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Trends Cardiovasc Med. 2019 Mar 28. pii: S1050-1738(19)30043-X. doi: 10.1016/j.tcm.2019.03.006. [Epub ahead of print]

Arson in the artery: Who set the atheroma aflame?

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Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, United States. Electronic address:


Inflammation drives the formation, evolution, and complication of atherosclerotic plaques. Yet, we have not yet captured the culprits who light the fire that burns within the atherosclerotic plaque. The arsonist remains at large. A rigorous analysis exculpates many of the usual suspects. Low-density lipoprotein (LDL) itself engenders little inflammation. Clinical trials do not support an actionable role of oxidized LDL in atherothrombosis. In contrast, triglyceride-rich lipoproteins do promote inflammation, and provide a promising target for intervention. Obese adipose tissue -especially visceral or ectopic lipid deposits -also incite inflammation. A newly recognized cardiovascular risk factor, clonal hematopoiesis provides a novel link between inflammatory pathways and atherosclerotic risk. Despite this progress, the jury is still out on who lit the plaque afire. The rigorous observer must still consider this an unsolved act of arson. We remain in "hot" pursuit of the causal culprit, the arsonist, and accomplices who set the artery wall ablaze.


Clonal hematopoiesis; Endotoxin; Inflammation; Microbiome; Triglyceride-rich lipoproteins


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