Artikel
Troponin I (Trop I) as a marker of vascular complications in subarachnoid haemorrhage (SAH)
Troponin (Trop I) als Marker für vaskuläre Komplikationen bei Subarachnoidalblutungen (SAB)
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Autoren
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Paiman Shalchian-Tehran
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Klinik für Neurochirurgie, Köln, Deutschland
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Habib Bendella
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Klinik für Neurochirurgie, Köln, Deutschland
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Alexander Erich Hartmann
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Klinik für Neurochirurgie, Köln, Deutschland
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Marcel Poels
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Klinik für Anästhesiologie und operative Intensivmedizin, Köln, Deutschland
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Makoto Nakamura
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Klinik für Neurochirurgie, Köln, Deutschland
| Veröffentlicht: | 4. Juni 2021 |
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Gliederung
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Objective: Trop I has been stated to be a marker of poor prognosis in patients with SAH. As a metabolic substrate released from cardiac tissue during myocardial functional insufficiency. In case of functional failure of the heart-brain axis with its origin in the diencephalon Trop I may increase without primary cardiac failure. This might occur in the presence of vasospasm (VS) after SAH followed by cerebral ischemia. It is unknown whether VS correlate to Trop I as an indicator of damage to the cerebro-cardiac axis and as a marker of the clinical condition.
Methods: Prospective monocentric ongoing protocol with so far 29 consecutive patients (16 f, 13 m; mean age 55,1 yrs) with SAH between March 2020 and October 2020.
Measurements of Trop I (normal value below 26,4 (ng/l) from day 1 for 10 days, in case of proven VS on digital subtraction angiography (DSA) till day 21. Routinely measurements of blood flow velocity (BFV - as mean flow in cm/s) by transcranial Doppler sonography (TCD) in the middle cerebral arteries (MCA) of both sides were performed. Documentation of Glascow Coma Scale at ictus, Hunt & Hess and Fisher grade, brain infarcts (CCT), delayed ischemic neurological deficit (DIND) by daily neurologic evaluation. Primary myocardial malfunction as the main cause of Trop I elevation were excluded by ECG and in some cases by cardiac sonography. Additionally cardiac co-morbidities were documented by pts. history.
Results: Half of the pts. (15/29) presented with elevated Trop I during their course on the intensive care unit (day 1 till day 14) (36 till 3333 ng/L.). 7 (25%) of these pts. developed after initial normal values during their stay an elevated Trop I (max. 3333ng/L), which in the majority started suddenly and with a very short interval to its highest value. On average these pts presented a higher Hunt & Hess (>3) and Fisher Grade (IV) on admission with a GCS Score of 11 points.
Within averaged 2,4 days vascular complications could be seen (i.e. increasing of BFV, events of CCT infarcts, VS in DSA). 3 pts. (10%) with Trop I elevation died within 7 days after initial bleeding and could not be followed up. Only one patient out of 29 had a history of cardiac comorbidity (tachyarrhytmia absoluta).
Conclusion: Daily estimation of Trop I can be a marker of delayed vascular complications in pts. during the first two weeks after initial subarachnoid bleeding. Trop I elevation may indicate risky cerebrovascular situations and can contribute to the better estimation of a poor prognosis.
