Flavanol-rich dark chocolate (DC) and green tea extract capsules (GT) were assessed for effects on markers of vascular health. Commercially available dark chocolate was analysed for flavanol and methylxanthine levels using HPLC. There was considerable variation between brands of high cocoa solid content, and epicatechin (EC) levels did not correlate with calculated % non-fat cocoa solids. EC-rich DC also had considerably high methylxanthine levels. EC-rich DC was used to assess acute endothelial fitness. EndoPAT index (PAT) was determined in fingertips (3 subjects). PAT was not affected by dark chocolate ingestion, but systolic blood pressure (SBP) increased significantly by 5.2±4.9 mmHg (p<O.04). In a further intervention study (3 subjects), no correlation was observed between flow-mediated dilation (FMD) and PAT before or after DC ingestion. Neither FMD nor PAT were affected by acute DC intake while SBP increased (+10.2±8.6 mmHg, p=O.058). Augmentation index (Alx) and• pulse wave velocity (PWV) remained constant. Acute FMD improved significantly by 2.8±2.0% (p<O.02) after intake of GT in another intervention study (6 subjects). DC, or DC and GT co-ingested, had no effect on FMD. SBP (+3.9±4.1 mmHg, p<O.05) and diastolic BP (DBP) (+4.1 ±2.9 mmHg, p<O.02) increased significantly after DC intake but not after GT, or DC and GT combined. Alx, PWV and area-under-the-shear-rate- curve remained unaffected by either dietary intervention. 5-hour urine specimen displayed higher concentrations of EC, 3'-O-methyl- EC and 4'-O-methyl-EC following intake of DC than GT, or DC and GT combined. No correlation was present between urinary flavanol metabolites and endothelial fitness markers. The presence of flavanols in the test foods may have been the underlying cause for FMD improvement following GT ingestion. After DC consumption, the beneficial effects of EC may have been counteracted by the pressor effects of the methylxanthines, which consistently led to BP increases in all 3 studies after DC ingestion.

Introduction:  Laboratory markers play an important role in early risk stratification diagnosis and management for patients presenting with different heart problems.  However, the role of such markers as diagnostic tests remains unclear when applied to real life patient’s cohorts, especially when it is accompanied by incorrect time of measurement and interpretation of final results. Methods:  We have assessed the role of a variety of markers (hFABP, myoglobin, cTnI, PAPP-A, hsCRP, hsp70, and ADP/ATP) with respect to their diagnostic and prognostic value using an evidence-based approach in pragmatic real life cohorts (patients with ACS, patienst undergoing cardiac surgery and patients with AF). Results:  Measurement of myoglobin and hFABP in patients presenting with ACS offers no additional value to the measurement of cTnI on admission and at 12 hours. PAPP-A measurement may be useful at detecting unstable plaque disease. Post-operative measurement of cTnI in patients undergoing cardiac surgery is useful at detecting post-operative complications and at predicting subsequent mortality. An inflammatory component, as indicated by the measurement of hsCRP may be associated with the initiation of AF. Conclusions:  The evaluation of biochemical marker in real-life patients cohorts is essential to understand the true relationships present in the exact patient cohorts that the tests will subsequently be used in. Larger studies are required for both new and current markers.

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Background: Diagnosis of acute coronary syndromes (ACS) in the Emergency Department (ED) is a topical and contentious issue. Current diagnostic techniques rely on hospital admission for troponin testing. Only a minority of those admitted prove to have ACS while unacceptable proportions of those discharged have unrecognised ACS. Aims: We aimed to evaluate the diagnostic and prognostic value of individual clinical findings and novel biomarkers in ED patients with suspected cardiac chest pain. We then aimed to derive a clinical decision rule (CDR) to potentially enable safe, immediate discharge of a proportion of patients from the ED while risk stratifying others to facilitate triage to an appropriate level of in-patient care. Methods: We recruited patients who presented to the ED with suspected cardiac chest pain. Variables that have previously been shown to predict diagnosis of acute myocardial infarction (AMI) or to predict outcome were prospectively recorded. Blood was drawn at presentation for levels of eight biomarkers. Patients underwent 12-hour troponin testing and were followed up for the composite primary outcome of AMI, death or urgent coronary revascularisation for six months. Variables that were univariate predictors (p<0.05) of outcome were entered into a multivariate analysis using recursive partitioning. Results: While many clinical findings and levels of all eight novel biomarkers were found to be significant predictors of outcome, none could be used individually to confirm or exclude ACS in the ED. We derived a nine-point CDR that combined clinical findings with biomarker levels to effectively stratify patients into four risk groups. 14.2% of patients were identified as being at ‘no risk’ and had a 0.0% outcome rate. The rule performed significantly better than two commonly used risk scores and may improve on triage decisions made in actual clinical practice. Conclusion: ACS remains a difficult diagnosis to confidently confirm or refute in the ED. Our CDR may help to avoid unnecessary hospital admissions while improving on triage decisions made for the remaining in-patients. Prospective validation of our findings is warranted.