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> “The art of simplicity is a puzzle of complexity”> > —Douglas HortonAtherosclerosis is a systemic disease, and it often affects multiple arterial beds at the same time. Why atherosclerosis hits first at the coronary, cerebral, or peripheral level in different patients is unknown. Also, few data are available on how the disease spreads to multiple sites, whether plaque growth progresses linearly over time or if it accelerates suddenly. The recent discovery that acute vascular events, such as myocardial infarction and stroke, are both consequences and causes of atherosclerosis acceleration, is groundbreaking.1 A neuroendocrine loop has been described as responsible for plaque growth after acute ischemia in animals and humans. This pathway primarily involves bone marrow (BM)–derived precursors, generating inflammatory cells that propagate to the plaque. Organs such as the BM and the spleen were not considered to play a significant role in the pathophysiology of atherosclerosis. Now we know that many actors of the atherosclerotic process are born in the BM and traffic through the spleen before reaching the artery wall.2 Studies using F-18-fluorodeoxyglucose-positron emission tomography show that metabolic activation of the BM and spleen takes place after acute coronary syndromes,3,4 and spleen metabolic activity also predicts future cardiovascular events.3 Enhanced BM myelopoiesis, extramedullary seeding of myeloid precursors, and monocytosis are consistent features observed in murine models of atherosclerosis and myocardial infarction, as well as in patients with atherosclerosis or risk factors.2,5Article, see p 564 A parallel line of research has produced a wealth …

Task for Today: Complete the Puzzle of Circulating Stem Cells and the Atherosclerotic Burden