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The past 20 years have seen significant changes in both the demographics and natural history of many cardiovascular diseases. Important reductions in case-fatality rates (such as in acute coronary syndromes) have resulted from improved diagnostics and treatment options and better understanding of natural history. For others (such as infective endocarditis), improvements have been limited and disappointing. While advances in therapy and the scientific evidence underpinning treatments have been crucial, the importance of accurate diagnosis has remained a key element for progress. Many of the principles needed for diagnosis are constant: the pre-eminence of a focused, accurate history, complete physical examination, and timely and relevant investigation endures. It is essential to have a secure knowledge of the strengths and limitations of interpretation of a frequently bewildering array of tests. Progress in this field has been rapid; advances in ultrasound, scintigraphy, and cardiac magnetic resonance stand out at the interface between structure and function central to good patient care.

Background: Coronary sinus (CS) blood sampling is important for measuring metabolites and biomarkers in cardiovascular research, but can be technically challenging. Here we demonstrate the use of the antecubital fossa for CS blood sampling as an alternative to femoral access, and a simple technique of paired venous and CS blood gas analysis for confirmation of valid CS sampling. We also demonstrate improvement in sampling accuracy by using a coronary guide wire to stabilize the sampling catheter in the CS. Methods: Paired blood samples from CS and peripheral vein were collected from patients at the time of primary PCI for acute myocardial infarction. Venous access for CS sampling was via the antecubital vein. Blood gas analysis was used to confirm a true CS sample (pO2[CS]

AIMS: Predicting the likely success of primary PCI to salvage potential infarcted myocardium is desirable. We compared early invasive parameters of coronary microcirculation function with the levels of circulating endothelin (ET-1) and 6-month ejection fraction after STEMI. METHODS AND RESULTS: Forty-four STEMI patients underwent assessment of coronary flow reserve (CFR) and index of myocardial resistance (IMR) on completion of PPCI and one day later. Cardiac magnetic resonance (CMR) at 24 h and 6 months assessed ejection fraction, oedema, late gadolinium enhancement, and salvage. In patients with depressed EF, there was no difference in IMR or CFR measured immediately after PPCI compared with those with preserved EF. However, by Day 1, CFR was significantly lower in those with depressed EF [2.0(1.5-2.3) vs. 2.6(2.1-3.3), P = 0.008]. In multivariable models, higher CFR post-PPCI [EST: +8.9 (SE 3.7) per 1 CFR unit, P = 0.03] and greater increase in CFR between post-PPCI and Day 1 [EST: +8.5 (SE 3.4) per 1 CFR unit, P = 0.01] were associated with higher salvage index. Circulating endothelin levels were significantly elevated in the low EF group at both 6 and 24 h, and 24 h levels correlated with CFR. CONCLUSION: Changes of the coronary microcirculation in the first day after PPCI are associated with 6-month ejection fraction and myocardial salvage. Depressed CFR at 24 h is associated with CMR imaging indices of MVO and haemorrhage and elevated endothelin levels.

Background— Changes in the myocardium in acute ischemia are dynamic and complex, and the characteristics of myocardial tissue on cardiovascular magnetic resonance in the acute setting are not fully defined. We investigated changes in edema and late gadolinium enhancement (LGE) with serial imaging early after acute myocardial infarction, relating these to global and segmental myocardial function at 6 months. Methods and Results— Cardiovascular magnetic resonance scans were performed on 30 patients with ST-elevation–myocardial infarction treated by primary percutaneous coronary intervention at each of 4 time points: 12 to 48 hours; 5 to 7 days; 14 to 17 days; and 6 months. All patients showed edema at 24 hours. The mean volume of edema (% left ventricle) was 37±16 at 24 hours and 39±17 at 1 week, with a reduction to 24±13 ( P P P =0.002). Of segments showing LGE at 24 hours, 50% showed resolution by 6 months. In segments with such a reduction in LGE, 65% also showed improved wall motion ( P r =0.9; P r =0.7). The difference in LGE between 24 hours and 6 months had profound effects on the calculation of salvage index (26±21% at 24 hours versus 42±23% at 6 months; P =0.02). Conclusions— Myocardial edema is maximal and constant over the first week after myocardial infarction, providing a stable window for the retrospective evaluation of area at risk. By contrast, myocardial areas with high signal intensity in LGE images recede over time with corresponding recovery of function, indicating that acutely detected LGE does not necessarily equate with irreversible injury and may severely underestimate salvaged myocardium.

Objectives: To investigate rates of and reasons for second and subsequent stent procedures in an unselected, “real-world” population. Background: Repeat stenting is the primary difference reported in clinical trials of alternative revascularization strategies. The incidence, indication, and outcome for repeat stenting in contemporary practice outside the more selective populations of trials and registries has not been described. Method: All patients undergoing a first percutaneous coronary intervention (PCI) procedure with stenting from January 2001 to August 2009 (10,509) from a large UK tertiary referral and district general hospital were identified. Mortality and the incidence, timing, and indication for repeat revascularization in this population were investigated from patient records. Results: Of 10,509 patients undergoing a first PCI and stent implant 23.5% underwent repeat angiography of which 11.2% required repeat PCI and 2% coronary artery bypass grafting (median follow-up of 3.8 years). A total of 1.3% went on to a third PCI. The commonest indication for repeat stenting was disease progression remote from the original stent (46%) and planned staged PCI (23%); 21% had a stent-related indication. Functional assessment before repeat stenting was used in one-third of stable patients. Mortality was 2.5% per annum. Conclusions: In contemporary practice, patients undergoing a first stenting procedure have a low subsequent mortality, and the substantial majority (86.4%) requires no further revascularization over a median 3.8 year follow-up. For those who do require repeat stenting, this is most commonly at a site remote from the first stent. © 2012 Wiley Periodicals, Inc.

Pericardial diseases are common but rigorous large-scale or randomized studies of current clinical practice remain limited. This article outlines a current and practical approach to the clinical assessment and investigation of pericarditis, pericardial effusions and constrictive pericarditis. The management of these conditions is discussed in line with best practice. Limited clinical trial data underlines the importance of bedside and investigative skills in assessing both the function and form of this organ and the treatment options.

BACKGROUND: Craniofacial abnormalities and increased pharyngeal collapsibility due to abnormal connective tissue suggest the possibility of an increased prevalence of obstructive sleep apnoea (OSA) in patients with Marfan's syndrome but the actual prevalence is uncertain. Aortic dilatation and dissection are life threatening manifestations of Marfan's syndrome and case reports have suggested a possible association with OSA but data from cohort studies are not available. METHODS: A sleep study was performed in 61 patients with Ghent criteria positive Marfan's syndrome (mean age 38.3 (SD 12.9) years; 37 females) and in 26 control subjects matched for age, gender, height and weight. OSA was defined using two conventional levels of apnoea-hypopnoea index (AHI), >5 and >15/h. In patients with Marfan's syndrome, aortic root diameter was measured by echocardiography. RESULTS: More patients with Marfan's syndrome than controls had OSA (AHI >5, 32.8% compared with 11.5%, mean difference +21.3%, 95% CI 4.2% to 38.3%, p = 0.04; AHI >15, 18.0% compared with 0%, mean difference +18.0%, 95% CI 8.4% to 27.7%, p = 0.02). AHI was correlated with aortic root diameter (r = 0.50, 95% CI 0.26 to 0.69, p = 0.0003), and mean aortic root diameter was significantly greater in patients with OSA (4.5 (SD 0.6) cm) compared with those without OSA (3.7 (0.6) cm) (mean difference 0.8 cm, 95% CI 0.4 to 1.2 cm, p

Introduction: Cinacalcet is a calcimirnetic agent used to treat secondary hyperparathyroidism in patients with end-stage renal disease on dialysis or bypercalcemia related to parathyroid carcinoma. This report describes recurring circulatory collapse in a patient treated with cinacalcet for unrelated refractory primary hyperparathyroidisrrm. Case summary: A white man, aged 54 years and weighing 68 kg, was admitted to the hospital with lethargy, dyspnea, and twitching in the extremities. He was diagnosed previously with primary hyperparathyroidism and nonischemic dilated cardiomyopathy. Surgical parathyroidectomy had been unsuccessful. His serum calcium concentration was 3.15 innol/L and was refractory to bisphosphonate therapy. Therapy with cinacalcet 30 ingld was reinitiated, resulting in a reduction in serum calcium concentration and greatly increased heart failure requiring inotropic drug therapy and hemofiltration. After 13 days of treatment, cinacalcet was withdrawn, and the patient's condition unproved. On reintroduction of cinacalcet 30 mg/d, the patient decompensated and required emergency circulatory support. Decompensation resolved 5 days after discontinuation of cinacalcet. Discussion: Based on a score of 7 on the Naranjo adverse drug reaction probability scale, cinacalcet was the probable cause of cardiogenic shock in this patient. Calcium-channel antagonist poisoning is associated with hypotension and bradycardia, whereas the calcium sensitizer levosimendan has been reported to improve low-output heart failure, suggesting that calcium may have inotropic properties. Conclusions: It appears that cardiac function in this patient had adapted to hypercalcermia and became destabilized after introduction of cinacalcet. Caution should be exercised when considering treatment with cinacalcet in patients with heart failure.

Contains fulltext : 156882.pdf (Publisher’s version ) (Open Access) RATIONALE: A number of randomized trials are underway, which will address the effects of angiotensin receptor blockers (ARBs) on aortic root enlargement and a range of other end points in patients with Marfan syndrome. If individual participant data from these trials were to be combined, a meta-analysis of the resulting data, totaling approximately 2,300 patients, would allow estimation across a number of trials of the treatment effects both of ARB therapy and of beta-blockade. Such an analysis would also allow estimation of treatment effects in particular subgroups of patients on a range of end points of interest and would allow a more powerful estimate of the effects of these treatments on a composite end point of several clinical outcomes than would be available from any individual trial. DESIGN: A prospective, collaborative meta-analysis based on individual patient data from all randomized trials in Marfan syndrome of (i) ARBs versus placebo (or open-label control) and (ii) ARBs versus beta-blockers will be performed. A prospective study design, in which the principal hypotheses, trial eligibility criteria, analyses, and methods are specified in advance of the unblinding of the component trials, will help to limit bias owing to data-dependent emphasis on the results of particular trials. The use of individual patient data will allow for analysis of the effects of ARBs in particular patient subgroups and for time-to-event analysis for clinical outcomes. The meta-analysis protocol summarized in this report was written on behalf of the Marfan Treatment Trialists' Collaboration and finalized in late 2012, without foreknowledge of the results of any component trial, and will be made available online (http://www.ctsu.ox.ac.uk/research/meta-trials). 01 mei 2015

Objective: Paragangliomas are rare tumors of neuroendocrine origin; approximately 30% of these tumors are related to an underlying genetic condition. Many of the hereditary paragangliomas, particularly those arising in the head and neck, have been linked to mutations in genes encoding different subunits of the succinate dehydrogenase (SDH) enzyme complex. The authors report an atypical presentation of a rare mutation in the SDH complex subunit C gene (SDHC).Methods: We reviewed the patient's clinical course, along with relevant literature for similar reported cases.Results: A 45-year-old woman with a background of multiple and recurrent paragangliomas (left glomus jugulare, right carotid body tumor, intrathyroidal and right lung paragangliomas) was found to have an intrapericardiac paraganglioma associated with excess levels of dopamine metabolites. Simultaneously, the proband's son was diagnosed with a macroprolactinoma at age 23 years. Genetic workup identified an underlying germline mutation in the gene encoding SDHC, consistent with the diagnosis of familial paraganglioma syndrome type 3. Current knowledge regarding the clinical implications of an SDHC gene mutation have been reviewed.Conclusion: Patients with SDHC gene mutations can develop paragangliomas within the pericardium. Our patient presented with multiple recurrent paragangliomas, in different locations, including within the pericardium. These tumors were functional, including a dopamine-secreting paraganglioma. The presence of multiple paragangliomas, the cardiac localization of tumors, the high risk of recurrence, and the elevation of 3-methoxytyramine levels should be taken into account when treating these patients. In addition, the diagnosis of macroprolactinoma in our patient's son reinforces the reported association between SDH mutations and the development of pituitary tumors.Abbreviations: MRI magnetic resonance imaging RET RET proto-oncogene SDH succinate dehydrogenase SDHB succinate dehydrogenase enzyme complex subunit B SDHC succinate dehydrogenase enzyme complex subunit C

Restoration of effective myocardial reperfusion by primary percutaneous coronary intervention (PPCI) in patients with STEMI is not predictable. A method to assess the likelihood of a suboptimal response to conventional pharmaco-mechanical therapies could be beneficial. We aimed to derive and

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy).The prevalence of MVO was reduced in the adenosine-treated patients (45%) compared to 85% of control patients (P=0.0043). We found that the size of MVO in adenosine-treated patients was significantly reduced (0.35g) compared to 0.91 g in the control group (P=0.027). There was no statistically significant difference in TIMI flow and clinical outcomes after primary PCI.Excel software was used to calculate the p-values. On recalculation using a newer version of the programme, the values are coming back different: Prevalence of MVO comparing adenosine to non-adenosine is now 0.15, therefore non-significant. Also the P-value for the mass of MVO in adenosine versus non-adenosine is 0.34, again non-significant.

Background: Aortic dissection is a life-threatening manifestation of Marfan's syndrome. Preliminary evidence suggests that obstructive sleep apnea (OSA) is associated with aortic disease in Marfan's syndrome. Objectives: To study the effect of OSA on aortic events in Marfan's syndrome. Methods: In patients with Marfan's syndrome, a sleep study was performed at baseline and OSA was defined as >5 events of apnea/hypopnea (A+H) per hour in bed. Operation because of progressive aortic dilatation and death because of aortic rupture were defined as ‘aortic events'. Kaplan-Meier survival analyses were used to compare event-free survival in patients with and without OSA. Cox regression models were used to explore the effects of covariates on event-free survival. Results: Data from 44 patients (mean age 37.4 years, 30 females) were available for analysis; 15 patients (34.1%) had OSA. The median follow-up time was 29 (interquartile range 24-36) months. Five patients had an aortic event within the follow-up time. Median event-free survival was 51.6 months. Event-free survival was significantly shorter in patients with OSA compared to patients without OSA (p = 0.012). In univariate analysis, A+H was associated with aortic events [hazard ratio (HR) 1.09, 95% confidence interval (CI) 1.01-1.18, p = 0.023]. Taking the interaction between BMI and A+H into account increased the HR for A+H (HR 1.75, 95% CI 1.003-3.048, p = 0.049). This association was no longer significant when other covariates were forced into the multivariate analysis. Conclusions: These data suggest that aortic event-free survival may be shorter in patients with Marfan's syndrome and OSA compared to patients without OSA, but more data from well-designed studies are needed to prove this association.

Granisetron is a highly potent and selective 5-hydroxytryptamine3 (5-HT3) receptor antagonist indicated for the prevention of cytotoxic-induced nausea and vomiting. Clinical trials have demonstrated granisetron to be effective and well tolerated at a standard dose of 40 micrograms/kg or 3 mg given i.v. as a 5-min infusion. In this study, the efficacy and safety of granisetron given as a 30-s infusion was assessed. A total of 21 patients, scheduled to undergo chemotherapy, received a single 3-mg i.v. dose of granisetron over 30 s, completed at 1 h before chemotherapy administration. Patients were allowed two further i.v. doses of granisetron at 3 mg within the 24-h assessment period. Changes from baseline values in vital signs were analysed prior to granisetron administration and at 30 s as well as 1, 10, 15, 30 and 60 min after granisetron administration. Holter ECG recordings were taken for 6 h prior to and 1 h after administration. No significant change was found in vital signs at 30 s or 1 min after granisetron infusion. There was a small but statistically significant fall in diastolic blood pressure as compared with baseline and a non-significant trend in favour of a reduction in heart rate at 10 and 15 min. No ECG abnormality was recorded post-infusion that had not been present pre-infusion. None of these changes was considered to be clinically relevant. The treatment was well tolerated. The most frequently reported adverse events were constipation (n = 6) and headache (n = 5). Maximal plasma levels of granisetron were within the range of 44.57-410 ng/ml except in one patient. The median values recorded for peak concentration (Cmax) and area under the curve (AUC) were 195 ng/ml and 71.2 ng h ml-1, respectively. In conclusion, granisetron at 3 mg was shown to be safe and well tolerated when given as a 30-s i.v. infusion to patients receiving chemotherapy for malignant disease.

Background Aortic blood flow in healthy people is characterised by helical flow in the ascending and descending aorta, with corresponding patterns of wall shear stress (WSS) imposed upon the wall of the aorta by moving blood. Flow and WSS patterns in the aortic root and sinuses of Valsalva, and the flow patterns in diseased aortas are incompletely defined. We describe the use of a validated, time-resolved, 3D flow MRI sequence to characterize flow and WSS in the aorta, focusing on the aortic root, and demonstrate the flow and WSS in the aorta of healthy volunteers and patients with prior aortic dissection.

Background Abnormalities of dystrophin expression cause Duchenne Muscular Dystrophy (D) or Becker Muscular Dystrophy (B). Since widespread use of non-invasive respiratory ventilation, many D patients who previously died in their early 20 s from respiratory failure are now surviving longer and developing cardiomyopathy. In B patients, disease progression is slower, however, development of progressive cardiomyopathy is highly frequent. One previously identified predictor of mortality in cardiomyopathy is myocardial fibrosis as detected by late gadolinium enhacement (LGE) cardiovascular magnetic resonance (CMR) imaging. Furthermore, a high percentage and typical inferolateral pattern of LGE has been previously reported in small numbers of patients with B/D, however, the relationship with left ventricular systolic dysfunction needs to be further evaluated.

Twenty-five patients (aged 62 +/- 2 years) with stable, moderate to severe ischemic congestive heart failure (CHF) (New York Heart Association class II/III: 15/10; ejection fraction 21.6 +/- 2%; and peak oxygen uptake 13.6 +/- 0.7 ml/kg/min) were studied to evaluate the ability of different methods to characterize autonomic tone in chronic CHF. Sympathovagal balance was assessed by: (1) heart rate variability in the time domain, assessed by the SD of RR intervals; (2) heart rate variability in the frequency domain, assessed by low- (0.03 to 0.14 Hz) and high- (0.18 to 0.40 Hz) frequency components of heart rate variability by autoregressive power spectral analysis; (3) 24-hour, daytime and nighttime heart rate; (4) submaximal heart rate during upright bicycle exercise, with respiratory gas analysis to obtain peak oxygen uptake; and (5) radiolabeled norepinephrine spillover. These methods did not correlate, with the exception of day and nighttime heart rate (r = 0.74; p < 0.001) and the expected inverse correlation between low and high frequency (r = -0.92; p < 0.001). No method correlated significantly with peak oxygen uptake, exercise tolerance or ejection fraction. After 8 weeks of physical training at home, all methods showed improvement in autonomic balance: increases in SD of RR intervals (+21%; p < 0.02) and high frequency (+41%; p < 0.007), and decreases in low frequency (-19%; p < 0.002), low-/high-frequency ratio (-48%; p < 0.03), norepinephrine spillover (-28.9%; p < 0.03), 24-hour heart rate (-2.7%; p < 0.005) and submaximal heart rate (-10.8%; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Kinetics of [3H]noradrenaline in the plasma were compared with plasma noradrenaline concentration in assessing overall sympathetic activity in six groups totalling 118 subjects. Arterial plasma noradrenaline in 21 control subjects was 204 +/- 14 pg/ml, similar to 20 patients with stable angina not treated with beta-blockers (194 +/- 25 pg/ml) and to 31 patients with stable angina treated with beta-blockers (232 +/- 19 pg/ml). Plasma noradrenaline was increased in 17 patients with unstable angina (366 +/- 50 pg/ml, P less than 0.01), in 14 patients with recent acute myocardial infarction (460 +/- 44 pg/ml, P less than 0.001) and in 15 patients with treated cardiac failure (582 +/- 78 pg/ml, P less than 0.001). Whole body clearance of noradrenaline from plasma was, however, reduced in each of the last three groups compared to controls by 20% (P less than 0.05), by 34% (P less than 0.01) and by 31% (P less than 0.01), respectively. In the 31 patients with stable angina on beta-blockers, clearance of noradrenaline was also reduced by 20% (P less than 0.05). Whole body noradrenaline spillover, a potentially more accurate measure of overall sympathetic activity than concentration of noradrenaline in plasma, was 235 +/- 20 ng min-1 m-2 in controls, was similar in subjects with stable angina (no beta-blockers; 260 +/- 34 ng min-1 m-2, beta-blockers; 200 +/- 17 ng min-1 m-2), but was increased in patients with unstable angina (310 +/- 27 ng min-1 m-2, P less than 0.05), with recent acute myocardial infarction (346 +/- 40 ng min-1 m-2, P less than 0.05) or with heart failure (438 +/- 65 ng min-1 m-2, P less than 0.01). Overall sympathetic activity is unchanged in stable angina, but is progressively increased in patients with unstable angina, recent myocardial infarction or heart failure. Plasma concentration of noradrenaline fails accurately to reflect this as a result of decreased clearance of noradrenaline in these patients. The results show the potential limitations of measurement of noradrenaline in the plasma as an index of overall sympathetic activity and the importance of assessing clearance.

Background: Anomalous origin of the left circumflex coronary artery from the right sinus of Valsalva or proximal right coronary artery is the most common congenital coronary anatomical abnormality. Whether such vessels are particularly predisposed to atherosclerotic disease in their proximal portion remains controversial. Successful balloon angioplasty has been described, but thus far only six isolated cases of stent deployment in anomalous circumflex vessels have been described in the interventional literature. Methods: Single-center retrospective case study of twenty-two patients with anomalous circumflex coronary arteries. Twelve patients (11/12 male, average age (63 ± 3) years) underwent successful percutaneous coronary intervention (PCI) with stent deployment in the retroaortic segment of the anomalous vessel. Results: Significant obstructive coronary disease in the retroaortic portion was found in the majority of anomalous left circumflex vessels (16/22, 73%), but did not predict the presence of significant two or three vessel coronary disease (P = 0.14, 0.63). PCI was successful in all cases attempted, with favourable short/medium-term event-free survival. Conclusions: The retroaortic portion of anomalously-arising circumflex coronary arteries is selectively predisposed to atherosclerotic disease. PCI to these vessels is feasible but may be technically challenging. © 2006 Wiley-Liss, Inc.

The safety and predictability of percutaneous coronary intervention (PCI) has improved dramatically in the last decade. The increased numbers of patients suitable for the procedures have placed pressure on existing health care systems. Treating patients with chronic stable angina on a day case basis without an overnight stay has several attractions,1 but there are some concerns over the safety of this approach. Troponin I is released rapidly following myocardial necrosis, it is highly sensitive, and may be more specific than other enzymatic markers of cardiac damage. Elevation of cardiac markers, mainly creatine kinase-MB, after both elective percutaneous and surgical revascularisation reflects myocardial necrosis and is associated with increased risk of in-hospital and long term adverse events.2 Glycoprotein (Gp) IIb/IIIa inhibitors appear to be particularly beneficial in reducing this complication,3 but day case intervention precludes overnight administration of Gp IIb/IIIa inhibitors. This audit determined the incidence of serum troponin I elevation after 6–8 hours in patients discharged the same day according to pre-specified clinical, angiographic, and procedural criteria. Two hundred and twenty nine consecutive patients were admitted for elective day case PCI from January to July 2002. This represents 30% of the total PCIs in our institution during this period (n = 762). Predetermined clinical and angiographic inclusion and exclusion criteria were …

An 80-year-old woman was referred with non-sustained palpitations, intermittent presyncope, and atypical chest pain. Examination revealed a loud “plopping” first heart sound and presystolic thrill at the lower left sternal edge. Echocardiography showed a large cystic lesion attached to the septal leaflet of the tricuspid valve, dilatation of the right heart chambers, and moderate tricuspid regurgitation (Figure 1). Three-dimensional contrast echocardiography confirmed the mobile …

A 50-year-old man had a large lateral left ventricular wall pseudoaneurysm with rupture after a limited myocardial infarction. This was diagnosed by the combination of flow in and out of the aneurysm and pulsatile flow in the pericardial cavity using color flow and continuous wave Doppler ultrasound. This report describes the case management, the use of echocardiography in this setting, and the implications of pseudoaneurysm formation.

Conventional surgery for revision of right ventricular outflow tract conduits is complex and demanding. Percutaneous implantation of pulmonary valves may not be feasible in all cases. We describe a safe, alternative hybrid transapical approach from the right ventricle that avoids the extensive dissection and potential complications of revision surgery.

Introduction Changes in myocardial tissue in acute ischaemia are dynamic and complex and the characteristics of myocardial tissue on cardiovascular magnetic resonance (CMR) in the acute setting are not fully defined. We investigated changes in oedema and late gadolinium enhancement (LGE) with serial imaging early after acute MI, relating these to global and segmental myocardial function at 6 months. Methods and Results CMR scans were performed on 30 patients with ST elevation MI (STEMI) treated by primary PCI at each of 4 time points: 12–48 h (TP1); 5–7 days (TP2); 14–17 days (TP3); and 6 months (TP4). All patients showed oedema at TP1. The mean volume of oedema (% LV) was 37±16 at TP1 and 39±17 at TP2 with a reduction to 24±13 (p Conclusions (1) Myocardial oedema was unchanged over the first week but decreased by 15 days; (2) a large majority of segments that were positive for oedema also showed LGE, assessed at 12–48 h; (3) In 46% of patients, LGE present on early scans had diminished in size by 6 months, (4) resolution of LGE was associated with improvement in function; (5) the reduction in LGE at the later time had a profound effect on the calculation of salvage index, which varied by up to ∼60%, depending on the time point used. (6) From a clinical perspective, the use of acute LGE may severely underestimate salvaged myocardium and should not be used to predict recovery of myocardial function.

INTRODUCTION: Up to 10% of patients presenting with chest pain and elevated troponin levels demonstrate non-obstructive coronary arteries on angiography, posing a clinical challenge in diagnosis, prognosis and management. The final diagnosis has important implications for the patient, including prescription for treatment and fitness for permissible activities, occupation and medical insurance. Cardiovascular magnetic resonance (CMR) is superior to other cardiac imaging modalities in tissue characterisation. We hypothesised that CMR, when performed early using conventional and novel tissue characterisation techniques, can determine the cause of acute myocardial injury in these patients and provide a diagnosis. METHODS: One hundred and twenty (n = 120) patients (mean age 50 ± 17 yrs; 50% female) presenting with chest pain, positive troponin I (normal 60 μg/L) and non-obstructive coronaries were prospectively recruited.Early CMR at 1.5T (median 3 days, IQR 1-6 days) included cine, T2W (dark-blood STIR), T1-mapping (ShMOLLI) and LGE imaging. Findings were compared to 50 controls matched for age and gender distributions.Image analysis included: the detection of oedema comparing T2 signal intensity of myocardium to skeletal muscle (>2.0) or remote myocardium (>2 SD); myocardial T1 times (areas of injury defined as an area of ≥40 mm2 with T1 >990 ms as validated for detecting oedema); and presence of LGE. RESULTS: When CMR was performed early using only conventional techniques (cine, T2W and LGE), there was a high diagnostic yield of 95%. Oedema was detected in 79% and LGE in 61% of patients.Based on CMR findings, including the type, pattern and regional distribution of injury, the commonest diagnosis was myocarditis (37%), followed by Takotsubo cardiomyopathy (23%), myocardial infarction (18%), acute regional stunning (9%; wall motion abnormality with oedema but no LGE), dilated cardiomyopathy (4%), hypertrophic cardiomyopathy (3%), and missed pulmonary embolism (1%). In 11/21 (52%) of patients with MI, a patent foramen ovale (PFO) was demonstrated on echocardiography with agitated saline contrast, suggesting these patients may have suffered a paradoxical coronary embolism. The remaining 5.0% (n = 6) of patients had no findings on T2W and LGE imaging. However, T1 mapping localised areas of injury in 4 out of the remaining 6 patients, improving the detection rate to 98%. CONCLUSIONS: Early CMR using conventional and novel T1-mapping techniques has a high diagnostic yield in patients presenting with acute chest pain, positive troponins but non-obstructive coronaries. T1 mapping detected additional areas of abnormality when conventional CMR was "normal", improving the detection rate to 98%. Early multiparametric CMR is able to localise areas of affected myocardium and is useful in the further management or diagnostic workup in this patient cohort.

BACKGROUND: High-risk percutaneous coronary intervention (PCI) procedures are being performed in greater numbers, in older patients with multiple comorbidities, and increasingly in the setting of acute coronary syndromes. Estimating inpatient PCI mortality and MACE risk (mortality, Q-wave myocardial infarction, urgent coronary artery bypass grafting and stroke) is essential in informing decision-making, consent, and operator and institutional benchmarking. There are a number of currently available risk scores that are often applied interchangeably. We investigated if there was concordance between contemporary risk scoring systems for inpatient mortality and MACE following PCI in patients at low, moderate or high-risk in a 'real life' cohort, depending upon method of presentation (elective, urgent, emergency). METHODS: We retrospectively identified 1,404 consecutive patients treated by PCI within a 6-month period in 2013. The New York risk score (NY) and National Cardiovascular Data Registry score (NCDR) were calculated for each patient to predict inpatient mortality risk and the Northwestern Quality Improvement score (NWQIP) and the Mayo Clinical Risk Score (MCRS) were calculated to predict inpatient MACE risk. Using the NY score as the reference for inpatient mortality and the NWQIP score as the reference for inpatient MACE, patients were divided into three risk groups (low < 1%; moderate 1-5%; high > 5%) and stratified into elective, urgent and emergency clinical presentations. Concordance was estimated using the Intraclass Correlation Coefficient (ICC) calculated with respect to each risk score and stratified by patient group. RESULTS: 757 patients were identified as low-risk (461 elective, 280 urgent, 16 emergency), 497 patients as moderate-risk (73 elective, 197 urgent, 227 emergency) and 150 patients as high-risk (4 elective, 43 urgent, 103 emergency) for inpatient mortality. 607 patients were identified as low-risk (382 elective, 225 urgent, 0 emergency), 594 patients as moderate-risk (97 elective, 237 urgent, 260 emergency) and 203 patients as high-risk (14 elective, 66 urgent, 123 emergency) for inpatient MACE events. The ICC indicated that risk scores correlated well for low-risk groups however were poorly concordant for high-risk groups (Table 1) and that this was true regardless of mode of clinical presentation (Table 2). heartjnl;100/Suppl_3/A41-b/T1F1T1 Abstract 71 Table 1 heartjnl;100/Suppl_3/A41-b/T2F2T2 Abstract 71 Table 2 CONCLUSIONS: Currently available PCI risk scores for both inpatient mortality and MACE are broadly concordant in low risk patient groups. However in patients at higher risk with multiple co-morbid factors, current tools are poorly concordant in predicting mortality and MACE. This has important implications for consent, and benchmark analysis of operator and institutional performance. Better understanding of choice of risk score for use in clinical practice is needed particularly as case mix and complexity evolve.

Introduction Repeat revascularisation after coronary angioplasty and stenting is well recognised, a feature of most prospective trials of percutaneous intervention (PCI) and is a major difference reported in trials comparing surgical to percutaneous revascularisation strategies. We investigated outcomes and repeat procedures in some 25 000 consecutive patients over 9 years from a UK teaching hospital. Methods Between January 2001 and August 2009, 24 521 patients presented to the John Radcliffe Hospital Oxford for coronary angiography. Revascularisation procedures in the follow-up period were analysed using the procedural database, stored angiographic images and from casenote review. Results 10 697 (43.6%) underwent PCI with stenting, 832 (3.4%) PCI alone, 4589 (18.7%) coronary artery bypass surgery (CABG) and 8133 (33.2%) medical treatment. Two thousand four hundred and seventy-seven of the 10 697 stented patients (23.2%) returned for a second angiogram and 1314 (12.3%) underwent further stenting and 211 (2.0%) CABG over a median follow-up of 4.25 years (IQR 2.13–6.13 years). Three hundred and eighty-four patients (29.2%) of those requiring a second stenting procedure underwent a third angiogram during the follow-up period and 161 (12.3%) underwent further stenting and 33 (2.5%) CABG. Rates of stenting for the fourth, fifth and sixth procedures were respectively 21%, 24% and 38% representing 0.3%, 0.1% and 0.02% of the initial stented cohort (Abstract 130 Figure 1). 59.9% of repeat PCI stenting procedures were elective, 38.1% urgent and 1.5% primary. Clinical indications for repeat stenting are shown in Abstract 130 Figure 2. A minority of patients (15.7%) required restenting for in-stent restenosis with most patients returning either with disease progression in an unstented area (45.2%) or for staged PCI (25.2%). Stent thrombosis as an indication for repeat stenting was rare (3.3%). Of those requiring restenting, 37.2% patients received drug eluting stents (DES) in their first stenting procedure and 62.8% received bare metal stents (BMS) alone. 5.4% of patients had both DES and BMS in the same procedure. This did not differ significantly from the ratio of DES/BMS in those patients undergoing stenting who did not require further revascularisation in the follow-up period (39% DES, 61% BMS, 14.8% both DES and BMS). 19.3% people requiring a second stenting procedure had multi vessel stenting at first PCI. Conclusion and Implications This study shows that in a large unselected ‘real world’ cohort of patients undergoing stenting, a substantial minority of patients undergoing a first stenting procedure will require repeat assessment (23%) and/or repeat stenting (12%). However the driving force behind repeat stenting procedures is progression of disease distant from the site of the first stent (45%) and staged PCI (25%) rather than isolated stent-related restenosis which accounts for under 16% of second stenting procedures and thus a minority of restenting cases.

Several changes in neuroendocrine activity follow failure of cardiac function to satisfy peripheral requirements and contribute to the clinical syndromes of heart failure. Afferent pathways are poorly understood and triggers are both central and peripheral, involving attenuation of atrial and arterial baroreceptor activity. Efferent sympathetic activity is generally increased with resulting vasoconstriction, but responses are organ-specific and differ among heart, kidney, lung and skeletal muscle. Changes in cardiac sympathetic activity are inadequately understood. Enhanced cardiac norepinephrine spillover contrasts with reduced tissue concentration and impaired activity of synthetic enzymes and neuronal catecholamine uptake. Beta-receptor down-regulation further complicates overall adrenergic responsiveness and the balance between enhancement of contractile function and reduction in arrhythmia threshold. Activation of the renin-angiotensin system is potentiated by the sympathetic nervous system and may contribute to vasoconstrictor hyporesponsiveness. Angiotensin II may in turn facilitate the central and peripheral effects of sympathetic activation and the release of vasopressin from the pituitary. Our understanding of the role of vasodilator peptides in heart failure remains rudimentary. It is likely that vasoconstrictor neuroendocrine response adversely influences optimal cardiac function in heart failure and may promote arrhythmogenesis. The neuroendocrine response in individual organs, however, requires intensive study.

Cardiovascular magnetic resonance using T1-mapping, T2-weighted and late gadolinium enhancement imaging provides a high diagnostic yield in patients presenting with acute chest pain, positive troponin and non-obstructive coronary arteries Vanessa M Ferreira, Erica Dall’Armellina, Stefan K Piechnik, Theodoros D Karamitsos, Jane M Francis, Robin Choudhury, Keith Channon, Rajesh Kharbanda, Colin Forfar, Oliver Ormerod, Bernard D Prendergast, Attila Kardos, Jim Newton, Matthias G Friedrich, Matthew D Robson, Stefan Neubauer

Background Native T1 mapping cardiac magnetic resonance (CMR) imaging allows for quantitative assessment of myocardial oedema following acute myocardial infarction (MI). Coronary flow reserve (CFR) measures the maximum increase in intracoronary blood flow and it is a marker of microvascular dysfunction consequent to ischemic damage. The relation between increasingly higher native T1 values and the underlying severity of microvascular damage due to ischemic insult is not known.We hypothesise that T1 values measured in areas of injured myocardium, correlate to invasive measurements of CFR and microvascular dysfunction. Methods We recruited 20 ST elevation MI (STEMI) patients post primary percutaneous coronary intervention. At 24 hours post procedure the patients underwent a repeat coronary angiogram with CFR measurement, and a 3T CMR. Matching short axis slices with full left ventricle (LV) coverage were acquired using functional steady-state free precession (SSFP) imaging, native T1 mapping, oedema T2W imaging and late gadolinium enhancement (LGE). For the comparisons among acute T1-mapping, T2W and LGE, we excluded apical slices due to partial volume effects and slices with off-resonance artifacts. In order to minimise ambiguity over acutely injured myocardium with low signal intensity and low T1 due to microvascular obstruction (MVO), patients with MVO on LGE were excluded from analyses. Each slice was segmented in a 6 equiangular segment model with the RV-LV junction as reference point. Global and segmental injured fractions by LGE and oedema were assessed; segmental T1 values were calculated in the injured myocardial segments with an injured fraction of at least 50% as determined by oedema and/or LGE. Results Out of the recruited patients, 6 were excluded due to microvascular obstruction on LGE. Fourteen underwent CMR and CFR at 24 hrs. The EF was 53 ± 10%, with a LV damaged fraction measured by oedema and LGE of 37 ± 15% and 30 ± 13%. The average T1 values in the injured areas were 1295 ± 61 msec (mean ± SD, range 1159-1388 msec) (normal values = 1196 ± 56 msec). There was a significant correlation (r = -0.7, p < 0.01) between the 24 hrs