Update on acute coronary syndromes: the pathologists' view

Area of Science:

• Cardiovascular Medicine
• Pathology
• Immunology

Background:

• Coronary heart disease mortality is declining, but morbidity, including acute coronary syndrome (ACS), remains a significant concern.
• ACS results from myocardial ischemia, manifesting as myocardial infarction or unstable angina.
• Plaque morphology, including rupture, erosion, and hemorrhage, dictates ACS development.

Purpose of the Study:

• To elucidate the distinct morphologies of coronary artery plaques responsible for ACS.
• To differentiate the characteristics of plaque rupture versus plaque erosion.
• To highlight the role of inflammation and macrophage subtypes in atherosclerosis and plaque instability.

Main Methods:

• Review of autopsy data to analyze plaque morphology in relation to patient demographics (age, sex).
• Histopathological examination of ruptured and eroded plaques, noting features like necrotic core, fibrous cap, inflammation, smooth muscle cells, and proteoglycans.
• Identification and characterization of macrophage subtypes (M1, M2, M(Hb)) at atherosclerotic plaque sites.

Main Results:

• Plaque rupture is the most common cause of ACS, particularly in men, and is associated with positive remodeling, large necrotic cores, and thin fibrous caps.
• Plaque erosion is more frequent in younger women and is characterized by negative remodeling, smooth muscle cells, and minimal inflammation.
• Plaque hemorrhage, from rupture or neovascularization, can rapidly expand plaques and precipitate unstable angina. Macrophage subtypes, including M(Hb) at hemorrhage sites, play crucial roles in the inflammatory process.

Conclusions:

• Distinct plaque morphologies (rupture, erosion, hemorrhage) underlie ACS, with differing prevalence based on sex and age.
• Atherosclerosis is an inflammatory disease involving key roles for macrophages and T-lymphocytes.
• Further understanding of plaque instability mechanisms and in vivo imaging are crucial for developing novel anti-atherosclerotic therapies.