Introduction: Coated-platelets (CP), a subpopulation of activated platelets, can be used as a surrogate marker for systemic thrombogenic propensity. Microthrombosis causes delayed cerebral ischemia (DCI) and is a major determinant of morbidity after subarachnoid hemorrhage (SAH). Association studies have reported increased morbidity and mortality after SAH depending on disease severity at admission.
Hypothesis: We hypothesized that severe clinical and radiological grades of SAH would be associated with increased CP and contribute to DCI.
Methods: Prospective cohort of 44 patients with non-traumatic, spontaneous SAH was enrolled. Clinical and radiological severity was recorded using Hunt and Hess (H&H), World Federation of Neurosurgeons Scale (WFNS), Simplified Applied Physiology Score (SAPS-II), Acute Physiology and Chronic Health Evaluation (APACHE-II) and modified Fisher scale (mFS). DCI and clinical vasospasm were used to assess in-hospital morbidity. CP levels were measured on predetermined days after SAH for each patient using flow cytometry. Mixed linear models were used to study test hypothesis.
Results: Cohort average age was 51.4 (IQR 44-58.5) and women representing 70.5% patients. Fifteen (34.1%) developed symptomatic vasospasm, and imaging identified 21 (47.7%) with DCI. During the first 5 days after SAH, scales indicating severe disease were associated with a 5-10% increase in CP. But this was only significant for mFS, 10.4% higher CP in grades 3 and 4 (95%CI: 1.5%, 19.4%; p=0.0251) than in those with grades 1 and 2. Similarly, higher clinical and radiological severity were associated with subsequent downtrending levels of CP after an initial rise but was only statistically significant for SAPS-II (upper tertile 0.8%/day vs middle tertile 1.7% vs lower tertile 1.02%/day, p=0.0297).
Conclusion: Higher initial CP levels among patients with severe clinico-radiologic findings, along with declining CP trends over 21 days, suggest that neurohumoral triggers may induce systemic thrombogenicity and contribute to DCI and clinical vasospasm after SAH.