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Association of lipoprotein lipase gene polymorphisms with coronary artery disease

Jeffrey L. Anderson, MD, FACC^* , Gretchen J. King, PhD^* , Tami L. Bair, BS^* , Sidney P. Elmer, BS^* , Joseph B. Muhlestein, MD, FACC^* , Jessica Habashi, BS^* , Lori Mixson, PhD and John F. Carlquist, PhD^*

^* Department of Medicine (Cardiology), University of Utah, LDS Hospital, Salt Lake City, Utah, USA
Department of Pathology, University of Utah, LDS Hospital, Salt Lake City, Utah, USA
Merck Research Laboratories, West Point, Pennsylvania, USA

View larger version (68K): [in a new window]   Figure 1 Computer-assisted photodocumentation showing examples of LPL HindIII (left) and PvuII (right) polymorphic genotyping using polyacrylamide gel electrophoresis of polymerase chain reaction amplification products.

View larger version (29K): [in a new window]   Figure 2 Odds ratio (OR) (diamonds = point estimates, with 95% confidence intervals [CIs]) for coronary artery disease (CAD) of carriage of HindIII (+) allele (genotypes +/+ or +/– vs. genotype –/–) (left), and PvuII (–) allele (genotypes –/– or –/+ vs. +/+ genotype) (right), for CAD versus no-CAD groups overall (open diamonds) and in prespecified subgroups (black diamonds). Size (area) of each diamond is proportional to size of respective (sub)group. Scale on abscissa is logarithmic with increments of 0.1 between 0.1 and 1.0 and 1 between 1 and 10. Chol = cholesterol; HTN = hypertension.