| Objective: Observe the therapeutic effect of urinary kallidinogenase onarteriosclerosis cerebral infarction and the effect of urinary kallidinogenase oninfarction area and plaque area by MRI black-blood imaging.Methods:60patients who were diagnosed cerebral infarction wereclassified as control group for20cases and experimental group for40cases.Cases in control group accepted common therapy for20days. Cases inexperimental group were applied urinary kallidinogenase combined withcommon therapy for14or20days, according to the general condition. NIHSSscores were recorded before treatment, the7thday after treatment and the lastday after treatment(the14thday or the20thday). Some laboratoryexaminations were necessary during the treatment, such as coagulationfunction, liver function and kidney function. Pay attention to blood pressureand side effects during the treatment. After treatment, improvement rate ofnerve function was calculated as following:(NIHSS scores before treatment–NIHSS scores after treatment)/NIHSS scores before treatment. Recovery:90%-100%; obvious improvement:46%-89%; improvement:18%-45%;inefficacy:0-18%. Deterioration is characterized as advanced NIHSS scoresafter treatment by18%.19cases of experimental group and20cases of controlgroup received MRI imaging and black-blood imaging before treatment, onthe14thday of treatment and the20thday of treatment, recording the infarctionarea, the plaque area and the type of plaque. MRI imaging parameter: axialview T1WI-SE, axial view T2WI-FSE, axial view T2-FLAIR, Y axes viewT2-FSE. Black-blood imaging parameter: FSE-DIR T1WI, FSE-DIRPDWI,FSE-DIR T2WI.The T1WI,FSE-T2WI,T2-FLAIR and DWI imaging ofSE sequences were applied for cerebral infarction examination.Results:34male cases and26female cases, ranging from46to76years old (average61.6±8.26years old) were included in the study.19cases wereapplied urinary kallidinogenase for20days. NIHSS scores in experimentalgroup were significantly reduced compared with control group on differentstages of treatment(P＜0.05).Efficiency in experimental group weresignificantly obvious compared with control group after treatment for14days.Cases of obvious improvement(NIHSS scores reduced by46%-89%) inexperimental group were significantly advanced compared with control group.None of the cases was found negative response to the treatment. Of19cases,6cases were coincidence with type Ⅳ-Ⅴ of plaque, with small area highsignal in equal signal plaque in black-blood imaging, namely the lipid core infiber plaque.10cases were coincidence with type Ⅵ of plaque, withpatching area high signal in equal signal plaque in black-blood imaging.2cases were coincidence with type Ⅶ of plaque, with low signal in equalplaque in black-blood imaging, namely the calcification in fiber plaque.1casewas coincidence with type Ⅷ of plaque, with equal signal plaque, namely thewhole fiber plaque without lipid core and necrosis.10cases in control groupwere characterized as type Ⅳ-Ⅴ or Ⅵ. Infarction area in experimentalgroup was significantly reduced compared with control group in differentstages of treatment(P＜0.05). As for the26cases of type Ⅳ-Ⅴ or Ⅵ, plaquearea was almost stable between control group and experimental group aftertreatment for14days(P＞0.05), but plaque area in experimental group wassignificantly reduced compared with control group after treatment for20days(P＜0.05).Conclusion: Urinary kallidinogenase could significantly improveneurological dysfunction and improve the efficiency as well as the prognosis.Cerebral infarction area was decreased with the treatment of urinaryKallidinogenose. While the therapeutic effect was obvious on unstable plaque,especially on the later stage of treatment. |
