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A novel apoA-I mutation (L178P) leads to endothelial dysfunction, increased arterial wall thickness, and premature coronary artery disease

G. Kees Hovingh, MD^*, Alison Brownlie, PhD, Radjesh J. Bisoendial, MD^*, Marie Pierre Dube, PhD, Johannes H.M. Levels, PhD^*, Wilma Petersen, BSc^*, Robin P.F. Dullaart, MD, PhD, Erik S.G. Stroes, MD, PhD^*, Aeilko H. Zwinderman, PhD, Eric de Groot, MD, PhD^*, Michael R. Hayden, MD, PhD, ChB^,||, Jan Albert Kuivenhoven, PhD^* and John J.P. Kastelein, MD, PhD^*,*

^* Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands
Xenon Genetics Inc., Vancouver, British Columbia, Canada
Department of Internal Medicine, Academic Hospital, Groningen, The Netherlands
Department of Clinical Epidemiology and Biostatistics, Academic Medical Center, Amsterdam, The Netherlands
^|| Center for Molecular Medicine and Therapeutics, Children and Women's Hospital, University of British Columbia, Vancouver, British Columbia, Canada

View larger version (16K): [in a new window]   Figure 1 Log-transformed (logFMD) results are significantly lower in carriers of the apoA-I (L178P) mutation compared with family controls. Inverted triangles = apoA-I (L178P) carriers; circles = family controls.

View larger version (28K): [in a new window]   Figure 2 Mean combined carotid intima media thickness (IMT) increase per year of age is significantly higher in heterozygotes compared with controls. The rate of progression of carotid wall thickening over time is similar in L178P heterozygotes and familial hypercholesterolemia (FH) patients. Solid circles = ApoA-I (L178P) carriers; open diamonds = patients with FH; + = family controls.

View larger version (11K): [in a new window]   Figure 3 Event-free survival is significantly lower in apoA-I (L178P) carriers than in controls. Bottom broken line = apoA-I (L178P) carriers; top line = family controls. p = 0.008.