Arterial plaque, fatty deposits known as atheromatous plaque, accumulates in artery walls. This buildup can begin early in life, with many individuals developing some form of atherosclerosis by their twenties. While many plaques remain stable and do not cause immediate problems, a particular type, termed “vulnerable plaque,” poses a sudden health risk. These plaques differ from stable ones due to features that make them prone to serious complications.
Characteristics of Vulnerable Plaque
Vulnerable plaques have distinct features that contribute to their instability. A defining characteristic is a thin fibrous cap, typically less than 65 micrometers thick, which covers the plaque’s core. This thin cap is a major determinant of vulnerability, unlike stable plaques which have a thick, robust fibrous cap.
Beneath this thin cap lies a large, lipid-rich necrotic core, a collection of dead cells, lipids, and cholesterol. This core forms primarily from the accumulation of fat droplets absorbed by the artery, leading to inflammation and the transformation of immune cells into fat-filled macrophages. The size of this necrotic core is another factor in plaque instability, as it contains highly thrombogenic material.
Inflammatory cells, predominantly macrophages, within the plaque and its cap further distinguish vulnerable plaques. These cells contribute to inflammation, which can weaken the fibrous cap by degrading collagen and reducing its synthesis. This inflammatory activity, combined with other stresses like high blood pressure, can cause the thin cap to crack. Other features associated with increased risk include outward vessel remodeling, microcalcifications, and intraplaque hemorrhage.
How Vulnerable Plaque Causes Cardiovascular Events
Vulnerable plaque leads to serious cardiovascular events primarily through a process known as plaque rupture. Unlike stable plaques that may gradually narrow an artery, vulnerable plaques can break open even if they do not severely obstruct blood flow. This rupture exposes the highly thrombogenic material within the plaque’s lipid-rich necrotic core to the bloodstream.
Once the plaque ruptures, the exposed contents trigger a rapid clotting response. Platelets, blood cells involved in clotting, rush to the site and clump, forming a blood clot or thrombus. This clot can quickly grow large enough to partially or completely block the artery, interrupting blood flow.
The location of this blockage determines the type of cardiovascular event. If rupture and clot formation occur in the coronary arteries, which supply blood to the heart, it can lead to a heart attack (myocardial infarction). When the blockage occurs in arteries leading to the brain, it can cause an ischemic stroke. While plaque rupture is the most common cause, other mechanisms like plaque erosion or calcified nodules can also lead to clot formation, though their precursors are less understood.
Detecting and Preventing Vulnerable Plaque
Detecting vulnerable plaque directly is challenging, as these plaques often do not significantly narrow arteries and may not be visible through conventional angiography. However, advanced imaging techniques offer ways to identify features suggestive of vulnerability. Invasive methods like Intravascular Ultrasound (IVUS) and Optical Coherence Tomography (OCT) are considered gold standards, providing detailed information on plaque morphology and composition. IVUS can help identify calcified and soft plaques, while OCT can quantitatively measure the fibrous cap thickness, often less than 65 micrometers in vulnerable plaques. Near-infrared spectroscopy (NIRS) can be used alongside IVUS to measure the lipid content within the plaque.
Non-invasive imaging techniques are also evolving for detection. Computed Tomography Coronary Angiography (CTCA) can identify features such as low-attenuation plaque, which indicates a lipid-rich necrotic core, and positive remodeling. Cardiovascular Magnetic Resonance (CMR) imaging and nuclear imaging techniques are additional non-invasive options being explored. These methods aim to identify high-risk plaque characteristics and assess vascular inflammation, which is a major driver of plaque progression.
Preventing the formation and progression of vulnerable plaque is a primary focus for reducing cardiovascular events. Managing established risk factors such as high cholesterol, high blood pressure, and diabetes is a foundational strategy. Adopting healthy lifestyle changes, including a balanced diet and regular exercise, plays a role in prevention. Pharmacological interventions are also widely used; statins, for instance, are lipid-lowering medications that help stabilize plaques, while anti-inflammatory medications can reduce the inflammatory processes within the arteries.