Cardiology: Bad matters made worse

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.

Figure 1. A cycle of damage and repair

During atherosclerosis, fat-carrying lipoproteins are retained in the artery wall. This induces an inflammatory response that is characterized by an influx of immune cells called monocytes, which differentiate into other inflammatory cells, such as macrophages and dendritic cells. Blood clots at sites of atherosclerosis can block the arteries and cause heart attacks. In a mouse model of atherosclerosis, Dutta et al. show that heart attack activates the sympathetic nervous system (SNS), and that this promotes monocyte production in the spleen. The authors demonstrate that the monocytes move from the spleen to the blood and then to atherosclerotic lesions in the arteries, where they accelerate the progression of these lesions (red arrow). However, monocytes are also likely to be important in the repair of heart muscle tissue (green arrow) following heart attack, and this dual role could complicate attempts to treat post-heart-attack atherosclerosis by targeting monocytes.