title: Relation of plasma lipoprotein(a) with myocardial viability and left ventricular performance in survivors of myocardial infarction.
abstract: Previous studies have reported that high serum lipoprotein(a) levels may be responsible for total occlusion of the infarct-related artery via inhibition of intrinsic fibrinolysis during acute myocardial infarction. We evaluated whether this would result in a greater extent of myocardial necrosis and impaired left ventricular function in patients with high lipoprotein(a) levels. Sixty-eight patients with prior myocardial infarction, who were not receiving thrombolytic therapy underwent coronary angiography and stress-redistribution-reinjection Tl-201 scintigraphy. Antegrade TIMI flow in the infarct-related artery was lower (1.54 +/- 1.14 vs 2.15 +/- 1.05; p = 0.03) and the collateral index was higher (1.3 +/- 1.0 vs 0.8 +/- 0.9; p = 0.07) in patients with high lipoprotein(a) levels (> 30 mg/dl) compared to those with low lipoprotein(a) levels (< or = 30 mg/dl). Regional wall motion score index was lower (0.8 +/- 0.8 vs 1.4 +/- 0.5; p = 0.008) and global ejection fraction was higher (46 +/- 10% vs 40 +/- 11%; p = 0.03) in patients with low lipoprotein(a) levels. On SPECT images, the number of non-viable defects was higher in patients with high lipoprotein(a) levels (4.0 +/- 2.5 vs 1.9 +/- 1.3; p = 0.0002), whereas the number of viable defects was higher in those with low lipoprotein(a) levels (2.5 +/- 1.8 vs 1.5 +/- 1.3; p = 0.02). We conclude that high lipoprotein(a) levels may prolong the occlusion of infarct-related artery during acute myocardial infarction and lead to a greater extent of myocardial necrosis and impaired left ventricular function.
authors.affiliation: Siyami Ersek Thoracic and Cardiovascular Surgery Centre, Istanbul, Turkey.
authors.forename: M
authors.initials: M
authors.lastname: Aksoy
authors.forename: Y
authors.initials: Y
authors.lastname: Kepekçi
authors.forename: O
authors.initials: O
authors.lastname: Göktekin
authors.forename: I
authors.initials: I
authors.lastname: Akdemir
authors.forename: M
authors.initials: M
authors.lastname: Gürsürer
authors.forename: A
authors.initials: A
authors.lastname: Emre
authors.forename: M
authors.initials: M
authors.lastname: Bilge
authors.forename: K
authors.initials: K
authors.lastname: Yesilçimen
authors.forename: B
authors.initials: B
authors.lastname: Ersek
mesh_terms: D000328:Adult; D001241:Aspirin / Q000627:therapeutic use; D017023:Coronary Angiography; D005260:Female; D006321:Heart / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D015912:Thrombolytic Therapy; D014022:Tissue Survival; D015899:Tomography, Emission-Computed, Single-Photon; D016277:Ventricular Function, Left
chemical_list: D017270:Lipoprotein(a); D001241:Aspirin