الفهرس 
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Abstract
Stroke is the second most common cause of death and the third most common cause of disability all over the world. TPA is the only FDA approved treatment for ischemic stroke. TPA was found to greatly eliminate stroke patients disability through its thrombolytic action. Recently, studies pointed to the crucial role of TPA in neuroplasticity participating in the recovery of ischemic stroke patients.
Matrix metalloproteinases are well-known inflammatory mediators that belong to a family of structurally related zinc-binding proteolytic enzymes that are widely distributed in human tissues. They degrade almost all components of extracellular matrix in both physiological and pathological processes.
MMPs are involved in the pathogenesis of atherosclerosis by the activation of migration and proliferation of smooth muscle cells and by induction and destabilization of atherosclerotic plaques .
Ischemic stroke (IS) and intracerebral hemorrhage (ICH) are both associated with activation and altered expression of matrix metalloproteinases (MMPs), mainly MMP-2 and MMP-9. Several reports have shown that serum levels of MMP-9 increase in the acute phase of stroke and MMP-2 levels increase after several days.
Circulating levels of MMP-9 have been proved associated with poor outcomes in stroke patients treated with tissue plasminogen activator (rTPA) . Furthermore, recent studies suggest that rTPA adverse effects may be mediated through MMP supregulation and activation .
The present study aimed to assess the relationship between serum level of matrix metalloproteinase 9 and both stroke severity (at the onset of stroke) and outcome of stroke (after 3 months) in acute ischemic stroke patients treated with thrombolytic therapy. Also to study the role of matrix metalloproteinase 9 as a predictor serum marker for rtPA complications.
The study was conducted on 50 patients with ischemic stroke who had received rTPA treatment (within 4.5 hours from stroke onset) (patient group) and 50 patients with ischemic stroke who had contraindications for treatment with rTPA (within 12 hours from stroke onset) (control group).
All included patients were subjected to the following:
History taking regarding: stroke risk factors (DM, HTN, AF, smoking, drug abuse, family history or past history of stroke).
Clinical assessment including: BMI and neurological assessment using the NIHSS at the onset of stroke and 24h after Rtpa and at day 7 from the onset.
Radiological assessment including:
1. C.T. or MRI brain at the onset of stroke and at day 7 from stroke onset. Infarction site and size were assessed using the pure ellipsoid model of ABC/2.
2. Cardiovascular assessment using echocardiography to assess the presence of valvular disease, ejection fraction , left atrium dilatation and cardiomyopathy.
3. Carotid and vertebrobasilar duplex to detect atherosclerosis or stenosis of the carotid and vertebrobasilar arteries.
Laboratory investigations including: Random blood sugar, complete blood count (WBC, PLT and HCT), lipid profile (cholesterol, TG, LDL and HDL) and uric acid
Serum level of MMP- 9 in all included subjects after 24 h of stroke onset.
The results of our study were summarized in the following:
There was no statistically significant difference with p-value >0.05 between group 1( patient group) and group 2( control group) regarding MMP-9 serum level measured 24 h from stroke onset.
There was a statistically significant difference between controlled hypertensive and non-controlled hypertensive subjects regarding the mean MMP-9 serum level with p-value =0.03.
In acute ischemic stroke patients treated with rTPA 6% (n=3 ) had haemorrhagic transformation as a complications from rTPA injection .While 94% (n=47) didn’t have any complications .Small sample size could not be used in statistical analysis.
There was no statistically significant difference between patients group and control group regarding NIHSS just after admission and before thrombolytic therapy.
There was a statistically highly significant difference between both groups regarding NIHSS after 24h and 7 days.
The mean value for door to needle time for rTPA treated patients was 94.8±66.7 and door to needle time ranged between 30-240 minutes.
The mean value for infarction size at day 7 for rTPA treated patients was 13.02±5.8 cm3 and for controls was 14.07±6.7 cm3 . There was no statistically significant difference between both groups regarding the infarction size (Pvalue=0.4).
The mean value for MRS after 3 months for rTPA treated patients was 1.9 ± 1.4 and MRS ranged between 0-6 ,while for controls was 3.6 ± 0.92 and MRS ranged between 1-6 .There was a highly statistically significant difference between both groups regarding MRS (Pvalue˂0.001).
The mean value for MMP- 9 serum level for rTPA treated patients was 1138.5±412.5 pg/ml and MMP-9 serum level ranged between 260-1971 pg/ml ,while for controls the MMP-9 serum level was 1131.06±367.4 pg/ml and MMP-9 serum level ranged between 355-2080 pg/ml. There was no statistically significant difference between study groups regarding the serum level of MMP-9 ( p-value˃0.9).
There was no statistically significant difference between females and males (P-value=0.8), regarding the mean level of MMP-9.
There was no statistically significant difference between diabetic and non-diabetic patients regarding the mean level of MMP-9.
There was a positive correlation between MMP-9 and age, NIHSS level before and after 24 hrs , and 7 days of treatment in addition to infarction size level , MRS and Time from door to needle (minutes) among group I; which indicated an increase in these variables will be associated with increase in MMP-9 level with p-value <0.05. There was a positive correlation betweenMMP-9 and each of NIHSS level before and after 24 hrs , 7 days of treatment and with infarction size levels, and MRS among group II; which indicated an increase in these variables will be associated with increase in MMP-9 level, but with no correlation with age.