Editor's Note: Commentary based on Lankeit M, Friesen D, Aschoff J, et al. Highly sensitive troponin T assay in normotensive patients with acute pulmonary embolism. Eur Heart J. 2010;31:1836-44.

Pulmonary embolism (PE) represents an acute illness that can present as a wide spectrum of severity, from patients who are relatively asymptomatic to those who have cardiogenic shock. Therefore, early accurate risk stratification is important for identifying high-risk patients who at the time of presentation may appear to be relatively stable. Elevated troponin in these patients has been shown to predict adverse events, with mortality equivalent to patients with MI who have Killip class III heart failure¹. However, most prior studies are limited by failure to exclude hemodynamically unstable patients who are obviously high-risk, in whom further risk stratification is not necessary.

Therefore, identifying patients who are clinically stable but who are likely to have subsequent complications would be important. To address this, Lankeit et al² measured high sensitivity troponin T (hsTnT) in 156 normotensive patients presenting with acute PE. Patients were excluded if they had evidence of cardiogenic shock or significant renal failure (GFR <30 mL/min; likely excluded due to the known association of increased TnT in patients with renal failure). Traditional TnT was considered elevated if it exceeded 30 pg/mL (or 0.03 ng/ml). For hsTnT, an upper limit of normal was defined as the 99 percentile of a normal population, which was 14 pg/mL. Significant complications, which included need for catecholamine administration, intubation, CPR, or death, were assessed over the subsequent 30 days.

The authors found that an increased hsTnT was present in almost two-thirds of hemodynamically stable PE patients PE; in contrast, elevated traditional TnT was present in only one-third. Therefore, half of the patients who had an increased hsTnT did not have an elevated traditional TnT. During follow-up, 8 patients (5%) had an adverse outcome which included death in 2 patients. HsTnT values were almost three times as high in patients who had a complication (median 72 vs 26 pg/ml). For identifying patients who had complications, using the traditional TnT, 50% of the patients would have been misclassified as low risk. In contrast, all patients with complications had an elevated hsTnT, resulting in a negative predictive value of 100%. Finally, while traditional TnT was not an independent predictor of adverse outcomes, hsTnT was (odds ratio 2.02), and, when combined with echocardiographic evidence of RV dysfunction, identified a cohort who had a 12 fold increase in adverse outcomes.

The results from this study expand the knowledge base of the role of hsTnT outside of MI and CHF into risk stratification for PE patients. The absence of increased values identified a lower risk cohort who likely can be evaluated in a less intense setting, potentially being able to admitted to a non-monitored setting, with rapid discharge. Patients with an increased hsTnT would require monitoring for longer periods.

Certain limitations of this study need to be considered, however. The positive predictive value of an increased hsTnT was only 8%; therefore, many patients with increased hsTnT values would not have a complication. Only a small number of patients had adverse events (only 5% of the patients). Hence, further study is necessary to confirm its utility. Another limitation of this study was the fact that in the 15% of patients treated with thrombolytics; it is possible that without being treated these patients would have had an adverse event, and increased the overall positive predictive value of hsTnT.

Another interesting finding from this study was confirmation that BNP had good prognostic value³, and in fact, was more sensitive and specific than hsTnT for identifying patients with complications. Therefore, it may be that similar to acute MI patients, a dual marker approach using both hsTnT and BNP could identify particularly high-risk patients in whom mechanical or pharmacologic intervention would improve overall outcomes.

References

1. Becattini C, Vedovati MC, Agnelli G. Prognostic value of troponins in acute pulmonary embolism: a meta-analysis. Circulation 2007;116:427-33
2. Lankeit M, Friesen D, Aschoff J, Dellas C, Hasenfuss G, Katus H, Konstantinides S, Giannitsis E. Highly sensitive troponin T assay in normotensive patients with acute pulmonary embolism. Eur Heart J 2010;31:1836-44.
3. Klok FA, Mos IC, Huisman MV . Brain-type natriuretic peptide levels in the prediction of adverse outcome in patients with pulmonary embolism: a systematic review and meta-analysis. Am J Respir Crit Care Med 2008;178:425-30.

Keywords: Heart, Hemodynamics, Risk, Shock, Cardiogenic, Troponin, Pulmonary Embolism

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