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Objective: Maladaptive repair contributes towards the development of heart failure following myocardial infarction (MI). The α v β 3 integrin receptor is a key mediator and determinant of cardiac repair. We aimed to establish whether α v β 3 integrin expression determines myocardial recovery following MI., Methods: 18 F-Fluciclatide (a novel α v β 3 -selective radiotracer) positron emission tomography (PET) and CT imaging and gadolinium-enhanced MRI (CMR) were performed in 21 patients 2 weeks after ST-segment elevation MI (anterior, n=16; lateral, n=4; inferior, n=1). CMR was repeated 9 months after MI. 7 stable patients with chronic total occlusion (CTO) of a major coronary vessel and nine healthy volunteers underwent a single PET/CT and CMR., Results: 18 F-Fluciclatide uptake was increased at sites of acute infarction compared with remote myocardium (tissue-to-background ratio (TBR mean ) 1.34±0.22 vs 0.85±0.17; p<0.001) and myocardium of healthy volunteers (TBR mean 1.34±0.22 vs 0.70±0.03; p<0.001). There was no 18 F-fluciclatide uptake at sites of established prior infarction in patients with CTO, with activity similar to the myocardium of healthy volunteers (TBR mean 0.71±0.06 vs 0.70±0.03, p=0.83). 18 F-Fluciclatide uptake occurred at sites of regional wall hypokinesia (wall motion index≥1 vs 0; TBR mean 0.93±0.31 vs 0.80±0.26 respectively, p<0.001) and subendocardial infarction. Importantly, although there was no correlation with infarct size (r=0.03, p=0.90) or inflammation (C reactive protein, r=-0.20, p=0.38), 18 F-fluciclatide uptake was increased in segments displaying functional recovery (TBR mean 0.95±0.33 vs 0.81±0.27, p=0.002) and associated with increase in probability of regional recovery., Conclusion: 18 F-Fluciclatide uptake is increased at sites of recent MI acting as a biomarker of cardiac repair and predicting regions of recovery., Trial Registration Number: NCT01813045; Post-results., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Background: The purpose of this study was to examine the relationship between left ventricular (LV) function, cytokine levels and site of myocardial infarction (MI) in patients undergoing coronary artery bypass grafting (CABG)., Methods: Sixty patients undergoing CABG were divided into three groups (n = 20) according to their history of site of myocardial infarction (MI): no previous MI, anterior MI and posterior/inferior MI. In the pre-operative period, detailed analysis of LV function was done by transthoracic echocardiography. The levels of adrenomedullin, interleukin-1-beta, interleukin-6, tumour necrosis factor-alpha (TNF-α) and angiotensin-II in both peripheral blood samples and pericardial fluid were also measured., Results: Echocardiographic analyses showed that the anterior MI group had significantly worse LV function than both the group with no previous MI and the posterior/inferior MI group (p < 0.05 for LV end-systolic diameter, fractional shortening, LV end-systolic volume, LV end-systolic volume index and ejection fraction). In the anterior MI group, both plasma and pericardial fluid levels of adrenomedullin and and pericardial fluid levels of interleukin-6 and interleukin- 1-beta were significantly higher than those in the group with no previous MI (p < 0.05), and pericardial fluid levels of adrenomedullin, interleukin-6 and interleukin-1-beta were significantly higher than those in the posterior/inferior MI group (p < 0.05)., Conclusions: The results of this study indicate that (1) patients with an anterior MI had worse LV function than patients with no previous MI and those with a posterior/inferior MI, and (2) cytokine levels in the plasma and pericardial fluid in patients with anterior MI were increased compared to patients with no previous MI.

Background: New generation cardiac troponin assays have sufficient precision to detect and quantify plasma troponin concentrations below the lower threshold of detection of the currently employed troponin tests. However, diagnostic performance of the newer generation assays in daily clinical practice is not well established., Aim: To evaluate the diagnostic performance of a sensitive assay as compared to a standard assay in a single reading at admission in the diagnosis of acute myocardial infarction (AMI) in patients presenting to the Emergency Department with chest pain., Methods: The study comprised 187 consecutive patients admitted to the Institute of Cardiology in Warsaw in June and July 2010 with chest pain in whom the attending physician ordered troponin assay to rule AMI in or out. In all of these patients, in addition to the standard Dimension Flex Troponin I (Siemens Healthcare Diagnostics, Inc.) the sensitive Architect Stat Troponin I (Abbott Diagnostics) test was assayed. The triage of patients as well as all diagnostic and treatment decisions were left to the discretion of the attending physician who was blinded to the sensitive troponin test readings. The final diagnosis was adjudicated by a team of two cardiologists on the basis of all the available medical records except for sensitive troponin test results., Results: Mean age of the study cohort (n = 187) was 64.3 ± 13.9 years and 119 (63.6%) were males. The final diagnosis of AMI was adjudicated in 84 (44.9%) patients (mean age 67.5 ± 12.9 years; 119 [63.6%] males). Receiver operating characteristic (ROC) analysis showed greater area under the curve (AUC) for the sensitive cardiac troponin assay compared to the standard assay (AUC = 0.916, 95% CI = 0.866-0.951 vs AUC = 0.863, 95% CI = 0.806-0.909, respectively; p = 0.02) in a single reading at admission. Sensitive assay was characterised by higher sensitivity (87%), specificity (88%), positive (86%) and negative (89%) predictive values in the detection of AMI compared to the standard troponin test (82%, 81%, 78%, and 85% respectively)., Conclusions: The newer generation sensitive cardiac troponin assay presented superior diagnostic accuracy in the diagnosis of AMI compared to the standard troponin test in a single reading at admission with improved sensitivity and specificity. The sensitive troponin assay has the potential to improve early detection and/or exclusion of AMI.