title: Conditioned blood reperfusion during angioplasty (CoBRA) treatment of acute myocardial infarction.
abstract: Acute myocardial infarct (MI) results in ischemia distal to lesions which puts heart muscle at risk for reperfusion injury (RI). Neutrophils, platelets and complement are putative mediators of RI. Recent advances in filtration technology provide integrated neutrophil and platelet removal together with complement-attenuating properties in a single blood-conditioning device. The present study characterizes the properties of a blood-conditioning filter and describes its clinical effect when used in conjunction with active hemoperfusion for acute MI. The filter reduces leukocytes by 99.9998 +/- 0.0002% (p<0.0001) and platelets by 99.9934 +/- 0.0069% (p<0.0001). Human plasma, derived from heparinized blood that was 'conditioned' by filtration, was studied using the Langendorff isolated rabbit heart preparation. The deposition of membrane attack complex and the resultant functional myocardial impairments [reflected in hemodynamic and biochemical measurements, including developed pressure, coronary blood flow, lymph-derived myocardial creatine kinase (CK)] are significantly attenuated by blood conditioning. Integration of the blood-conditioning filter into an active hemoperfusion system during primary percutaneous transluminal coronary angioplasty (PTCA) for acute MI (n=8) did not delay the procedure or cause any complications. Reperfusion of occluded coronary arteries with 300 cm3 of conditioned blood led to significant improvement in echocardiographic global wall motion scores (in standard deviations) following treatment (-1.64 +/- 0.18 to -1.45 +/- 0.15, p=0.02). Initial reperfusion of totally occluded coronary arteries with conditioned blood leads to acutely improved ventricular function. Collectively, these data provide a strong indication for continued investigation of conditioned blood reperfusion in angioplasty following acute MI for the long-term effect upon recovery of salvagable myocardium.
authors.affiliation: Department of Cardiology, William Beaumont Hospital, Royal Oak, Michigan, USA.
authors.forename: M B
authors.initials: MB
authors.lastname: Patel
authors.forename: K S
authors.initials: KS
authors.lastname: Kilgore
authors.forename: G A
authors.initials: GA
authors.lastname: Ortolano
authors.forename: C L
authors.initials: CL
authors.lastname: Gryboski
authors.forename: M A
authors.initials: MA
authors.lastname: Qureshi
authors.forename: P
authors.initials: P
authors.lastname: Marcovitz
authors.forename: K B
authors.initials: KB
authors.lastname: Naylor
authors.forename: J L
authors.initials: JL
authors.lastname: Park
authors.forename: B
authors.initials: B
authors.lastname: Wenz
authors.forename: N
authors.initials: N
authors.lastname: Gikakis
authors.forename: R J
authors.initials: RJ
authors.lastname: Freedman
authors.forename: B R
authors.initials: BR
authors.lastname: Lucchesi
authors.forename: W W
authors.initials: WW
authors.lastname: O'Neill
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary / Q000379:methods*; D000818:Animals; D015938:Complement Membrane Attack Complex / Q000378:metabolism / Q000494:pharmacology; D004562:Electrocardiography; D005260:Female; D005374:Filtration / Q000379:methods; D006801:Humans; D066298:In Vitro Techniques; D007937:Leukapheresis; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000503:physiopathology / Q000601:surgery*; D010865:Pilot Projects; D010983:Plateletpheresis; D011446:Prospective Studies; D011817:Rabbits; D015424:Reperfusion / Q000379:methods*; D015427:Reperfusion Injury / Q000209:etiology / Q000517:prevention & control; D013318:Stroke Volume; D016277:Ventricular Function, Left
chemical_list: D015938:Complement Membrane Attack Complex