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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:884.)
© 2002 American Heart Association, Inc.

Editorials

Comparative Genetics of Atherosclerosis and Restenosis: Exploration With Mouse Models

Xiaosong Wang; Beverly Paigen

From The Jackson Laboratory, Bar Harbor, Me.

Correspondence to Beverly Paigen, The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609. E-mail bjp@jax.org

Ischemic heart disease is a consequence of coronary atherosclerosis. In addition to coronary bypass surgery, a common and often successful treatment 0is angioplasty, expanding the internal lumen of the coronary artery with a balloon. However, 30% to 50% of angioplasty patients soon develop significant restenosis, a narrowing of the artery through migration and growth of smooth muscle cells. Stents introduced into the coronary artery to keep it open after angioplasty considerably reduce the incidence of restenosis, but 10% to 50% of patients receiving stents still develop restenosis.¹ Recent clinical trials that use local radiation to the treated artery or drugs released by the stent, such as sirolimus and paclitaxel, are reported to improve the clinical outcomes^2–5 but may only provide transient protection. Even after these efforts, restenosis remains a major clinical problem in light of the more than 800,000 angioplasty procedures in the United States each year and the generally disappointing results of efforts to prevent restenosis with systemically delivered drugs in humans.

See page 955

An understanding of the genetic factors underlying restenosis will help identify those patients resistant to restenosis for whom treatment is most likely to be successful. More importantly, identifying the critical genes involved will clarify the molecular mechanisms controlling restenosis, providing possibilities for substantially more effective therapeutic control of this significant problem.

Exploring the genetics of restenosis has now begun in experimental animals with significant implications for the human condition. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Kuhel et al⁶ have compared the . . . [Full Text of this Article]

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