title: Extracorporeal double filtration plasmapheresis in acute atherothrombotic brain infarction caused by major artery occlusive lesion.
abstract: Extracorporeal double filtration plasmapheresis (EDFP) can quickly lower plasma viscosity and fibrinogen concentration. EDFP has the potential to improve cerebral microcirculation in acute ischemic stroke and ultimately to salvage penumbral tissue. However, no evidence is available to show that EDFP can increase cerebra blood flow (CBF). Therefore, we investigated whether EDFP could increase CBF by quantitative CBF measurements and documented the clinical effects of EDFP in acute ischemic stroke. EDFP was performed ten times in seven patients diagnosed as having acute atherothrombotic brain infarction caused by major artery occlusive lesion. They also fulfilled one of the following entry criteria: 1) diffusion/perfusion mismatch demonstrated by MRI on admission; 2) a hemispheric syndrome, but only a small lesion on diffusion weighted MRI (<25% of MCA territory); or 3) progressing stroke. Exclusion criteria were 1) contraindication of heparin or 2) spontaneous improvement of symptoms. Time from stroke onset to EDFP varied from 5 hr to 7 days. Plasma viscosity was quickly lowered by EDFP without affecting RBC counts, Hb, or Hct in all patients. Positron emission tomography (PET) with 15-O labeled H2O measurements revealed a significant CBF increase from 36.4 +/- 8.3 ml/100 g/min to 40.7 +/- 6.8 ml/100 g/min in the affected hemisphere (P=0.048). Definite CBF improvement was also demonstrated by single photon emission computed tomography (SPECT) in one of two patients who had severe stenosis of the middle cerebral artery. Furthermore, this patient showed remarkable improvement of hemiplegia immediately following EDFP (NIHSS score: 18 to 13). In conclusion, EDFP can increase CBF in ischemic brain tissue in acute atherothrombotic brain infarction. Further clinical studies should focus on the efficacy of EDFP on outcome of patients with this stroke subtype.
authors.affiliation: Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Suita, Osaka, Japan. yazhaseg@hsp.ncvc.go.jp
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Hasegawa
authors.forename: Masafumi
authors.initials: M
authors.lastname: Tagaya
authors.forename: Shigeru
authors.initials: S
authors.lastname: Fujimoto
authors.forename: Kohei
authors.initials: K
authors.lastname: Hayashida
authors.forename: Takenori
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: Kazuo
authors.initials: K
authors.lastname: Minematsu
mesh_terms: D000368:Aged; D001783:Blood Flow Velocity; D001809:Blood Viscosity; D002545:Brain Ischemia / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D002544:Cerebral Infarction / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D002560:Cerebrovascular Circulation; D006801:Humans; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D010956:Plasmapheresis / Q000379:methods*; D014055:Tomography, Emission-Computed