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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1326.)
© 2004 American Heart Association, Inc.

In Memoriam

Gardner Craddock McMillan

Momtaz Wassef

From the Atherosclerosis Research Group, Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, Bethesda, Md.

Correspondence to Dr Momtaz Wassef, Leader, Atherosclerosis Research Group, Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, Two Rockledge Center, 6701 Rockledge Drive, Suite 10196, Bethesda, MD 20892. E-mail WassefM@NHLBI.NIH.GOV

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The cardiovascular medicine community lost a leading light with the death, in April 2004, of Gardner C. McMillan. He recognized, early on, the complexity of human and experimental atherosclerosis. Dr McMillan’s observations, thoughts, and articulate advocacy were always at the forefront of a major shift in how we conceptualize atherogenesis. He led the way in transforming contemporary atherosclerosis and vascular biology research.

Gardner McMillan began his career in medicine by earning a medical degree from McGill University in Montreal, Canada in 1944, taking prize-winning honors in anatomy (the John Munro Elder Prize). He developed a keen interest in pathology during his early postgraduate days, which was solidified with a Masters degree in 1946 and a PhD degree in 1948 under the sponsorship of another pioneering leader of atherosclerosis research, George Lyman Duff. He remained in Dr Duff’s department as a Markel Scholar in Medical Science and began his research career with investigations of human and experimental atherosclerosis. Gardner’s keen interest in comparative pathology enabled him to grasp the magnitude of the contribution that animal models could make toward better-understanding atherosclerosis in humans. His research markedly influenced ensuing research directions in arteriosclerosis. Among his early work was the paradoxical observation that experimental diabetes (induced by alloxan) inhibited the atherosclerosis resulting from feeding cholesterol to the rabbit.¹ As a result of this fundamental research, we came to recognize that some lipoprotein particles are atherogenic whereas others are not, and it likely fuelled Dr McMillan’s lifelong suspicion that the cause of atherosclerosis was . . . [Full Text of this Article]