ABSTRACT
Objective To study the correlation between hyperhomocystinemia and the property of cerebral artery plaque,and the pathogenic mechanism of hyperhomocystinemia resulting in acute cerebral stroke.Methods 60 patients with acute ischemic stroke were chosen.30 patients with normal homocysteine were classified as control group.The other 30 patients with hyperhomocystinemia were classified as observation group.High resolution magnetic resonance imaging(HRMRI) and multi contrast plaque imaging technique were used to measure the cerebral artery plaque burden,the fat ratio of plaques,the hemorrhage within the plaque and fibrouscap rupture.The number of inflammatory cells in the plaque and the density of the new blood vessels were identified using the transfer constant of the contrast medium.Results In the observation group,4 cases with low-risk plaques (13.33％),10 cases with middle-risk plaques (33.33 ％) and 16 cases with high-risk plaques (53.33 ％).In the control group,13 cases with low-risk plaques (43.33％),6 cases with middle-risk plaques (20.00％),11 cases with high-risk plaques (36.67％).The number of intraplaque hemorrhage were 18 cases (60.00％) in the observation group,and 8 cases (26.67％) in the control group.The number of fibrouscap rupture were 21 cases (70.00％) in the observation group,and 13 cases (43.33％) in the control group.Risk stratification of vulnerable plaques in cerebral atherosclerosis (U =-2.032,P =0.042),intraplaque hemorrhage (x2 =6.79,P =0.009) and fibrouscap rupture (x2 =4.34,P =0.037) in the observation group was higher than that in the control group.The number of inflammatory cells in plaques and the density of the new blood vessels in the observation group was (0.188 ± 0.265)Ktrans/min,which in the control group was (0.118 ± 0.183)Ktrans/min.The number of inflammatory cells in the plaque and the density of the new blood vessels in the observation group was higher than that in the control group (t =11.831,P =0.000).Conclusion Hyperhomocystinemia causes intraplaque hemorrhage,fibrouscap rupture,inflammatory cell activity and neovascularization in plaques,accelerates cerebral atherosclerosis and increases the incidence of ischemic stroke events.