title: Increased cerebral CO(2) reactivity after heparin-mediated extracorporal LDL precipitation (HELP) in patients with coronary heart disease and hyperlipidemia.
abstract: OBJECTIVE
  There is experimental and clinical evidence that hypercholesterolemia leads to an impairment of endothelial function in coronary and cerebral arteries. Using transcranial Doppler sonography, we examined CO(2) reactivity as a marker of cerebral vasoreactivity in patients with coronary heart disease and hyperlipidemia before and after drastic lowering of LDL cholesterol, lipoprotein(a) [Lp(a)], and fibrinogen levels by heparin-mediated extracorporal LDL precipitation (HELP).
  
  
  METHODS
  CO(2) reactivity was determined in 13 patients with coronary artery disease and hyperlipidemia undergoing regular HELP therapy. Middle cerebral artery mean blood flow velocity (MFV) was detected by transcranial Doppler. CO(2) reactivity was calculated as the percent change of MFV during hypercapnia, induced by ventilation of carbogene (5% CO(2), 95% O(2)), to normocapnia. Patients with extracranial or intracranial stenoses were excluded. Other parameters such as blood viscosity, heart rate, and blood pressure were measured to control hemorheologic and systemic influences on CO(2) reactivity.
  
  
  RESULTS
  A single HELP treatment reduced total cholesterol, LDL cholesterol, Lp(a), triglycerides, and fibrinogen levels by >50% (P<0.001). Blood viscosity significantly decreased from 1.24+/-0.04 to 1.07+/-0.02 mPa (P<0.001). Blood pressure, heart rate, and MFV did not change significantly. CO(2) reactivity increased from 22% +/- 21% to 36% +/- 18% (P<0.05).
  
  
  CONCLUSIONS
  Fast and drastic removal of LDL cholesterol, Lp(a), and fibrinogen from plasma results in an improvement of cerebrovascular reactivity in patients with coronary heart disease and hyperlipidemia. The clinical use of HELP in patients with impaired cerebrovascular reactivity might be promising.
authors.affiliation: Department of Neurology and Institute of Clinical Chemistry, Klinikum Grosshadern, Ludwig-Maximilians-Universität, Munich, Germany.
authors.forename: T K
authors.initials: TK
authors.lastname: Pfefferkorn
authors.forename: H P
authors.initials: HP
authors.lastname: Knüppel
authors.forename: B R
authors.initials: BR
authors.lastname: Jaeger
authors.forename: J
authors.initials: J
authors.lastname: Thiery
authors.forename: G F
authors.initials: GF
authors.lastname: Hamann
mesh_terms: D000368:Aged; D000925:Anticoagulants / Q000627:therapeutic use*; D001781:Blood Component Removal; D001809:Blood Viscosity; D002245:Carbon Dioxide / Q000494:pharmacology*; D002536:Cerebral Arteries / Q000000981:diagnostic imaging; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D011232:Chemical Precipitation; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood*; D003327:Coronary Disease / Q000503:physiopathology* / Q000628:therapy; D005112:Extracorporeal Circulation; D005340:Fibrinogen / Q000032:analysis; D006493:Heparin / Q000627:therapeutic use*; D006801:Humans; D006949:Hyperlipidemias / Q000503:physiopathology* / Q000628:therapy; D017270:Lipoprotein(a) / Q000097:blood; D008875:Middle Aged; D011446:Prospective Studies; D014280:Triglycerides / Q000097:blood; D017585:Ultrasonography, Doppler, Transcranial
chemical_list: D000925:Anticoagulants; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D017270:Lipoprotein(a); D014280:Triglycerides; D002245:Carbon Dioxide; D005340:Fibrinogen; D006493:Heparin