Although increases in cTnI (cardiac troponin I) and cTnT (cardiac troponin T) always indicate myocardial damage, the test is not able to identify the mechanisms responsible for this damage, which may not be due to ischaemia, but rather to other clinical conditions. In the present issue of Clinical Science, Filusch and co-workers have assessed cTnT using a high-sensitive assay in patients with pulmonary arterial hypertension. Their study suggests that, even in patients with extracardiac diseases, high-sensitive troponin assays could lead to better risk stratification of patients in whom conventional cTnT assays show values within the ‘normal’ range. These findings support the hypothesis that increased levels of cTnI and cTnT are an index of cardiac tissue damage, even in patients with extracardiac diseases, thus enabling appropriate diagnosis and, when necessary and available, specific treatment.

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