Correlation between fibrinogen level and cerebral infarction.

OBJECTIVE: To investigate the correlation between plasma fibrinogen level and cerebral infarction (CI) as well as the difference of fibrinogen among subtypes of CI. METHODS: A case-controlled study was conducted with 131 cases of CI and 148 controls. Plasma fibrinogen levels were detected by the Clauss method. RESULTS: High fibrinogen level (3.09 +/- 0.94 g/L) was correlated with CI (OR = 2.47, 95% CI: 1.51-4.04, P < 0.005) at the onset stage of the disease. Persistent high fibrinogen level (3.14 +/- 0.81 g/L) at 6-month after stroke onset was detected and correlated with CI (OR = 4.34, 95% CI: 1.80-10.51, P = 0.001). Higher fibrinogen level was correlated with total anterior circulation infarction (TACI), partial anterior circulation infarction (PACI), and posterior circulation infarction (POCI) (OR = 4.008, P < 0.001). Higher fibrinogen level was correlated with extracranial atherosclerosis (OR = 3.220, P < 0.05, but not with intracranial atherosclerosis. CONCLUSION: Fibrinogen level may be a risk factor of CI and probably correlates with subtypes of CI and distributions of atherosclerosis.

Higher serum triglyceride level in patients with acute ischemic stroke is associated with lower infarct volume on CT brain scans.

We investigated the relationship between serum triglyceride level and acute ischemic stroke severity using infarct volume on CT brain scans as a marker. A total of 121 consecutive acute ischemic stroke patients (53 males and 68 females, age 47-93 years) with anterior circulation (75%), posterior circulation (9%) or lacunar infarcts (16%) were examined. All patients were admitted within 24 h of the symptom onset, and CT scans were taken over the subsequent 24-72 h. With adjustment for the infarct type, age, sex, timing of CT imaging (24-36, >36-48 or >48-72 h since admission), atrial fibrillation, hypertension, fasting cholesterol and glucose levels, a higher (> or =1.70 mmol/l) fasting serum triglyceride level (within 24 h after admission) was associated with a lower infarct volume (p = 0.014). In line with a recent report on milder clinical symptoms in acute ischemic stroke patients with higher triglycerides, the results suggest an independent association between serum triglyceride level and stroke severity.

Insular cortical ischemia is independently associated with acute stress hyperglycemia.

BACKGROUND AND PURPOSE: Acute poststroke hyperglycemia has been associated with larger infarct volumes and a cortical location, regardless of diabetes status. Stress hyperglycemia has been attributed to activation of the hypothalamic-pituitary-adrenal axis but never a specific cortical location. We tested the hypothesis that damage to the insular cortex, a site with autonomic connectivity, results in hyperglycemia reflecting sympathoadrenal dysregulation. METHODS: Diffusion-weighted MRI, glycosylated hemoglobin (HbA1c), and blood glucose measurements were obtained in 31 patients within 24 hours of ischemic stroke onset. Acute diffusion-weighted imaging (DWI) lesion volumes were measured, and involvement of the insular cortex was assessed on T2-weighted images. RESULTS: Median admission glucose was significantly higher in patients with insular cortical ischemia (8.6 mmol/L; n=14) compared with those without (6.5 mmol/L; n=17; P=0.006). Multivariate linear regression demonstrated that insular cortical ischemia was a significant independent predictor of glucose level (P=0.001), as was pre-existing diabetes mellitus (P=0.008). After controlling for the effect of insular cortical ischemia, DWI lesion volume was not associated with higher glucose levels (P=0.849). There was no association between HbA1c and glucose level (P=0.737). CONCLUSIONS: Despite the small sample size, insular cortical ischemia appeared to be associated with the production of poststroke hyperglycemia. This relationship is independent of pre-existing glycemic status and infarct volume. Neuroendocrine dysregulation after insular ischemia may be 1 aspect of a more generalized acute stress response. Future studies of poststroke hyperglycemia should account for the effect of insular cortical ischemia.

Prediction of early clinical severity and extent of neuronal damage in anterior-circulation infarction using the initial serum neuron-specific enolase level.

CONTEXT: Prompt and precise measurement of neuronal damage in acute cerebral infarction is important to determine the prognosis of functional outcome. A feasible biochemical marker such as the neuron-specific enolase (NSE) level has been used to detect various diseases involving the central nervous system. OBJECTIVE: To determine whether the initial serum NSE level is a useful marker for predicting the severity of clinical neurological deficits and the extent of neuronal damage in acute anterior-circulation infarction. DESIGN: Case-control study with biochemical-clinicoradiological correlation. SETTING: Tertiary care center. PARTICIPANTS: Eighty-one patients and 77 age- and sex-matched control subjects. MAIN OUTCOME MEASURES: Patients with anterior-circulation infarction underwent intravenous serum NSE sampling within 24 hours after symptom onset. Recent infarction was confirmed by T2-weighted and diffusion-weighted magnetic resonance imaging of the brain about 1 week after the onset of stroke. Volumetric analysis of infarction was also performed. The National Institutes of Health Stroke Scale score was measured on admission to the hospital and 1 week after symptom onset. RESULTS: The patients' initial serum NSE levels were statistically significantly higher than the controls (P<.05). The initial serum NSE level highly correlated with the volume of infarction seen on T2-weighted magnetic resonance imaging of the brain (r = 0.62, P<.001) and with the National Institutes of Health Stroke Scale score obtained on hospital admission (r = 0.42, P =.002) and on the seventh day after the onset of stroke (r = 0.44, P<.001). CONCLUSION: The initial serum NSE level is a reliable predictor for the extent of neuronal damage and the severity of clinical neurological deficits in acute anterior-circulation infarction.

Tissue plasminogen activator and plasminogen activator inhibitor in patients with acute ischemic stroke: relation to stroke etiology.

Recent studies suggest that high plasma levels of tissue-type plasminogen activator (tPA) and its inhibitor (plasminogen activator inhibitor-1, PAI-1) are markers of an increased risk of atherothrombotic ischemic events such as stroke and myocardial infarction. In this prospective study, we measured tPA antigen, PAI-1 antigen and activity, as well as tPA/PAI-1 complex in patients with acute stroke. Stroke subtypes were classified according to the TOAST criteria. From 132 consecutively screened patients, 89 (100%) were enrolled in this study, including 42 patients (47%) with large artery atherosclerosis (LAA), 32 (36%) with small vessel occlusion (SVO), and 15 (17%) with cardioembolism (CE). Nineteen age-matched neurologic patients without manifestations of cerebrovascular disease served as control subjects (CS). Patients with acute stroke had significantly higher plasma levels of tPA antigen (p < 0.001), PAI-1 antigen (p < 0.05) and PAI activity (p < 0.05) than patients in the control group. t-PA antigen, PAI activity and tPA/PAI-1 complex levels were similar regardless of stroke etiology. Only PAI-1 antigen was lower in patients with cardioembolic stroke than in stroke patients with LAA (p < 0.05). Plasma tPA antigen, PAI-1 antigen, and PAI activity are significantly increased in patients with acute ischemic stroke. Except for PAI-1 antigen, this increase appears not to be related to the underlying stroke etiology.