High-sensitivity troponin useful for diagnosis and prognosis in patients with acute coronary syndrome
- Correspondence to
: Eugenio Stabile
Department of Cardiology, Centro Polidiagnostico Stabile, via diaz 32, Salerno 84100, Italy;
High-sensitivity cardiac troponin (hs-cTnT) determination has improved cTnT evaluation in patients with acute coronary syndrome (ACS). The hs-cTnT ‘normal value’ is considered to be <99th percentile (0.014 ug/l). Hs-cTnT can diagnose an acute myocardial infarction (AMI) earlier than common cTnT determinations, even in patients with previous CAD.1 ,2 Some studies have shown higher specificity of hs-cTnT in AMI diagnosis, compared with common cTnT determinations.3 Hs-cTnT is also a better predictor of death and heart failure in patients with chest pain and ACS during follow-up.1 ,2 ,4
The APACE study, a multicentre prospective trial, enrolled a total of 1181 consecutive patients who were admitted to the emergency department because of chest pain and/or other symptoms suggestive of AMI for less than 12 h duration. Patients who presented with symptoms that lasted for more than 12 h or with renal failure requiring dialysis were excluded.
Patients underwent hs-cTnT determination at presentation, and within 3 h, unless the diagnosis of AMI was certain. The 99th percentile of hs-cTnT was the cut-off point, with a coefficient of variation <10% (achieved at 0.013 ug/l). Samples were assayed in a blinded fashion. Final diagnosis of ACS was obtained by two independent cardiologists (the authors did not provide a measure of agreement between the cardiologists). Clinical follow-up was done 30, 90 and 360 days after hospital discharge. The primary endpoint was death from all causes.
A total of 351 patients had ACS during hospitalisation. Of these, 187 (53%) had AMI and 164 (47%) had unstable angina (UA). Hs-cTnT was below the 99th percentile in 112 patients (31.9%, 11 of whom had AMI, 5.9%) and above the 99th percentile in 239 patients (68.1%). In the 9/11 AMI patients with follow-up hs-cTnT at 3 h, all of them were positive, with 7/67 patients with UA with follow-up hs-cTnT becoming positive.
During follow-up, mortality from all causes was higher in patients with ACS and elevated hs-cTnT versus those with ACS and normal hs-cTnT (7.5% vs 0% at 30 days, p=0.003; 10.8% vs 0% at 90 days, p<0.001; 17.5% vs 2.0% at 360 days, p<0.001). Patients with ACS and normal hs-cTnT had an increased AMI rate at the 360-day follow-up (15% vs 5.4%; p=0.004) but a low-death rate, similar to patients with non-cardiac chest pain, indicating high-cardiovascular risk.
Due to the hs-cTnT determination, Meune et al were able to diagnose an AMI in 94% of cases at admission and in 100% of the cases, if the assay was repeated at 3 h.
There is a physiologic continuum between UA and AMI and the hs-cTnT appears to be useful for the early diagnosis of AMI; serial measurements support the concept of a continuum. We speculate that hs-cTnT determination to diagnose AMI, will improve patient outcomes by leading to earlier AMI treatment.
Due to the high sensitivity of hs-cTnT test, however, physicians should be wary of interpretation to avoid AMI misdiagnosis in patients with minimal cTnT increases, which are common in patients affected by other diseases.4 Patients with ACS and normal hs-cTnT, and a higher AMI rate at 360-day follow-up, were younger and already on statins, aspirin and clopidogrel treatment, with normal renal function. This reflects that these patients had a higher baseline risk. Physicians should always be wary of ACS, even if circulating troponin is normal at onset. Careful follow-up for risk factor modification is important.