High-sensitivity cardiac troponin for the rapid diagnosis of acute coronary syndrome in the emergency department : a clinical and cost-effectiveness evaluation
In the emergency medicine community, such a change is generating concern. A higher sensitivity assay will potentially result in earlier identification of those individuals experiencing an MI (as well as possibly those who can be safely discharged from the ED with no further investigations). However,...
Canadian Agency for Drugs and Technologies in Health
|Series:||CADTH optimal use report
|Collection:||National Center for Biotechnology Information - Collection details see MPG.ReNa|
|Summary:||In the emergency medicine community, such a change is generating concern. A higher sensitivity assay will potentially result in earlier identification of those individuals experiencing an MI (as well as possibly those who can be safely discharged from the ED with no further investigations). However, the use of high-sensitivity assays may also be associated with lower clinical specificity. Such lower specificity could potentially result in higher rates of false-positive tests; that is, situations where patients are incorrectly identified as having NSTEMI. Therefore, the use of hs-cTn assays could lead to conducting additional investigations and undertaking more vascular interventions (e.g., angiogram). These additional investigations and interventions carry the potential to increase the pressure on EDs, cardiology referrals, and possibly cardiac catheterization suites. These could result in additional costs to the health care system and cause increased anxiety to patients|
When patients with chest pain (or other symptoms suggestive of acute coronary syndrome [ACS]) present at an emergency department (ED), investigations are rapidly conducted to rule out ACS. ACS represents a spectrum of clinical presentations of myocardial ischemia ranging from ST-segment elevation myocardial infarction (STEMI) to non-STEMI (NSTEMI) and unstable angina (UA).1-3 STEMI is diagnosed by specific electrocardiogram (ECG) findings and portends a high risk of cardiac death. NSTEMI and UA are typically caused by myocardial ischemia, but of differing severity depending on the presence of myocardial infarction (MI), and are often clinically indistinguishable because of the similarity in symptoms and transient or non-specific ECG findings of ischemia at presentation. In 2000, the European Society of Cardiology and the American College of Cardiology (ESC/ACC) jointly redefined myocardial necrosis to incorporate cardiac troponin (cTn) assays as a diagnostic determinant.
In 2007, the ESC/ACC/American Heart Association (AHA) updated the definition of MI and advocated a "rise and/or fall" of cTn during a six to nine-hour time period using the 99th percentile in a reference population as the cut-off for classifying an acute and evolving MI.3 The time frame for the assessment of cTn, after the first measurement, has been reduced to three to six hours in the third universal of MI (2012).4 Therefore, in patients with suspected MI, but without ECG STEMI criteria, the cTn level is the discriminating criterion between NSTEMI and UA. In Canada, there are two cTn tests available: cardiac troponin T (cTnT) and cardiac troponin I (cTnI). As of 2012, the manufacturer of the cTnT reagent started to remove the conventional reagent and replace it with a high-sensitivity cTnT (hs-cTnT) reagent. High-sensitivity cTnI (hs-cTnI) is not yet available, but its introduction to the market is expected within the next year.
|Item Description:||Title from PDF cover. - "March 2013."|
|Physical Description:||1 PDF file (iii, 103 pages) illustrations|