Lipoprotein(a) and inflammation in human coronary atheroma: association with the severity of clinical presentation
George Dangas, MD*  ,
Roxana Mehran, MD,
Peter C. Harpel, MD*  ,
Samin K. Sharma, MD, FACC* ,
Santica M. Marcovina, PhD||,
Geoffrey Dube, BS*  ,
John A. Ambrose, MD, FACC* and
John T. Fallon, MD, PhD*
* Cardiovascular Institute, Mount Sinai School of Medicine, New York, New York, USA
Department of Medicine (Division of Hematology), Mount Sinai School of Medicine, New York, New York, USA
Department of Pathology, Mount Sinai School of Medicine, New York, New York, USA
Cardiology Research Foundation, Washington Hospital Center, Washington, D.C., USA
|| Department of Medicine, Northwest Lipid Research Laboratories, University of Washington, Seattle, Washington, USA
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Figure 1 Demonstration of two Lp(a) stains, utilizing the polyclonal apoprotein(a) antibody (left panel) and the monoclonal apoprotein(a) antibody a-6 (right panel). The positive staining occupies the same plaque areas in both stains, but the polyclonal antibody stains with greater intensity. Lp(a) occupies the majority of the plaque. Original magnification x40 (brown = peroxidase developed with 3-3'-diaminobenzidine).
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Figure 2 Comparative staining of an atherosclerotic plaque of a rest angina patient: eosin (A), alpha-actin (B), KP-1 (C) and polyclonal apoprotein(a) antibody (D). The distribution of Lp(a) and macrophages is nearly identical (C, D). Smooth muscle cells occupy a certain portion of the Lp(a) area, but they also localize in Lp(a) negative area.
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Figure 3 Correlation between Lp(a) and KP-1 in rest angina (r2 = 0.77, p < 0.0001).
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Figure 4 Correlation between Lp(a) and alpha-actin in crescendo exertional angina (r2 = 0.38, p < 0.001).
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