Transient ventricular dysfunction syndrome: the evolving nomenclature.

I thank Lippi and Targher for their kind remarks about my editorial in CHEST (February 2008),1 which describes “tricks of the trade” for assessing pulmonary embolism prognosis. They raise two important questions: (1) Should measurement of natriuretic peptides such as brain natriuretic peptide or pro-brain natriuretic peptide be incorporated into routine prognostic assessment of acute pulmonary embolism? (2) Do brain natriuretic peptide levels provide clinically useful, complementary information above and beyond troponin measurement? Troponin measurement has several advantages over natriuretic peptides. First, any elevation of troponin, even a “troponin leak,” carries a markedly increased adverse prognosis for survival over the ensuing 30 days. Second, troponin as a pulmonary embolism biomarker has been far more extensively studied than natriuretic peptides. Third, the normal range for natriuretic peptides and the level at which they indicate a poor prognosis for pulmonary embolism remain uncertain. Fourth, the negative predictive value for a normal troponin level is almost 100%. Therefore, it is hard to conceive how natriuretic peptides can yield incrementally useful clinical information to indicate a favorable prognosis. Fifth, dissecting the contribution of occult or overt concomitant heart failure to elevated natriuretic peptide levels in the presence of pulmonary embolism is difficult. For now, we know that normal troponin levels indicate a likely excellent prognosis. I hope that some day soon, we will be able to use the combination of elevated troponin levels plus elevated natriuretic peptide levels as an indicator of an especially ominous prognosis. However, that day has not yet arrived. Therefore, routine measurement of natriuretic peptides is not quite ready for prime time when assessing the prognosis of a patient with acute pulmonary embolism.