Validation of the shared decision-making model in the context of a patient presenting to the emergency department with chest pain of possible cardiac origin.

The intention of this thesis was to investigate the feasibility of clinical shared decision-making. If physicians are to contribute to a shared decision process, they will need to be able to communicate unbiased information to their patients clearly. Thus, physicians need to provide some form of quantitative risk estimate. Physicians estimated the probability that a patient presenting with chest pain had Acute Coronary Syndrome. The patients details were then entered into a structured clinical risk calculator and the results were compared. It was found that although both methods held comparable predictive power, the physician’s estimate did not correlate well with the structured estimate. This suggests that physicians do not utilise a quantitative risk estimate. It then found that the correlation between risk estimates increased as further investigations were performed. However, neither estimation method could predict these test results. It was hypothesised that physicians utilise a dichotomous decision process. Thus, as positive and negative test results erode the intermediate risk group and populate the high and low risk groups, the correlation between methods increases. It was concluded that a dichotomous decision process would provide a considerable hurdle to the shared decision-making process, as it would limit the communicability of the physicians thought process. However, the potential benefits of shared decision-making encourage future researchers to find a way to overcome this hurdle

Comparison of high sensitivity and contemporary troponin assays for the early detection of acute myocardial infarction in the emergency department

Current guidelines define acute myocardial infarction (AMI) by the rise and/or fall of cardiac troponin with ≥1 value above the 99th percentile. Past troponin assays have been unreliable at the lower end of the range. Highly sensitive assays have therefore been developed to increase the clinical sensitivity for detection of myocardial injury.Three hundred and thirty-two patients with chest pain suggestive of AMI were prospectively recruited between November 2006 and April 2007. Serial blood samples were analysed to compare Roche Elecsys high sensitivity troponin T (hsTnT), Abbott Architect troponin I 3rd generation (TnI 3) and Roche Elecsys troponin T (TnT) for the diagnosis of AMI.One hundred and ten (33.1%) patients were diagnosed with AMI. Test performance for the diagnosis of AMI, as quantified by receiver operating characteristic area under the curve (95% confidence intervals) for baseline/follow-up troponins were as follows: hsTnT 0.90 (0.87-0.94)/0.94 (0.91-0.97), TnI 3 0.88 (0.84-0.92)/0.93 (0.90-0.96) and TnT 0.80 (0.74-0.85)/0.89 (0.85-0.94). hsTnT was superior to TnT (P < 0.001/0.013 at baseline/follow-up) but equivalent to TnI 3. For patients with a final diagnosis of AMI, baseline troponins were raised in more patients for hsTnT (83.6%) than TnI 3 (74.5%) and TnT (62.7%). A delta troponin of ≥20% increased the specificity of hsTnT from 80.6% to 93.7% but reduced sensitivity from 90.9% to 71.8%.hsTnT was superior to TnT but equivalent to TnI 3 for the diagnosis of AMI. Serial troponin measurement increased test performance. hsTnT was the most likely to be raised at baseline in those with AMI. A delta troponin increases specificity but reduces sensitivity