High-Sensitivity Troponin I Can Predict Mortality in Stable Patients Suspected to Have CAD The biomarker was more sensitive compared with other conventional troponin assays and predicted near-term MACE in low-risk patients.

Heightened levels of high sensitivity troponin I (hsTnI) can predict the near-term risk of death, acute myocardial infarction (MI), and hospitalization for unstable angina in stable symptomatic patients suspected to have coronary artery disease (CAD), according to a new study published in the Journal of American College of Cardiology.

Predicting MACE in the PROMISE trial population

The study aimed to evaluate patients enrolled in the PROMISE trial. Patients who had available hsTnI level were analyzed for the association between the serum level of hsTnI and the primary outcome of death, acute MI, or the hospitalization for unstable angina at 1 year. The secondary outcome was a composite of cardiovascular death or acute MI. The study showed that patients with serum hsTnI in the upper quartiles had higher risk clinical profiles. Also, an elevated hsTnI level independently predicted the primary outcome of death, acute MI, or hospitalization of unstable angina (HR: 1.54 per increase in log-hsTnI interquartile range; P < 0.001) and the secondary outcome of cardiovascular death or acute MI (HR: 1.52 per increase in log-hsTnI interquartile range; P < 0.001).

Limited options to risk stratify these patients

Stable patients with symptoms suggestive of CAD were difficult to categorize based on their risk of developing serious cardiovascular complications. The currently-used risk scores tended to overestimate the risk and the use of other diagnostic modalities such as CTA and stress testing was limited due to their variable availability from one location to another and their need for specialized interpretation. hsTnI represented a promising tool for these patients. In contrast to other high sensitivity troponin methods, hsTnI was detected in almost all the study subjects. Additionally, it was of a prognostic benefit for near-term events in both men and women. In the accompanying editorial, Dr. Paul Collinson (Department of Clinical Blood Sciences, St. George’s University Hospitals NHS Foundation Trust, Jenner Wing, Cranmer Terrace, London) commented, “The study by Januzzi et al. adds further compelling evidence to the concept of troponin as a risk marker in the healthy or stable coronary artery disease group.” He added, “Their study has 2 unique aspects. First, it covers the group between the ‘apparently’ healthy persons and those who are symptomatic but have a low level of symptomatic coronary artery disease. Second, the study investigators used a highly sensitive assay that routinely detects troponin in 100% of healthy individuals.”

While previous studies showed an association between high levels of hsTn and adverse outcomes in patients with CAD, the authors claimed that their data was ‘unique’ as they used hsTnI to predict adverse outcomes in patients with only symptoms suggestive of CAD (not established disease). However, the authors acknowledged some limitations such as the low event rate in their study and the low number of patients with kidney disease (and thus the inability to study the prognostic value of hsTnI in these patients). Lastly, the study did not identify a cutoff value of hsTnI that defined patients at higher risk. The authors concluded, “It is reasonable to hypothesize that patients with stable chest pain syndromes with relatively higher hsTnI could merit more aggressive diagnostic or therapeutic management. Besides typical recommendations for higher risk patients, such as avoidance of tobacco use, exercise prescription or more aggressive medical management of risk factors, proceeding directly to coronary CTA imaging or invasive angiography may be an option for such patients, although it is premature to make such a recommendation.”