Aneurysmal subarachnoid hemorrhage (aSAH) is associated with high socio-economic burden. Prothrombotic states of early brain injury (EBI) and delayed cerebral ischemia (DCI) after aSAH determine morbidity and mortality. To understand how activated platelets might contribute to such prothrombotic states, we studied trends in coated-platelets during EBI and DCI periods. Serial blood samples from a prospective cohort of aSAH patients were collected and assayed for coated-platelet levels. Patient's coated-platelet level during post-hospital discharge follow-up served as an estimate of baseline. Occurrence of DCI, Montreal cognitive assessment (MOCA) score of < 26, and modified Rankin scale (mRS) of 3-6 were considered poor clinical outcomes. Non-linear regression analysis detected a transition between periods of rising and declining coated-platelet levels at day 4. Additional regression analyses of coated-platelet trends before day 4 showed differences among patients with modified Fisher 3-4 [4.2% per day (95% CI 2.4, 6.1) vs. - 0.8% per day (95% CI - 3.4, 1.8); p = 0.0023] and those developing DCI [4.6% per day (95% CI 2.8, 6.5) vs. - 1.9% per day (95% CI - 4.5, 0.5); p < 0.001]. Differences between peak coated-platelet levels and baseline levels were larger, on average for those with DCI [18.1 ± 9.6 vs. 10.6 ± 8.0; p = 0.03], MOCA < 26 [17.0 ± 7.8 vs. 10.7 ± 7.4; p = 0.05] and mRS 3-6 [24.8 ± 10.5 vs. 11.9 ± 7.6; p = 0.01]. Coated-platelet trends after aSAH predict DCI and short-term clinical outcomes. The degree of rise in coated-platelets is also associated with adverse clinical outcomes.
BackgroundSpontaneous subarachnoid hemorrhage (SAH) is a disabling form of hemorrhagic stroke that affects young individuals and is responsible for short-term and long-term cognitive deficits. Delayed cerebral ischemia (DCI) is postulated to be the major determinant for this morbidity. Cerebral vasospasm (CVS) is a major contributor of DCI. Treatment of symptomatic CVS can consist of intra-arterial vasodilators or angioplasty. This study reports preliminary data on cognitive outcomes in a prospective cohort of patients with spontaneous SAH who received vasodilator therapy for anterior cerebral artery (ACA) vasospasm.Aim1. Determine role of delayed cerebral ischemia (DCI) and CVS after spontaneous SAH on short-term cognitive outcome.2. Determine if ACA vasospasm predicts short-term cognitive outcome.3. Determine if treatment of ACA vasospasm results in improvement in short-term cognitive outcome.MethodsThirty-five patients with clinical follow-up at 3 months after SAH were selected from a prospective cohort. DCI was defined as a new hypodensity on CT scans located in a vascular territory, with or without symptoms (decrease of consciousness or focal deficits), due to CVS and not explained by other causes (e.g. rebleeding, hydrocephalus, cardioembolic sources, hypoxia, electrolyte disturbances, or seizures). CVS was defined as ≥25% narrowing on digital subtraction angiogram (aCVS) or Transcranial Doppler mean flow velocity ≥120 cm/sec (sCVS). Cognitive outcomes were assessed using Montreal Cognitive Outcome Assessment (MOCA) and poor cognitive outcome was defined as MOCA score <26. Fisher’s exact tests and logistic regression were performed to analyze the study questions.ResultsAverage age of the study cohort was 53.1 ± 11.5 years with 71% of the patients being women. DCI occurred in 16/35 (45.7%) patients. In the absence of sCVS, DCI predicted poor cognitive outcomes (3/5 with DCI, 60% vs 1/10 without DCI, 10%; p = 0.04). Patients with anterior cerebral artery or anterior communicating complex (ACA/ACom) related aneurysmal SAH were less likely to have MOCA < 26 (ACA/ACom vs others (3/12, 25% vs 11/23, 47.8%; p = 0.28). Of the 22 patients who underwent digital subtraction angiogram for clinical indication, 10 were found to have ACA CVS and were treated. Patients with SAH due to ACA/ACom location aneurysms displayed low MOCA scores less often than those with SAH in other locations (2/5; 40% vs 4/5; 80%; p = 0.15). A two-factor logistic regression model found that, while holding treatment status constant, the odds of a poor cognitive outcome were 4.6 times higher (90% CI on odds ratio: 1.0, 21.3; p = 0.0998) among those with SAH outside of ACA/ACom aneurysms.ConclusionsOur study reaffirms that occurrence of DCI after SAH predicts poor cognitive outcome at 3 months. The fact that cognitive outcomes were not superior in patients treated for CVS suggests that a complex pathophysiology determines outcomes after SAH. Relatively poor cognitive outcome among patients with SAH in locations other than ACA/ACom alludes to involv...
Introduction: Mean platelet volume (MPV) is a common platelet index that estimates average platelet size. In retrospective cohorts, MPV is reported to be higher, on average, in patients who have experienced acute cardiovascular or cerebrovascular events. Aneurysmal subarachnoid hemorrhage (aSAH) is often associated with increased thrombogenic state due to reactive platelets resulting in delayed cerebral ischemia (DCI). Hypothesis: We assessed whether trends in MPV over the first 21 days after aSAH predicts occurrence of DCI. Methods: The present study enrolled a prospective cohort of 47 patients with aSAH. Clinical (H&H, WFNS) grades and daily MPV was recorded. Patients surviving atleast 7 days following aSAH were included for analysis to determine temporal trend of MPV. Mixed linear regression model was used to compare MPV trends between groups defined by clinical grades of varying severity. Segmented linear regression analysis was performed to identify transition point for patients developing DCI in comparison to those without DCI Results: Average age of cohort was 53.3±13.2 years with 68% women. Thirty-five of the 47 (74.5%) were H&H I-III as compared to 21/47 (44.7%) with WFNS 4-5. Thirty-two patients developed DCI. Baseline MPV was no different (~10.5fL) among patients with different clinical grades. In 32 patients who developed DCI, a transition point at 3 days was identified prior to which MPV increased by 0.13fL/day (95% CI 0.04, 0.23; p=0.0047) followed by a decline of 0.03fL/day (95% CI 0.02, 0.04; p=0.0006). Similar trend was not seen in those without DCI. Rate of decline in MPV were steeper among patients with H&H I-III and WFNS 1-3 as compared to those with H&H IV-V and 4-5 [0.26fL/day; 90% CI 0.004, 0.048, p=0.051 and 0.23fL/day; 90% CI 0.003, 0.042, p=0.06 respectively]. Conclusion: Rise in MPV during the first 3 days after aSAH with DCI followed by a decline indicates release of larger platelets after aSAH and possible association with DCI. Absence of declining trend MPV among higher clinical grade aSAH patients suggests persistence of reactive platelets in circulation.
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