title: Risk factors for progression of aortic atheroma in stroke and transient ischemic attack patients.
abstract: OBJECTIVE
  Aortic atheroma is an independent risk factor for stroke and undergoes temporal progression. Clinical and risk factor associations of such progression are unknown. Hyperhomocysteinemia has been linked with atherosclerosis, including that in the cerebral vasculature. This study investigated associations between elevated homocysteine levels and other stroke vascular risk factors and the risk of aortic atheroma progression in patients with cerebrovascular disease.
  
  
  METHODS
  Fifty-seven stroke and 21 transient ischemic attack patients underwent multiplanar transesophageal echocardiograms within 1 month of symptom onset and again at 9 months. Aortic atheroma was graded and stratified by use of existing criteria. Stroke risk factors; use of anticoagulant, antiplatelet, and hypolipidemic drugs; and clinical and etiological subtypes of stroke were recorded and compared in patients stratified for the presence or absence of aortic atheroma progression.
  
  
  RESULTS
  Of the 78, 29 (37%) progressed, 32 (41%) remained unchanged, and 17 (22%) regressed. Progression was most marked at the aortic arch (P=0.005), followed by the ascending segment (P<0.04). In nearly two thirds of the patients in whom aortic atheroma remained unchanged over 9 months, no atheroma was evident on baseline transesophageal echocardiogram. Only homocysteine levels > or =14.0 micromol/L (P=0.02), total anterior cerebral infarct (P=0.02), and large-artery atherosclerosis (P=0.005) significantly correlated with progression.
  
  
  CONCLUSIONS
  Among vascular risk factors, elevated homocysteine levels are associated with aortic atheroma progression. Stroke and transient ischemic attack patients with aortic atheroma should undergo assessment of homocysteine levels, which, if elevated, may be treated with vitamins in an effort to arrest aortic atheroma progression.
authors.affiliation: Cerebrovascular Program, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Md, USA.
authors.forename: Souvik
authors.initials: S
authors.lastname: Sen
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Oppenheimer
authors.forename: Joao
authors.initials: J
authors.lastname: Lima
authors.forename: Barry
authors.initials: B
authors.lastname: Cohen
mesh_terms: D000925:Anticoagulants / Q000627:therapeutic use; D001018:Aortic Diseases / Q000150:complications / Q000175:diagnosis* / Q000188:drug therapy; D001161:Arteriosclerosis / Q000150:complications / Q000175:diagnosis* / Q000188:drug therapy; D003710:Demography; D018450:Disease Progression; D017548:Echocardiography, Transesophageal; D005260:Female; D006710:Homocysteine / Q000097:blood; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000150:complications / Q000175:diagnosis*; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D002546:Ischemic Attack, Transient / Q000150:complications / Q000175:diagnosis*; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012075:Remission, Spontaneous; D012307:Risk Factors; D020521:Stroke / Q000145:classification / Q000150:complications / Q000175:diagnosis*; D016896:Treatment Outcome
chemical_list: D000925:Anticoagulants; D000960:Hypolipidemic Agents; D010975:Platelet Aggregation Inhibitors; D006710:Homocysteine