How does inflammation play a role in the pathogenesis of acute coronary syndrome?

Inflammation is a critical component in the pathogenesis of acute coronary syndrome and is primarily linked to the destabilization of atherosclerotic plaques. When inflammation occurs within the arterial wall, immune cells such as macrophages and T-lymphocytes are recruited to the site. These cells contribute to processes that weaken the fibrous cap that covers the plaque. As inflammation increases, enzymes that degrade the extracellular matrix can further compromise the stability of the plaque.

Once the fibrous cap becomes thin and brittle due to this inflammatory process, it is more susceptible to rupture. When a plaque ruptures, it exposes its inner contents to the bloodstream, creating a surface that promotes the formation of a blood clot (thrombosis). This clot can then occlude the coronary artery, resulting in the cessation of blood flow to the heart muscle, which manifests as acute coronary syndrome.

Therefore, the role of inflammation in promoting plaque instability and rupture is central to understanding how acute coronary syndrome develops. This process underscores the significance of managing inflammation not only in the context of coronary artery disease but also as a potential therapeutic target to prevent acute coronary events.