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He who saves a life,…deserves the merit as if he has saved a world
(Talmud, Sanhedrin 37a)
An audit conducted in 1995 based on the definitions provided by the WHO showed that 65% of patients clinically suspected, were confirmed as having myocardial infarction (MI), whereas 35% clinically suspected were not confirmed. The latter, unconfirmed, group received significantly less-appropriate medical therapy and had a significantly worse 30-day mortality (40% vs 16%; p<0.0011). At that time, commercial cardiac troponin assays were becoming available as specific markers of cardiomyocyte damage.
The transition to the routine use of cardiac troponins within the UK was accompanied by some confusion and concerns.2 The British Cardiac Society proposed a set of definitions to assist this change: (a) ACS (acute coronary syndrome) with UA (unstable angina), (b) ACS with myocyte necrosis, (c) ACS with clinical MI. The third of these groups related to ‘traditional MI’ while the first related to the condition of UA as defined by negative/undetectable troponin. In between was a group of patients with unknown natural history. Studies then emerged that demonstrated 30-day mortality rates (4.5%, 10.4% and 12.9%; p<0.0013) and 6-month mortality rates (8.6%, 18.7% and 19.2%; p<0.001), which indicated that ‘ACS with myocyte damage’ was not just a ‘small MI’, but rather a ‘full MI’ with the accompanying mortality. Moreover, this was compounded by inadequate routine use of secondary prevention therapies and hence a cause for concern.
The beginning of the troponin era was made more confusing by the range of analytical results and decision values given by the then available assays due to the lack of analytical standardisation and quality standards. Indeed, none of the first-generation assays could measure the upper end of the normal range, which …
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