Volume 12, Number 2, March-April 2005

Risk of death, MI and patterns of care delivered in non-ST elevation ACS patients with intermediate elevations in cardiac troponin T: a UK DGH experience
Kausik Ray, James Bolton, Alice Veitch, Paul Sheridan, Michael Gillett, Ahmed Al Rifai, Ramasamy ManivArmane, Alan Brennan, Gillian Payne, Wazir Baig

Prior studies have suggested a gradation in clinical risk with increasing elevations of cardiac troponins in patients with non-ST elevation acute coronary syndromes (ACS). We hypothesised that patients with cardiac troponin-T (cTnT) between 0.01-0.1 µg/L might be perceived as a low-risk group and consequently receive less active medical treatment.
Data were drawn from a UK district general hospital ACS registry between 2001 and 2002, and from the Office of National Statistics. A total of 255 patients were found to have had a non-ST elevation ACS with a cTnT rise between 0.01-0.10 µg/L.
Minor elevations in cTnT below 0.1 µg/L were found to be associated with a 20.1% risk of cardiovascular death or myocardial infarction (MI) at six months, with no ascending grade of risk from the lowest to the highest quintile. The use of statins (48.6%), angiotensin- converting enzyme (ACE) inhibitors (46.7%) and combined antiplatelet treatment (7.5%) was low, as was the use of angiography (8.2%) and stress testing (8.2%). In patients not undergoing early angiography, non-use of statins and ACE inhibitors was associated with twice the risk of death or MI (p=0.02). In a multivariate analysis, ST segment depression and non-use of ACE inhibitors were significant markers of risk.
Patients with non-ST elevation ACS and a cTnT between 0.01–0.1 µg/L are a universally high-risk group with no gradation of risk throughout this range. In a representative UK district general hospital (DGH), use of cardioprotective medication and cardiovascular assessment is low. An increased use of statins, ACE inhibitors and antiplatelet drugs, together with early angiography, might improve prognosis in this group.

Br J Cardiol 2005;12:AIC22-26.

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