL-18) and serum creatinine were taken at 0, 1, 2, 4, 6 and 48 h post contrast. Urinary NGAL and urinary cystatin C (CysC) were collected at 0, 6 and 48 h. Incidence of major adverse clinical events (MACE); acute myocardial infarction, heart failure hospitalisation, stroke and death were recorded at 1 year. Results CIN occurred in 28 (9.3%) patients and were independently associated with older age, diabetes, higher Mehran score, larger contrast volume and anaemia (p 0.05). A Mehran score ≥10 performed prior to procedure achieved an AUC of 0.65, p = 0.006. MACE occurred in 7 (25.0%) CIN patients but only 17 (6.2%) non-CIN patients (p 10, 6 hr NGAL and 4 hr L-FABP improved specificity to 96.7%. [Figure 2][3] highlights a proposed pathway of how biomarkers could be used to identify CIN early and facilitate timely therapeutic intervention to reduce morbidity and mortality. ![Abstract 208 Figure 1][4] Abstract 208 Figure 1 Median plasma NGAL (ng/ml) and serum L-FABP (ng/ml) in AKI and non-AKI ![Abstract 208 Figure 2][4] Abstract 208 Figure 2 Proposed patient pathways Abstract 208 Table 1 Summary of NGAL (ng/ml) and L-FABP (ng/ml) in AKI and non-AKI patients ![][5] Conclusions/implications Mehran risk score, 6 h plasma NGAL and 4 h serum L-FABP performed best at early CIN prediction. CIN patients were four times more likely to develop MACE and had a trebling of mortality risk at 1 year. The implications of our results, translated to the design of safer elective coronary intervention services able to more efficiently manage the increasing volume of contrast studies, should be a key health priority for cardiac and renal services. [1]: #F1 [2]: #F3 [3]: #F2 [4]: pending:yes [5]: /embed/graphic-3.gif

In the past five years, four new oral anticoagulants (NOACs) - dabigatran, rivaroxaban, apixaban and edoxaban - became available for prevention of stroke and systemic embolism among atrial fibrillation (AF) patients. This study compares the health and economic outcomes for AF patients treated with

Aims The present study aims to investigate patterns of beta-blocker usage in a national primary care cohort. Methods and results This is a retrospective cohort study utilising the UK General Practice Research Database from 2004 to 2008. Inclusion criteria were (i) a first diagnosis of chronic heart failure (CHF), myocardial infarction (MI) or angina, and (ii) first-ever prescription of beta-blocker on or after 1st April 2004. Outcome measures were discontinuation of beta-blockers over time, initiation dosages, titration patterns, incidence of adverse events (AEs) and associated prescribing actions. A total of 12,493 patients (68.0% male; mean age 58.0±SD 17.6years) were included. Of these, 27% had discontinued beta-blockers within 1year of initiation, increasing to 39% by 2years and 50% by 3years. Persistence appeared to be greater in the MI cohort compared with angina or CHF cohorts. Beta-blocker dose at initiation averaged approximately 33% of guideline recommended target, rising to 40% in those who continued with therapy. Dyspnoea, fatigue and dizziness were the most common incident AEs at 98, 53 and 49 per 1000 patient years, with little difference between indications. Conclusion A quarter of patients with cardiovascular disease who are commenced on a beta-blocker are no longer taking the drug by one year. This rises to 50% by three years, a finding that is consistent irrespective of whether the prescription is for prognostic (CHF or post MI) or symptomatic (angina) benefit. There is an urgent need to understand and address the prescribing difficulties of beta-blockers in these at-risk patients.

There is an established body of evidence from epidemiological studies which indicates that an elevated resting heart rate is independently associated with atherosclerosis and increased cardiovascular morbidity and mortality, in both the general population and in patients with established cardiovascular disease. Clinical trial data suggest that in patients with coronary artery disease, an elevated heart rate identifies those at increased risk of adverse cardiovascular outcomes, and that lowering of heart rate may reduce major cardiovascular events in patients with an elevated heart rate and symptom-limiting angina. These results suggest that an increased heart rate may have an adverse impact on the atherosclerotic process and increase the risk of a cardiovascular event in patients with coronary artery disease. The precise pathophysiological mechanisms that link heart rate and cardiovascular outcomes have yet to be defined. Possibilities may include indirect mechanisms related to autonomic dysregulation and those due to an increase in heart rate per se, which can increase the ischaemic burden and exert local haemodynamic forces that can adversely impact on the endothelium and arterial wall. For these reasons, heart rate should be considered as a therapeutic target in the treatment of patients with coronary artery disease.

A 70-year-old man presented with a 6 month history of grade II exertional chest tightness. At peak exercise on treadmill he developed borderline ST segment depression in lead V4. Cardiac catheterisation showed angiographically minor stenosis in the proximal left anterior descending artery (fig 1). However, on intravascular ultrasound, there was at least moderate atheroma burden in this segment, although the lumen was well preserved due to positive remodelling (fig 2). This is a striking example of the Glagov phenomenon (first described in 1987)1 whereby positive remodelling of the arterial wall enables lumen diameter to be maintained up to a plaque burden of 40–45% diameter, but above 40–45%, reduction in lumen occurs due to inability of the artery to expand further. Figure 1 Angiographically minor stenosis in the proximal left anterior descending artery. Figure 2 Intravascular ultrasound of the same segment showing at least moderate atheroma burden (blue), with preservation of the lumen (red) due to positive remodelling—the Glagov phenomenon.

Reducing heart rate may improve outcomes in patients with CVD.

Clinical imaging trials have assessed the impact lipid management has on atherosclerosis. Dr Ian Menown explains.

Aims To evaluate the role of novel biomarkers in early detection of acute myocardial infarction (MI) in patients admitted with acute chest pain. Methods and results A prospective study of 664 patients presenting to two coronary care units with chest pain was conducted over 3 years from 2003. Patients were assessed on admission: clinical characteristics, ECG (electrocardiogram), renal function, cardiac troponin T (cTnT), heart fatty acid binding protein (H-FABP), glycogen phosphorylase-BB, NT-pro-brain natriuretic peptide, D-dimer, hsCRP (high sensitivity C-reactive protein), myeloperoxidase, matrix metalloproteinase-9, pregnancy associated plasma protein-A, soluble CD40 ligand. A ≥12 h cTnT sample was also obtained. MI was defined as cTnT ≥ 0.03 µg/L. In patients presenting

To evaluate the prognostic role of novel biomarkers for the risk stratification of patients admitted with ischemic-type chest pain, a prospective study of 664 patients presenting to 2 coronary care units with ischemic-type chest pain was conducted over 3 years beginning in 2003. Patients were assessed on admission for clinical characteristics, electrocardiographic findings, renal function, cardiac troponin T (cTnT), markers of myocyte injury (heart fatty acid-binding protein [H-FABP] and glycogen phosphorylase BB), neurohormonal activation (N-terminal-pro-brain natriuretic peptide [NT-pro-BNP]), hemostatic activity (fibrinogen and D-dimer), and vascular inflammation (high-sensitivity C-reactive protein, myeloperoxidase, matrix metalloproteinase-9, pregnancy-associated plasma protein-A, and soluble CD40 ligand). Aor=12-hour cTnT sample was also obtained. Myocardial infarction (MI) was defined as peak cTnTor=0.03 microg/L. Patients were followed for 1 year from the time of admission. The primary end point was death or MI. Elevated fibrinogen, D-dimer, H-FABP, NT-pro-BNP, and peak cTnT were predictive of death or MI within 1 year (unadjusted odds ratios 2.5, 3.1, 5.4, 5.4, and 6.9, respectively). On multivariate analysis, H-FABP and NT-pro-BNP were selected, in addition to age, peak cTnT, and left ventricular hypertrophy on initial electrocardiography, as significant independent predictors of death or MI within 1 year. Patients without elevations of H-FABP, NT-pro-BNP, or peak cTnT formed a very low risk group in terms of death or MI within 1 year. A very high risk group had elevations of all 3 biomarkers. In conclusion, the measurement of H-FABP and NT-pro-BNP at the time of hospital admission for patients with ischemic-type chest pain adds useful prognostic information to that provided by the measurement of baseline and 12-hour cTnT.

A prospective, multicenter trial was conducted in patients with nontraumatic chest pain in 4 hospitals to determine whether an 80-lead body surface map electrocardiogram system (80-lead BSM ECG) improves detection of ST-segment elevation in acute myocardial infarction (STEMI) compared with a standard 12-lead electrocardiogram (ECG) in an emergency department (ED) setting. A trained ED or cardiology staff member (technician or nurse) recorded a 12-lead ECG and 80-lead BSM ECG from each subject at initial presentation. Serial biomarkers (total creatine kinase [CK], CK-MB, and/or troponin) were obtained according to individual hospital practice. Of the 647 patients evaluated, 589 had available biomarkers results. Eighty-lead BSM ECG improved detection of biomarker-confirmed STEMI compared with the 12-lead ECG for CK-MB-defined STEMI (100% vs 72.7%, P = .031; n = 364) or troponin-defined STEMI (92.9% vs 60.7%, P = .022; n = 225). Specificity for STEMI was high (range, 94.9%-97.1%) with no significant difference between 80-lead BSM ECG and 12-lead ECG. Right ventricular involvement complicating inferior STEMI was detected by 80-lead BSM ECG in 2 (22%) of 9 patients with CK-MB-defined MI and in 2 (22%) of 9 patients with troponin-defined MI. The infarct location missed most commonly on 12-lead ECG but detected by 80-lead BSM ECG was inferoposterior MI. We conclude that BSM using 80-lead BSM ECG is more sensitive for detection of STEMI than 12-lead ECG, while retaining similar specificity.

Ivabradine is not only the first of a new class of selective If channel inhibitors, but is also the first new medical treatment for stable angina to be approved in Europe for 10 years. By selectively reducing heart rate without adversely affecting myocardial contractility or blood pressure, ivabradine offers a valuable new option for patients with stable angina in whom beta-blockers are not tolerated or are contraindicated.

Advances in coronary stent technology, both in terms of stent design and function, have significantly improved the safety and efficacy of percutaneous coronary intervention, including marked reduction in restenosis. This has led to its use in increasingly challenging clinical and lesional subsets, with potential for increased risk of stent-associated thrombosis. In this article we outline the development of passive stent coatings, and evaluate the ongoing role of such coatings in the contemporary era of antiproliferative drug-eluting stents.

Aims To compare prospectively the impact of pre-hospital care by a physician-staffed mobile coronary care unit with patients managed initially in-hospital, all with acute myocardial infarction. Methods and results This was a single centre registry of consecutive patients (n=750) admitted with acute myocardial infarction to the coronary care unit and cardiology wards of the Royal Victoria Hospital, Belfast between 1998 and 2001. For the 750 patients, in-hospital mortality was 11% and was significantly lower for those managed pre-hospital (8% vs 13%, P =0.04): patients who received fibrinolytic therapy (n=474), the in-hospital mortality was significantly lower in the pre-hospital group (7% vs 13%, P =0.02). Those managed pre-hospital had significant reduction in the median delay times (25th, 75th percentiles) from onset of symptoms to call for help 1.0 (0.5, 2.2) vs 2.0 (0.9, 6.0) h, P

We prospectively evaluated a rapid-access chest pain clinic in terms of clinical diagnoses, outcomes, morbidity and mortality at 3 months follow-up in patients, and cost-effectiveness. All patients seen at the clinic from February 1999 to December 2000 were assessed. Referring doctors indicated the management they would have provided had the clinic been unavailable, to allow a cost-effectiveness analysis. Overall, 709 patients were referred, 471 (66%) from General Practitioners, 212 (30%) from Accident and Emergency doctors and 26 (4%) from other sources. All had recent onset, or increasing frequency of ischaemic-type chest pain (excluding those with suspected myocardial infarction or rest chest pain angina). Fifty-one (7%) had acute coronary syndromes, 119 (17%) had stable ischaemic heart disease, 144 (20%) had possible ischaemic heart disease, and 395 (56%) were considered to have non-ischaemic symptoms. Some 70% of patients were seen within 24 h. Only 57 patients (8%) were admitted. Had the clinic been unavailable, 160 patients would have been admitted. Out-patient cardiology appointments were arranged for 116 patients (16%), and 429 patients (60%) were discharged directly. Follow-up data at 3 months were obtained from 565/567 eligible patients (99.6%). No major cardiac events (death/myocardial infarction) occurred in those with non-ischaemic chest pain. There were five deaths (including one due to cancer) and three patients had a myocardial infarction (event rate 1%). There were eleven readmissions for angina: six were in patients with acute coronary syndromes, and four of these six were awaiting revascularization. The estimated net saving was pound 58/patient. A rapid-access chest pain clinic offers a prompt, safe and cost-effective service in a challenging group of patients.

There is increasing awareness of the limitations of standard biochemical markers of cardiac damage in patients with acute coronary syndromes. A desire to improve sensitivity and specificity has led to the search for markers uniquely expressed by the myocardium. The cardiac troponins T and I (cTnT and cTnI) have been found to have excellent sensitivity and specificity and are superior to creatine kinase-MB (CK-MB) as indicators of myocardial necrosis.1 Using cTnT or cTnI as a diagnostic marker, the positivity rate in studies has varied from 20–48%, with death and acute myocardial infarction (MI) varying from 11–30% in 28 months follow up.2-4 These variations are largely caused by differences in risk among the populations studied and differing lengths of follow up. Troponins have proven useful for the diagnosis and subsequent risk stratification of patients presenting with acute chest pain.5 6 A raised troponin concentration may also identify those who are most likely to benefit from additional therapeutic measures.7 Nevertheless, is cTnT superior to cTnI? The troponin complex is situated on the thin filament of the striated muscle contractile apparatus and consists of troponin T (39 kD), troponin I (26 kD), and troponin C (18 kD), each coded by a separate gene.8 Specific cardiac and skeletal muscle isoforms are expressed in cardiac and skeletal striated muscle in adults. Troponins are mainly bound to the myofibrils, although 6–8% of cTnT and 2.8–4.1% of cTnI is cytosolic.9 This affects release kinetics. There is rapid early release of cytosolic cTnT after ischaemic injury, followed by more prolonged release of myofibrillar troponin, resulting in a biphasic release pattern. As cTnI has a smaller cytosolic pool, release is likely to be monophasic. Concentrations of both begin to rise in the 4–8 hours following injury and peak at 12–24 hours.7-9 cTnT may remain raised …

Summary Patients with acute chest pain suggestive of had higher sensitivity for the diagnosis of acute myocardial ischaemia, and normal or non-diagnostic coronary syndromes (myocardial infarction and electrocardiograms, form a difficult subgroup for unstable angina) than conventional markers (cTnI diagnosis and early risk stratification. We prospect- 48%, cTnT 38%, CKMB mass 30% or myoglobin ively evaluated the role of troponin T (cTnT), tro- 27%). At 3 months, a new cardiac event had ponin I (cTnI), CKMB mass and myoglobin, in the occurred in 42/214 (20%). Significantly higher diagnosis and risk stratification of 214 patients with event rates occurred when any of the biochemical acute chest pain of 24 h and non-diagnostic or markers was elevated, but the statistical significance normal ECGs admitted directly to the Cardiac Unit was highest for patients with elevated cTnI of the Royal Victoria Hospital Belfast from the ( p