The early hours after an acute stroke are crucial; it is the most useful time for effective management. With the rising burden of stroke and marked heterogeneity in stroke manifestation and outcome, it is necessary to find accurate, reliable, and simple predictors of functional recovery. Also, the natural recovery patterns must be investigated more so that we can better assess the effectiveness of the available therapeutic interventions and their contribution to recovery process (Bhatia et al. 2004).
In this study, we assessed the role of some important hemorheological parameters (such as blood viscosity hematocrit (Htc), platelet aggregation, and leukocyte count), protein C, protein S, antithrombin III, and serum albumin as prognostic factors which can early predict the outcome after ischemic stroke.
Albumin is an important functional protein in the blood; it maintains the normal permeability of the microvessel wall, reduces blood viscosity, and inhibits platelet aggregation (Wei-Hai et al. 2014). In recent years, there has been increasing interest in the association between serum albumin levels and stroke. Many studies have demonstrated an inverse relation between the concentration of serum albumin, stroke risk, and functional outcome (Babu et al. 2013).
Our results revealed that the serum albumin at admission is an independent predictive factor of the functional outcome in ischemic stroke patients by linear regression statistical analysis which is done to test for significant predictors of outcome. It suggests that patients with low serum albumin level within 24 h after the onset of stroke may have a poor functional outcome and it may be caused by low neuroprotective effects.
Many recent studies have shown the prognostic role of serum albumin level in cases of acute ischemic stroke. Our results agreed with Wei-Hai et al. (2014), Babu et al. (2013), Yoon et al. (2008), and Kasundra and Sood (2014) who investigated the effect of serum albumin at admission, on the functional outcome in ischemic stroke patients. They concluded that serum level of albumin at admission is considered as a good indicator of the functional outcome and trials for the correction of hypoalbuminemia in acute ischemic stroke would be helpful to decrease the risk of poor outcome.
Belayev et al. (2001) found that moderate-dose albumin therapy markedly improves functional outcome in ischemic stroke patients and reduces infarction volume and brain swelling.
High-dose albumin treatment for acute ischemic stroke was assessed in a randomized, double-blind, placebo-controlled trial, and the results were not encouraging further studies to test the role of albumin on a larger scale, at a different dose, and over a longer duration of follow-up were suggested by the authors (Ginsberg et al. 2013).
In the present study, there was a statistically significant negative correlation between hematocrit and clinical outcome. An elevated hematocrit can enhance atherosclerosis by increasing protein infiltration into the vessel wall, promoting platelet adhesion to the subendothelium and by causing stagnation of blood flow (Irace et al. 2003).
Our results agreed with Levy et al. (1986), Diamond et al. (2003), and Allport et al. (2005) who pointed out that hematocrit is inversely related to neurologic outcome in acute ischemic stroke and showed that the effect of hematocrit on outcome is not related to sex, age, diabetes, or hypertension. Czlonkowska et al. (1997) also demonstrated that hematocrit is an important predictor factor of 30-day fatality in ischemic stroke.
On the other hand, our results were opposed by Ozaita et al. (1987) who concluded that hematocrit has no effect on the short-term outcome of ischemic stroke cases. However, their findings also showed that there was only a tendency to elevated hematocrit in the first days in cases with severe admission deficit. Moreover, Bhatia et al. (2004) found that hematocrit is not a predictive factor of 30-day fatality in ischemic stroke.
The importance of the effect of hematocrit on stroke outcome explains the role of hemodilution therapies that may potentially improve stroke outcome. Previous hemodilution strategies have aimed to increase cerebral blood flow and salvage penumbral tissue. Unfortunately, early hemodilution trials in management of human acute ischemic stroke were negative, and the failure of translation from the trials of animal models has been attributed to different time windows and methodologic limitations in human (Asplund 2004).
Leukocyte count has an established role in predicting incident cerebrovascular and cardiovascular diseases, but the relationship between leukocyte count and acute ischemic stroke outcome is not well investigated (Elkind et al. 2004). In this study, a statistically significant negative correlation was found between total leukocyte count and clinical outcome (p value = 0.015).
Our results agreed with many recent studies; Furlan et al. (2014) in their study which was conducted on 170 cases with acute ischemic stroke found that the risk of stroke leading to disability at discharge was 1.04 times greater for every increase of 1 × 109 in leukocyte count on admission. Also, survival curves showed that high leukocyte count was associated with worsening in the 30-day mortality in patients with acute ischemic stroke.
Also, Liang et al. (2016) in their study which included 8829 patients with acute ischemic stroke reported that increased leukocyte on admission is an independent predictor of stroke severity on admission, higher degree of disability at discharge, and 30-day mortality.
Our study disagrees with an older study which studied the effect of leukocytosis on stroke outcome and reported that increased total leukocyte count on admission was related only to initial stroke severity but not to functional outcome (Kammersgaard et al. 1999).
Blood viscosity assumes a vital role in the pathophysiology of vascular diseases as a factor determining global cardiovascular load, and as a variable influencing regional tissue perfusion. Additionally, a high blood viscosity increases the risk of thromboembolic events and is correlated with the presence of systemic inflammation (Pop et al. 2002).
Our study found a statistically significant positive correlation between blood viscosity and size of infarction (p-value = 0.028) but failed to find any relation between blood viscosity and stroke outcome. This result was agreed with Zhou and Yang (1990) who reported that blood viscosity has positive correlation with the size of the cerebral infarction and postulated that the hematocrit and the blood viscosity should be reduced immediately for treating the larger cerebral infarction.
Platelet aggregation is a vital step in thrombus formation; several studies have demonstrated that platelets are activated in the acute phase of ischemic stroke. However, the impact of enhanced platelet activation in the clinical and functional outcome of acute ischemic stroke was still not well investigated. Recently, many studies have demonstrated that enhanced platelet activation is related to larger infarct size and poor clinical and functional outcome in patients with acute ischemic stroke (Zeller et al. 2005; Yip et al. 2005).
This study found a significant difference between cases and control group as regard platelet aggregation (p value 0.000) which agreed with Fateh-Moghadam et al. (2007) who reported that patients with acute ischemic stroke had significantly enhanced platelet aggregability compared to patients who presented with TIA. Also systemic platelet activation is enhanced in patients with acute stroke or TIA and returns to baseline levels at 3-month follow-up. Moreover, at 3-month follow-up, persistent platelet activation is associated with increased incidence of recurrent stroke.
However, in this study, there was no statistically significant correlation between platelet aggregation and clinical outcome. This finding coincided with Bhatia et al. (2004) who found that stroke outcome was not affected by platelet aggregation and there was no significant difference amongst expired patients and survivors regarding platelet aggregation. On the contrary, Iwamoto et al. (2005) concluded that enhanced platelet aggregation is associated with poor prognosis and that platelet function test helps to predict outcome in stroke patients.
The role of the natural anticoagulants, antithrombin III, protein C, and protein S, in patients with ischemic stroke, remains uncertain. This study aimed to find out whether their levels in peripheral blood correlate with the severity of neurological deficit or can predict clinical outcome and recurrence. There was no significant correlation between antithrombin III, protein C, and protein S and stroke outcome.
The patients included in this study were above 46 years old while natural anticoagulants deficiency may play a role in stroke in young adults. Additionally, natural anticoagulants deficiency is considered as one of the main risk factors of venous infarctions with less clear role in arterial infarctions.
Our results partially coincided with Haapaniemi et al. (2002) who found no correlation between the levels of the natural anticoagulants and etiology of stroke, any stroke risk factor, or neurological scores, except that the antithrombin III level on admission showed significant correlation with stroke severity and disability at 3 months. Moreover, natural anticoagulant levels did not predict recurrence of ischemic stroke.