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. 2024 Oct 15;150(16):1217-1219.
doi: 10.1161/CIRCULATIONAHA.124.070087. Epub 2024 Oct 14.

Pathogenesis of Atherothrombotic Events: From Lumen to Lesion and Beyond

Peter Libby  1
Affiliations

Pathogenesis of Atherothrombotic Events: From Lumen to Lesion and Beyond

Peter Libby. Circulation. .
No abstract available

Keywords: acute coronary syndrome; atherosclerosis; inflammation; myocardial infarction; thrombosis.

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Conflict of interest statement

Dr Libby is an unpaid consultant to or involved in clinical trials for Amgen, Baim Institute, Beren Therapeutics, Esperion Therapeutics, Genentech, Kancera, Kowa Pharmaceuticals, Novo Nordisk, Novartis, and Sanofi-Regeneron. Dr Libby is a member of the scientific advisory board for Amgen, Caristo Diagnostics, CSL Behring, Elucid, Kancera, Kowa Pharmaceuticals, Olatec Therapeutics, Novartis, PlaqueTec, Polygon Therapeutics, TenSixteen Bio, Soley Thereapeutics, and XBiotech, Inc. Dr Libby’s laboratory has received research funding in the last 2 years from Novartis, Novo Nordisk and Genentech. Dr Libby is on the Board of Directors of XBiotech, Inc. Dr Libby has a financial interest in Xbiotech, a company developing therapeutic human antibodies; in TenSixteen Bio, a company targeting somatic mosaicism and clonal hematopoiesis of indeterminate potential to discover and develop novel therapeutics to treat age-related diseases; and in Soley Therapeutics, a biotechnology company that is combining artificial intelligence with molecular and cellular response detection for discovering and developing new drugs, currently focusing on cancer therapeutics. Dr Libby’s interests were reviewed and are managed by Brigham and Women’s Hospital and Mass General Brigham in accordance with their conflict-of-interest policies.

Figures

Figure:
Figure:. The focus in understanding the pathophysiology and prevention and management strategies for acute coronary syndromes has evolved over time.
This figure depicts various stages in our concept of acute coronary syndromes (ACS) going from left to right. The initial focus concentrated on focal flow – limiting stenoses that could be bypassed surgically or treated percutaneously. Revascularization can undoubtedly relieve angina pectoris but does not necessarily forestall future ACS events. A great deal of attention then focused on the ruptured plaque as a cause of acute coronary syndromes, recognizing that many myocardial infarctions arise from lesions that do not critically limit blood flow. The substrate of rupture is typically a thin-capped atherosclerotic plaque with a large lipid core. Yet, we now recognize that many such plaques do not rupture or cause clinical events. In an era of effective lipid lowering, superficial erosion may be becoming more common as a cause of ACS. The mural thrombi associated with erosion generally have a platelet-rich “white” character. More recently, the focus has shifted to considerations of the overall burden of atherosclerotic plaque rather than concentrating on a single or a few obstructive lesions. Continued improvements and implementation of medical therapy may lessen the need for invasive treatments going forward.
See this image and copyright information in PMC

References

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