| Background and Objective:Theprogressivecerebralinfarctionisamajorcauseof death and disability in patients with stoke.The progress of the acute cerebralinfarction is associated with severe atherosclerosis, thrombosis extended or form again,great vascular lesions or collateral vessels obstruction, cerebral edema progress,hemorrhagic transformation of cerebral infarction, cerebral ischemic reperfusion injury,platelet-leukocyte increased aggregation and so on.Direct thrombin inhibitor argatrobancan reduce secondary micro thrombus of the ischemia penumbra,reduce ischemic injuryand improve neurological function deficit, and also can lower all kinds of cytokines leadto inflammate and thrombosis, to reduce the expression of P-select element on theplatelet surface and platelet-leukocyte aggregation, reduce leukocyte activation,inhibition of vascular atherosclerosis.Many clinical and animal experiments havedemonstrated argatroban could be effective in treatment of acute cerebral infarction andhave not increased the risk of bleeding. This study was to evaluate the efficacy andsafety of argatroban in the treatment of progressive cerebral infarction.Subjects and Methods:The progressive cerebral infarction patients are choosedfrom January2010to December2013in Shenyang Military Region General HospitalNeurology, met the inclusion criterias:①within48h of onset, NIHSS (NationalInstitutes of Health Stroke Scale)≥2;②within6h to5d after the onset of neurologicdeterioration,the difference between aggravating NIHSS and that on the onset≥2;③thefirst onset or have not legacy limb paralysis sequelae past, and does not affect the rating,mRS (Modified Rankin Scale)≤1;④all patients accorded with diagnostic criteria set bythe academic meeting of the fourth national cerebrovascular diseased in1995,anddiagnosed by the head CT and MRI;⑤parents could not be thrombolysis treatment forvarious reasons;⑥all informed consents by the patient and family members.Exclusion criteria:①With serious cardiac insufficiency and hypohepatia (glutamic oxalacetictransaminase or glutamic-pyruvic transaminase is greater than the normal value1~1.5times);②Severe hypertension(BP>180/110mmHg);③w ithblood disease or bleedingtendency such as hemorrhagic cerebral infarction, gastrointestinal bleeding, urinary tractbleeding, or blood coagulation dysfunction.All patients received the treatments afteradmission include promoting blood circulation to remove blood stasis, scavenging freeradicals, improving brain metabolism, control of blood pressure, blood glucose, bloodlipids and so on.On this basis, continuous intravenous pumping the argatroban(60mg/d)48h on the aggravation of the day and the next day,continuous intravenous pumpingargatroban(10mg)3h twice a day followed by5d,a total of7d treatment,and thencontinue to give antiplatelet therapy, promoting blood circulation to remove blood stasis,etc.Grouping in accordance with the time of the aggravation, the presence of greatvascular stenosis or not, severe degree, OCSP classification and the area of theinfarction, NIHSS and mRS were used respectively to evaluate each group degree ofnervous functional defects and the comprehensive ability of life before treatment and7dand14d after treatment.Results:Participants included100patients with progressive cerebral infarction,60males and40females, average age is (63.76±9.39). The NIHSS and mRS of all of thepatients7d,14d after treatment were significantly lower compared with beforetreatment,the difference was statistically significant(P<0.05),the total effective rate was68%.The NIHSS and mRS of both early progress group and late progress7d,14d aftertreatment was significantly decreased, the difference was statistically significant (P<0.05);The NIHSS of both great vascular stenosis group and no great vascular stenosisgroup and the mRS of no great vascular stenosis group7d,14d after treatment weresignificantly lower compared with before treatment,the difference was statisticallysignificant(P<0.05);There was no statistically significant difference (P>0.05) betweenthe mRS of great vessels stenosis group7d,14d after treatment and before treatment;TheNIHSS and mRS of mild and moderate groups7d,14d after treatment were significantlydecreased, the difference was statistically significant (P<0.05);There was no statistically significant difference (P>0.05) between the NIHSS and mRS of severe group7d,14dafter treatment and before treatment; The NIHSS and mRS of anterior circulationinfarction group (TACI+PACI)7d,14d after treatment and NIHSS of posteriorcirculation infarction group14d after treatment were significantly lower compared withbefore treatment, the difference was statistically significant (P<0.05);There was nostatistically significant difference (P>0.05) between the NIHSS and mRS of posteriorcirculation infarction group (POCI)7d after treatment and before treatment;The NIHSSand mRS of patients with cerebral infarction on the side of right and left7d,14d aftertreatment were significantly reduced compared with before treatment, the differencewas statistically significant (P<0.05);The NIHSS and mRS of patients with bilateralcerebral infarction7d,14d after treatment was no statistically significant difference (P>0.05) compared with the treatment did before;Agatroban is effective for each group.Thedifference of curative effect grade between great vascular stenosis group and no greatvascular stenosis group was statistically significant (P<0.05), the curative effect gradecomparison between each other was no statistically significant difference (P>0.05).Conclusion:Argatroban is safe and effective within48h of the onset of acuteprogressive cerebral infarction patients, regardless of the progress of time,the severity ofthe onset, the scope of brain ischemia,the area of infarction or the presence ofintracranial vascular stenosis.The neurological function improvement is moresignificant especially mild-moderate neurofunction deficit,no extracranial or intracranialvascular stenosis, anterior circulation ischemia and patients with unilateral progressivecerebral infarction. |
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