Elevated high-sensitive troponin T on admission is an indicator of poor long-term outcome in patients with subarachnoid haemorrhage: a prospective observational study

Jonatan Oras, Christina Grivans, Andreas Bartley, Bertil Rydenhag, Sven-Erik Ricksten, Helene Seeman-Lodding

Patients with subarachnoid haemorrhage (SAH) frequently develop cardiac complications in the acute phase after the bleeding. Although a number of studies have shown that increased levels of cardiac biomarkers after SAH are associated with a worse short-term prognosis, no prospective, consecutive study has assessed the association between biomarker release and long-term outcome. We aimed to evaluate whether the cardiac biomarkers, high-sensitive troponin T (hsTnT) and N-terminal pro B-type natriuretic peptide (NTproBNP), were associated with poor 1-year neurological outcome and cerebral infarction due to delayed cerebral ischaemia (CI-DCI). In this single-centre prospective observational study, all consecutive patients admitted to our neurointensive care unit from January 2012 to December 2013 with suspected/verified SAH with an onset of symptoms <72 hours were enrolled. Blood samples for hsTnT and NTproBNP were collected during three consecutive days following admission. Patients were followed-up after 1 year using the Glasgow Outcome Scale Extended (GOSE). Poor neurological outcome was defined as GOSE ≤4. One hundred and seventy seven patients with suspected SAH were admitted during the study period; 143 fulfilled inclusion criteria and 126 fulfilled follow-up. Forty-one patients had poor 1-year outcome and 18 had CI-DCI. Levels of hsTnT and NTproBNP were higher in patients with poor outcome and CI-DCI. In multivariable logistic regression modelling age, poor neurological admission status, cerebral infarction of any cause and peak hsTnT were independently associated with poor late outcome. Both peak hsTnT and peak NTproBNP were independently associated with CI-DCI. Increased serum levels of the myocardial damage biomarker hsTnT, when measured early after onset of SAH, are independently associated with poor 1-year outcome. Furthermore, release of both hsTnT and NTproBNP are independently associated with CI-DCI. These findings render further support to the notion that troponin release after SAH is an ominous finding. Future studies should evaluate whether there is a causal relationship between early release of biomarkers of myocardial injury after SAH and neurological sequelae.