Update December 8, 2018

 

 

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The integrative pathophysiology of atherosclerosis, ischemic heart disease, and the systemic inflammatory response. Atherosclerosis develops over many years (1) and can lead to myocardial infarction (2), while the stress of acute myocardial infarction (2) also produces an “echo” in atherosclerotic plaques (1). Acute myocardial infarction causes pain and anxiety that triggers sympathetic outflow from the central nervous system (3). β3 adrenergic stimulation mobilizes leukocyte progenitors from their bone marrow niche. These progenitor cells can migrate to the spleen, where they can multiply in response to hematopoietic growth factors. The proinflammatory monocytes then leave the spleen and enter the atherosclerotic plaque (1), where they promote inflammation that can render a plaque more likely to provoke thrombosis and hence acute myocardial infarction (2). IL, interleukin. Reproduced with permission from Libby P, Nahrendorf M, Swirski FK: Leukocytes Link Local and Systemic Inflammation in Ischemic Cardiovascular Disease: An Expanded “Cardiovascular Continuum.” J Am Coll Cardiol. 2016 Mar 8;67(9):1091-1103.192

 

When neurofibromatosis causes large tumors or tumors that press on a nerve, surgery can help ease symptoms. Some people may benefit from other therapies, such as stereotactic radiosurgery or medications to control pain.

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