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ObjectiveTo investigate percutaneous coronary intervention (PCI) practice in an international cohort of patients with spontaneous coronary artery dissection (SCAD). To explore factors associated with complications and study angiographic and longer term outcomes.MethodsSCAD patients (n=215, 94% female) who underwent PCI from three national cohort studies were investigated and compared with a matched cohort of conservatively managed SCAD patients (n=221).ResultsSCAD-PCI patients were high risk at presentation with only 8.8% undergoing PCI outside the context of ST-elevation myocardial infarction/cardiac arrest, thrombolysis in myocardial infarction (TIMI) 0/1 flow or proximal dissections. PCI complications occurred in 38.6% (83/215), with 13.0% (28/215) serious complications. PCI-related complications were associated with more extensive dissections (multiple vs single American Heart Association coronary segments, OR 1.9 (95% CI: 1.06–3.39),p=0.030), more proximal dissections (proximal diameter per mm, OR 2.25 (1.38–3.67), p=0.001) and dissections with no contrast penetration of the false lumen (Yip-Saw 2 versus 1, OR 2.89 (1.12–7.43), p=0.028). SCAD-PCI involved long lengths of stent (median 46mm, IQR: 29–61mm). Despite these risks, SCAD-PCI led to angiographic improvements in those with reduced TIMI flow in 84.3% (118/140). Worsening TIMI flow was only seen in 7.0% (15/215) of SCAD-PCI patients. Post-PCI major adverse cardiovascular and cerebrovascular events (MACCE) and left ventricular function outcomes were favourable.ConclusionWhile a conservative approach to revascularisation is favoured, SCAD cases with higher risk presentations may require PCI. SCAD-PCI is associated with longer stent lengths and a higher risk of complications but leads to overall improvements in coronary flow and good medium-term outcomes in patients.

Background The prognosis and treatment of the 2 main types of cardiac amyloidosis, immunoglobulin light chain (AL) and transthyretin (ATTR) amyloidosis are substantially influenced by cardiac involvement. ATTR amyloidosis has better prognosis than AL despite more amyloid infiltration. This paradox suggests additional mechanisms of damage in AL amyloidosis. The aim of this study was to assess the presence and ?prognostic significance of oedema in a large population of patients with cardiac amyloidosis and compare findings among those with TTR and AL types. Methods and results 286 patients (100 with systemic AL amyloidosis (including 49 patients scanned prior to commencing chemotherapy), 163 with cardiac ATTR amyloidosis, 12 with suspected cardiac ATTR amyloidosis (grade 1 on 99mTc-DPD) and 11 asymptomatic individuals with amyloidogenic transthyretin(TTR) mutations), and 30 healthy volunteers were recruited. All subjects underwent CMR with T1 and T2 mapping, and ECV quantification. Left ventricular(LV) mass and ECV were higher in ATTR compared to AL whilst LV ejection fraction(EF) was significantly lower(p Conclusion Patients with AL amyloidosis have a worse prognosis compared to ATTR despite having less cardiac amyloid infiltration. T2 was significantly higher in untreated AL amyloidosis consistent with oedema, and was an independent predictor of prognosis. The higher ECV in ATTR was consistent with higher amyloid infiltration. These findings highlight the unique role of CMR with multiparametric mapping for characterising the cardiac effects of systemic amyloidosis and risk stratification in this population.

Over a decade of research has shown nitric oxide (NO) to be a ubiquitous modulator of biological phenomena from cell signal to effector and from physiology to pathophysiology. The involvement of NO in cardiovascular biology has contributed significantly to our understanding of complex disease states including atherosclerosis, systemic and pulmonary hypertension, endotoxic shock, pre-eclampsia,1cardiomyopathy,2 and cardiac allograft rejection.3 However, the emerging role of NO in the maintenance of cell physiology from immunomodulation to calcium signalling has highlighted the importance of this fascinating molecule in cytostasis. This dichotomy of effector function is the “double edged sword” of NO in biological systems. However, the balance between cytostatic and cytotoxic effects of NO may lie in the tissue concentration of NO produced, the particular NO synthase (NOS) isoform activated (that is, “high output” or “low output”), and the complex interaction with other free radicals such as superoxide. However, a much greater understanding of the molecular and cellular actions of NO as a physiological regulator has resulted in a body of recent research increasing our understanding of NO, and thus NO releasing agents, in cytoprotection. Current evidence is outlined below. NO is produced by the catalytic action of NOS on the substrateL-arginine. The reaction involves the oxidation of one of the guanidinonitrogens of arginine and the process involves the oxidation of NADPH (nicotinamide adenine dinucleotide phosphate, reduced form) and the reduction of molecular oxygen. Three NOS enzymes have been characterised: type I (ncNOS), type II (iNOS), and type III (ecNOS). ncNOS and ecNOS are calcium dependent and low output enzymes associated with NO production in the picomolar range, whereas iNOS is a calcium independent and high output enzyme associated with NO production in the nanomolar (nmol) range. All three NOS isoforms have been shown to be present in …

Background Microparticles (MP) are sub-micron vesicles shed from eukaryotic cells following activation or apoptosis. They appear to have a role in the genesis and progression of atherosclerosis, leading to symptomatic coronary artery disease (CAD). It is now established that the levels of MP are elevated in CAD however, the MP signature associated with the spectrum of CAD is yet to be established. Methods 42 patients undergoing PCI (11 STEMI, 13 NSTEMI and 18 stable angina) were prospectively enrolled. MP levels from venous blood taken prior to PCI were measured by flow cytometry. Results (Figure 1): Patients with STEMI expressed significantly higher levels of CD62P+ platelet-derived MP (median 14.5%, IQR 8.1–20.3%) compared to NSTEMI (median 1.2%, IQR 0.4–19%, p + (ICAM-1) endothelial cell-derived MP. Conclusions The MP signature associated with CAD appears to differ with STEMI showing a predominantly pro-thrombotic signal and NSTEMI a pro-inflammatory signal. This suggests not only differing underlying pathophysiology but also indicated a potential new tool in rapid assessment and risk stratification.

Aims To compare optical coherence tomography (OCT)-derived plaque characteristics of the culprit and non-culprit coronary arteries in patients with Non ST elevation myocardial infarction (NSTEMI) and stable angina pectoris (SA). Methods Assessment of clinical data, angiographic, and OCT imaging including the analysis of plaques was performed. Plaque composition, thickness, arc, length, volume and relative volume were recorded. The presence of thrombus, microvessels, macrophages, cholesterol crystals and calcific nodules were recorded (in percentage of frames) as well. Results To date, 12 patients (8 NSTEMI and 4 SA) were included and analysed. Mean age of this predominantly male group was 55.36 ± 7.9 years. In total OCT was performed in 31 coronary arteries (12 culprit and 19 non culprit) - corresponding to a total of 1992 frames were analysed. Artery level analysis revealed a higher lipid content in culprit arteries as documented by a wider maximum lipid arc (221.91 ± 87.5 vs. 139.2 ± 42.0; p = 0.009) and higher relative lipid volume index (6.35 ± 4.8 vs. 3.3 ± 2.8; p = 0.08). Furthermore, in culprit arteries average cap thickness was smaller (340μ±41μ vs. 400μ±81μ; p = 0.03), and the incidence of macrophages was higher (% of frames 7.8 ± 6.2 vs. 3.2 ± 4.6; p = 0.02). Conclusions In this three-vessel OCT study culprit arteries in both NSTEMI and SA were noted to have more vulnerable features than non-culprit arteries however, larger studies are required to establish this finding.

Objective To determine the feasibility of a fast track pathway for high risk Non ST elevation acute coronary syndrome (NSTEACS) patients and to determine outcomes when compared with a conventional pathway of treatment. Methods This was a retrospective analysis comparing high risk NSTEACS patients admitted via a fast track pathway, with age and sex matched controls admitted via the conventional pathway. Results Over a period of 26 months, 96 patients were admitted through the Fast Track NSTEACS group and 78 patients through the control group. There was shorter duration of hospital stay for the fast track group (mean hospital stay, 3.4; SD 3.63 days) compared to the control group (mean hospital stay, 5.6 days (SD: 4.07), p Conclusion Admission of high-risk NSTEACS patients by fast track pathway resulted in shorter time from admission to angiography and shorter hospital stay, but had no significant effect on patients’ 6-month mortality risk or peak troponin release when compared to those admitted via existing pathways.

Introduction The use of primary percutaneous coronary intervention (PCI) in octogenarians to treat ST elevation myocardial infarction (STEMI) is less than in other age groups. This is due in part to underrepresentation in clinical trials and perceived increased risk. We present long-term survival of a large cohort of elderly patients following primary PCI in London. Methods This was an observational study of 10 249 consecutive patients undergoing primary PCI for STEMI at eight London heart attack centres between January 2005 and November 2011. Patient9s details were recorded at the time of procedure into the British Cardiac Intervention Society (BCIS) database. Outcome was assessed by all-cause mortality. Anonymous datasets from the eight centres were merged for analysis. The primary end-point was all-cause mortality at a median follow-up of 3.0 years (IQR range 1.2–4.6 years). Results A total of 1051 octogenarians (10.3% of the study population) with an average age of 84.2 years (IQR 80–101) were treated with primary PCI during the study period. Over time, the annual proportion of octogenarians gradually increased from 9.1% in 2005 to 10.5% in 2010. Unsurprisingly, when compared to patients under 80, octogenarian STEMI patients included a higher proportion of women, and had a higher prevalence of hypertension, hypercholesterolaemia, multi-vessel disease, previous infarction and previous CABG (table 1). They additionally were less likely to undergo radial access, receive GPIIb/IIIa inhibitors or a drug-eluting stent. When compared with younger patients, primary PCI in octogenarians was less likely to achieve TIMI flow grade 3. However between 2005 and 2011 the rates of post-procedural TIMI flow grade 3 increased significantly from 80.5% in 2005 to 90% in 2011 (p for trend 0.05). The cumulative incidence of all-cause mortality during follow-up was significantly higher in the octogenarian group compared to the younger subgroup (51.6% vs 12.8%, p Conclusions Octogenarians constitute an important subgroup of STEMI patients. Data from London9s experience would suggest that primary PCI rates are increasing in this group and that despite the high long term mortality, acute/year one rates survival rates are very encouraging.

Background Carotid intima media thickness (CIMT) has been used as a risk stratification tool for coronary artery disease (CAD). However, there is insufficient prospective data regarding carotid plaque (CP) and severity of CAC in asymptomatic diabetic subjects. Aim Our aim was to determine if CIMT and presence of CP were predictors of prevalence and severity of CAC. Methods One hundred and eight (n = 108) diabetic patientsrecruited for the PROCEED study (Progression of Coronary Atherosclerosis in Asymptomatic Diabetic Subjects – Evaluation of the role of CT Coronary Angiography and bio-markers of Endothelial Dysfunction and Vascular Inflammation) a prospective study in asymptomatic Type II diabetic subjects, evaluating the progression of atherosclerosis, underwent both carotid ultrasound and CAC scan. Measures of carotid atherosclerosis include CIMT and presence of carotid plaque. Coronary calcium scan was done by dual source multi slice scanner ((Siemens Medical Systems, Forchheim, Germany) and carotid ultrasound was performed using 9–12 MHz linear transducer (GE Vivid E9). Results The mean age of the study population was 61.3 + 8.7 years and Body Mass Index (BMI) 31.1 + 6.8. There were 65 (60.2%) males, 9 (8.3%)with h/o current smoking, 87(80%) with hypertension, 71 (65.7%) with hyperlipidaemia, 50 (46%) with micro vascular disease and 15 (13.9%) with a h/o premature ischaemic heart disease (IHD) . Mean CIMT was 0.82 ± 0.17 mm and CP was noted in 43(40%) patients. Mean CIMT did not differ significantly in patients with micro-vascular disease (MVD) as compared to those without (0.85 ± 0.18 mm vs 0.80 ± 0.17 mm). 32 (30%) patients had a CAC score of zero.76 (70%) had CAC >0, of which, 53(49%) had CAC score 1–400 and 23(21%) had a CAC score > 400. Association between CAC and CP was stronger on univariate (p = 0.002) and borderline on multivariate (p = 0.05) regression analysis. A significant association between prevalence of carotid plaque and severe CAC (>400Au) was noted in a Chi square analysis (p 0.019), Odds Ratio of 3.81 (95% CI of 1.44–10.06) whereas correlation between CAC and IMT was poor(r = 00.03) on bivariate analysis. Conclusion Presence of CP was independently associated with severity of CAC whereas CIMT was not, even in this high risk diabetic population. Carotid plaque evaluation may have important clinical implication by identifyingsub group of high risk population in asymptomatic diabetes.

Introduction During Primary Percutaneous Coronary Intervention (PPCI) post ST-Segment Myocardial Infarction (STEMI), distal embolisation of thrombus may lead to failure to re-establish normal flow in the infarct-related artery. Manual thrombus aspiration has been shown to improve coronary perfusion as assessed by time to ST-segment resolution and myocardial blush grade. Evidence supporting the benefit of thrombus aspiration on clinical outcomes, however, is limited and inconsistent. We aimed to assess the impact of manual thrombectomy on mortality in patients presenting with STEMI across all PPCI centres in London over a 5 year period from 2007 until 2012. Methods This was an observational cohort study of 9935 consecutive patients with STEMI treated with PPCI between 2007 and 2012 at eight tertiary cardiac centres across London, UK. Patient9s details were recorded at the time of the procedure into the British Cardiac Intervention Society (BCIS) database. Outcome was assessed by all-cause mortality. Anonymous datasets from the eight centres were merged for analysis. The primary end-point was all-cause mortality at a median follow-up of 2.0 years (IQR range 1.1–3.1 years). Results Of the 9935 consecutive STEMI patients presenting for PPCI, 2859 had mechanical thrombectomy. Patients who had manual thrombectomy were significantly younger (average age 60.6 vs 62.9) and were less likely to have had a previous myocardial infarction (11.9% of thrombectomy patients vs 14.7% of non-thrombectomy patients). Patients receiving manual thromectomy were found to be significantly more likely to have had PPCI via a radial approach (33.1% in thrombectomy patients vs 19.9% in non-thromectomy patients). Procedural success (defined as TIMI 3 flow at the end of procedure) was found to be significantly more likely in patients receiving manual thrombectomy (89.5% vs 86.7%) (table 1). Patients with thrombectomy use had similar unadjusted all-cause mortality rates to those without thrombectomy use (12.7% vs 16.5%, p=NS) during the 5-year follow-up period (figure 1). After multivariable adjustment thrombectomy use was associated with significantly decreased mortality rates (HR: 0.82, 95% CI 0.68 to 0.9, p=0.04). Conclusion Mechanical thrombectomy use appears to be associated with improved outcome, in the form of decreased mortality, in this large observational trial.

Background Primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy in patients with ST-segment elevation myocardial infarction (STEMI). We evaluated whether direct transfer to a cardiac centre performing primary percutaneous coronary intervention (PPCI) leads to improved survival compared with transfer via a non-PPCI performing hospital in STEMI patients in a regional network. Methods This was an observational cohort study of 10 108 patients with STEMI treated with PPCI between 2004 and 2011 at eight tertiary cardiac centres across London, UK. Patient9s details were recorded at the time of the procedure into the British Cardiac Intervention Society (BCIS) database. Outcome was assessed by all-cause mortality. Anonymous datasets from the eight centres were merged for analysis. The primary end-point was all-cause mortality at a median follow-up of 3.0 years (IQR range 1.2–4.6 years). Results 6492 patients (64.2%) were transferred directly to a PCI performing centre (direct) and 3616, (35.8%) were transferred via a non-PCI performing centre (indirect). There were higher rates of previous MI and previous CABG in the indirect group, with higher rates of poor LV function in the direct group (table 1). Median time to reperfusion (symptom to balloon) in transferred patients was 58 min longer compared to patients admitted directly (p 0.0001) at presentation compared to those transferred directly. Kaplan-Meier analysis demonstrated no significant difference in mortality rates between patients with and without transfer (12.3% direct vs 14.3% indirect, p=0.060). Age-adjusted Cox analysis revealed inter-hospital transfer for PPCI was associated with all cause mortality (HR 0.89 (95% CI 0.79 to 0.99)), however this was not maintained after multivariate adjustment (HR 0.84 (95% CI 0.62 to 1.14)). Conclusions In this large registry survival appear comparable in patients with STEMI admitted directly versus transferred for primary PCI. This is despite longer symptom to balloon times. This unexpected finding may reflect the earlier initiation of medical therapy (eg, anti-platelets and GpIIb/IIIa receptor inhibitors) and earlier pharmacological reperfusion, reflected by lower IRA TIMI 0 rates at angiography in the patients transferred from a non-PCI hospital.

Introduction Primary percutaneous coronary angioplasty (PPCI) is the preferred reperfusion strategy following an acute ST elevation myocardial infarction (STEMI). Since 2005 24/7 primary PCI has been the first line treatment for an acute STEMI in our centre. 93% of patients are direct access admissions by London Ambulance but a significant proportion (up to 20%) do not fulfil the diagnostic criteria for STEMI and are termed “false activations”. Data on the outcome of this cohort of patients is limited. Aim To review the clinical outcome of patients presenting to our heart attack centre with false activation PPCI. Method From January 2008 until October 2010, we identified 209 false PPCI activations defined as patients with incomplete diagnostic criteria for acute STEMI: absence of chest pain and/or typical ECG features (ST elevation or new LBBB). Data was collected via a “false activation” database together with retrospective review of case records. Results Complete data was available in 165 cases. 71% were male and 29% were female (mean age 67). The mean length of stay was 4 days (range 1–33). 71% presented with chest pains and 29% had no chest pains, but presented with breathlessness, palpitations or syncope. The ECG abnormality was non-specific ST-T changes in 22%, LBBB in 19%, left ventricular hypertrophy in 15%, fixed ST elevation or Q waves in 14%, early repolarisation changes in 10%, RBBB in 8% and other ECG abnormalities in 12%. The final diagnosis was non-ST elevation acute coronary syndrome (NSTEACS) in 19%, sepsis in 19% and congestive heart failure (CHF) in 15%. Stable angina was observed in 8% and syncope in 7%. Musculoskeletal or non-cardiac chest pains were noted in 8% and 7% of the patients respectively. 2% of the patients had pulmonary embolism and in 5%, a gastric cause for presentation was diagnosed. 14% had other cardiac problems, including arrhythmia, dilated cardiomyopathy, hypertension, pericarditis, pericardial effusion and late presentation STEMI. 15% had other diagnoses. The mean follow-up period was 18.7 months, during which 21.5% of false PPCI activation admissions died (n=45). 25% (n=11) died during the index admission and 33% (n=15) died within 30 days of admission. The overall 30-day mortality for false activations was 7.2%, which is higher than the overall PPCI mortality of 6.0% (including cardiogenic shock) (p=0.008) and 3.3% (excluding shock) (p Conclusion Patients presenting with false PPCI activation have a high observed mortality. This is probably due to significant associated comorbidities, including occult cardiac disease. Thus, false PPCI activation is not a benign phenomenon and masks underlying significant disease. Robust pathways are required to minimise delay in further investigations and a need for risk stratification for a significant proportion who present with NSTEACS.

Background Microvascular dysfunction is associated with adverse outcome in patients with acute coronary syndrome (ACS). During ACS platelet and monocyte derived chemokines, in conjunction with adhesion molecule expression, promote the inflammatory process. Activated platelets express p-selectin which binds to the p-selectin glycoprotein ligand on the monocyte forming platelet monocyte aggregates (PMA). PMA expression is a sensitive marker of platelet activation and inflammation. Although platelet monocyte interaction is a normal physiological process, in the presence of platelet activation, activated (CD62+ PMA) may be directly involved in the pathophysiology of intracoronary inflammation and microvascular dysfunction in ACS. Aim To investigate the relationship between microvascular dysfunction and PMA expression in patients with stable angina and non-ST elevation myocardial infarction (NSTEMI). Methods Six patients with stable angina undergoing elective PCI and six patients with NSTEMI undergoing non-elective PCI were recruited. Microvascular dysfunction was assessed by measuring the coronary wedge pressure (CwP) and the index of Microvascular resistance (IMR) using a single pressure-temperature sensor-tipped coronary wire from the simultaneous measurement of distal coronary pressure and thermodilution derived mean transit time (Tmn) of a bolus of saline injected at room temperature into the coronary artery during maximum hyperaemia. Blood samples were taken from the coronary artery (distal to the culprit lesion), aorta and the right atrium for PMA estimation. PMAs were assessed using fluorescent monoclonal antibodies and flow cytometry. Total PMAs were calculated and expressed as a percentage of the total monocyte count. Activated CD62+ PMAs were expressed as a percentage of total PMAs. Results As expected CwP was higher in patients with NSTEMI (46.5 (SD) 18.8) compared with the stable angina patients (Mean (SD) 21.1 (9.3) p=0.01). IMR was also higher in patients with NSTEMI (Mean (SD) 27.6 (12.6)) compared with patients with stable angina (Mean (SD) 20.7 (5.4) p=0.2). Total PMAs were non-significantly higher in patients with NSTEMI (Mean (SD) 14 (4.8)) compared with stable angina (Mean (SD) 10.9 (4.3) p=0.07). CD62+ PMAs were significantly higher in patients with NSTEMI (Mean (SD) 26.9 (12.2)) compared with stable angina (Mean (SD) 13.7 (5.1) p=0.02) Abstract 27 figure 1. CwP correlated positively with total PMA (p=0.01) in NSTEMI but not in stable angina patients. However, IMR correlated positively with total PMAs in both stable angina (p=0.02) and NSTEMI (p=0.08) Abstract 27 figure 2. Conclusions PMAs are elevated in stable coronary disease and ACS with elevated activated CD62+ PMA a hallmark of ACS. PMAs correlate with measured microvascular dysfunction during PCI in stable angina and NSTEMI. This study supports the hypothesis that PMA formation may be important determinants of platelet activation, inflammation and microvascular dysfunction in coronary disease.

Editor,—We write in response to the editorial “Diabetes and coronary artery disease: time to stop taking the tablets”.1 The authors highlight previous studies where diabetic patients treated with sulphonylureas have an excess cardiovascular mortality during myocardial infarction compared with diabetic patients treated by other means. As Connaughton and Webber point out ischaemic preconditioning has refocused our attention on these trials. The profound protective effects of ischaemic preconditioning are thought to be mediated by opening of a KATP channel, while the hypoglycaemic action of sulphonylureas is mediated by closure of these channels within the membrane of β cells in the islets of Langerhan. The authors suggest that it may be simply a case of “adding a potassium channel opener along with insulin during [myocardial infarction] MI” to improve outcome in diabetics presenting with infarction. However, recent findings suggest this is an oversimplification and probably incorrect. One problem is that, there are at least two different KATP channels within cardiac myocytes. Evidence is emerging that it is the mitochondrial and not the cell membrane KATPchannels that initiates the cardioprotective effects of preconditioning. This conclusion is based on recent work from Marban’s group.2-4 These investigators show that …