Abstract
Heart attacks occur when lipoprotein-driven inflammation called atherosclerosis triggers blood clotting in the arteries. It seems that the attacks can, in turn, accelerate atherosclerosis by fanning the inflammation. See Letter p.325 Patients who have a myocardial infarction are at high risk of recurrent events. This study shows for the first time that myocardial infarction and stroke accelerate atherosclerosis. The authors were able to demonstrate that myocardial infarction leads to activation of the sympathetic nervous system, which, in turn, leads to the release of haematopoietic stem cells and progenitor cells. These cells seeded in the spleen and augmented the production of monocytes displaying an enhanced atherogenic phenotype. These findings were correlated with patient data showing that prior beta-blocker therapy was associated with a decrease in circulating monocytes after myocardial infarction. These findings suggest that interventions that interrupt the supply of monocytes could attenuate atherosclerosis and may improve long-term patient outcomes.
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