| Objective To observe the the efficacy of atrovastatin on acute cerebral infarction andits influence on blood lipids, high sensitivity-C reactive protein (hs-CRP), carotidintima-media thickness (IMT) and plaque, in order to further explore the atorvastatintreatment of acute cerebral infarction and the possible mechanism of action.Methods (1) The Fourth National Cerebrovascular Disease Conference revised thevarious types of brain disease diagnostic points diagnostic criteria, confirmed by brain CT orMRI. Select the exclusion criteria and were randomly divided into two groups based on62cases of acute cerebral infarction onset2weeks to develop inclusion and exclusion criteria toexclude non-compliant cases, randomized controlled study would be consistent with thestandard. Treatment group:31cases of atorvastatin therapy), take atorvastatin20mg/d andAspirin100mg/d; control group:31cases, in addition to not taking atorvastatin calcium, theother treatment with atorvastatin treatment group. February of continuous treatment,2weeksafter treatment, February detects the following indicators:(1) determination of the U.S.National Institutes of Health Stroke Scale (NIHSS) score to determine the efficacy ofatorvastatin, while observe the drug’s adverse reactions to explore the safety of atorvastatintreatment of cerebral infarction.(2) detected before and after treatment in patients withhyperlipidemia, to study atorvastatin lipid effects of statins calcium;(3) detection of carotidB-ultrasound, to study atorvastatin of carotid artery plaque.(4) detection of ultra-sensitiveCRP (hs-CRP), in order to study the atorvastatin anti-inflammatory effects of statins.Results (l) Treatment group and control group of clinical data: the comparability ofcarotid IMT, blood lipids and inflammatory markers: Before treatment, the gender makeup ofthe two groups, the average age and NIHSS score, no significant difference (p>0.05). Therewas no significant difference (P>0.05).(2) Atorvastatin calcium NIHSS score in acutecerebral infarction treatment: the treatment group and control group before and after treatment have increased, and the difference between groups was statistically significant (P <0.05).(3)Treatment for2weeks after the atorvastatin group decreased (P <0.05) than the averagepre-treatment TG, LDL cholesterol (LDL-C) and high sensitivity-C reactive protein (hs-CRP),water, The level of the control group hypersensitivity-C response (hs-CRP), also lower thanits pre-treatment (P <0.05), but the treatment group decreased significantly (P <0.05).Treatment group two months later than the pre-treatment TC and LDL-C and hs-CRP levelsdecreased (P <0.05), but the treatment of hs-CRP levels between the two groups two monthsafter the difference count significance (P <0.05).(4) After2weeks of treatment in bothgroups were not statistically significant (P>0.05), Two months after the treatment group thanbefore treatment, after two weeks of treatment, IMT decreased with the IMT differencebetween pre-treatment groups and group within the difference was not statistically significant.Plaque score the treatment group (P>0.05); before and after treatment than before treatmentafter the February increase, the difference was statistically significant (P <0.05). Differencebetween groups was not statistically significant.(P>0.05). Conclusion atorvastatin the Tingearly in patients with acute cerebral infarction, lipid-lowering, anti-inflammatory, stablereversal of plaque role, and thus improve the prognosis of patients with early.Conclusion Acute cerebral infarction with low dose (20mg) atorvastatin statinscalcium through lipid lowering in patients with acute cerebral infarction, inflammatory, stablereversal of plaque role of pleiotropic mechanism to improve the prognosis of patients withearly. |
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