Atherosclerotic plaque consists of fat, cholesterol, calcium, and other blood substances. This plaque can accumulate on the inner walls of arteries, a process called atherosclerosis, which causes them to harden and narrow. This restriction in blood flow is the underlying cause of many cardiovascular diseases and increases the risk of serious health complications.
The Formation of Atherosclerotic Plaque
The development of atherosclerotic plaque begins with damage to the endothelium, the thin layer of cells lining the inside of an artery. This injury makes the artery wall more permeable, allowing substances like low-density lipoprotein (LDL) cholesterol to accumulate within the vessel wall. Once LDL particles cross the damaged endothelium, they become trapped in the artery’s inner layer, the intima.
Once in the intima, LDL particles undergo oxidation, which triggers an inflammatory response. The body dispatches white blood cells, specifically monocytes, to the site. These monocytes migrate into the artery wall and transform into larger cells called macrophages, which then engulf the oxidized LDL particles in an attempt to remove them.
As macrophages consume large amounts of oxidized LDL, they become engorged and transform into “foam cells” because of their bubbly appearance. The accumulation of these foam cells is the first visible sign of plaque, forming a “fatty streak” along the artery wall. This collection of foam cells continues to grow, creating a lipid-rich core within the developing plaque.
To contain this growing lesion, the body attempts to wall it off by forming a protective cover. Smooth muscle cells from the artery’s middle layer migrate to the surface of the plaque. These cells proliferate and deposit proteins, including collagen, to create a fibrous cap over the plaque’s core. The resulting mature plaque consists of a lipid core, dead cells, calcium deposits, and the overlying fibrous cap.
Factors Contributing to Plaque Development
Several risk factors can initiate or accelerate plaque formation and are categorized as modifiable or non-modifiable. Modifiable risk factors are those that can be managed through lifestyle or medical treatment. High blood pressure (hypertension) is a contributor, as the increased force of blood flow exerts mechanical stress on the artery walls, leading to injury.
Other modifiable factors also promote plaque development:
- Tobacco use, as its chemicals can directly harm the endothelium, increase LDL oxidation, and promote inflammation.
- High levels of LDL cholesterol in the blood, which provide the raw material for plaque buildup.
- Diabetes mellitus, which accelerates the process through elevated blood sugar that can damage blood vessels.
- Obesity and a sedentary lifestyle, which are linked to atherosclerosis by contributing to other risk factors like hypertension and high cholesterol.
Non-modifiable risk factors are beyond an individual’s control. Age is a primary factor, as the cumulative effects of minor endothelial injuries build up over a lifetime. Genetics also plays a role, with a family history of premature cardiovascular disease indicating a greater inherited predisposition. An individual’s sex can influence risk, as biological males generally develop atherosclerosis earlier than pre-menopausal females.
Plaque Progression and Complications
Once formed, atherosclerotic plaques can be either stable or unstable. Stable plaques have a thick, intact fibrous cap that securely covers the lipid core. These plaques tend to grow slowly and, while they can narrow an artery and restrict blood flow, they are less prone to breaking open. The symptoms associated with stable plaques, such as angina during exertion, are often predictable because they relate to the artery’s fixed narrowing.
Unstable plaques pose a more immediate threat, characterized by a thin fibrous cap, a large lipid core, and a high degree of inflammation. The thin cap is structurally weak and can be easily ruptured by the stresses of blood flow. Unstable plaques do not need to be large to be dangerous, as many acute events are caused by the rupture of plaques that were not significantly obstructing blood flow.
The most serious complications occur when an unstable plaque ruptures. The exposure of the plaque’s core to the bloodstream triggers a rapid clotting response. The body perceives the rupture as an injury and forms a blood clot, or thrombus, at the site. This clot can grow large enough to completely block the artery, cutting off blood supply to downstream tissues.
This sudden blockage of blood flow is the cause of major cardiovascular events. If the thrombosis occurs in a coronary artery, it results in a myocardial infarction (heart attack). Should this event happen in an artery supplying the brain, it causes an ischemic stroke. In the peripheral arteries, such as those in the legs, it can lead to acute limb ischemia.
Diagnosis and Medical Intervention
Diagnosing atherosclerosis involves identifying risk factors and visualizing the plaques. A physician will start with a physical exam and a review of personal and family medical history. Blood tests are used to measure levels of cholesterol, triglycerides, and glucose, which help assess an individual’s risk profile for conditions that contribute to plaque formation.
To directly visualize plaque buildup, healthcare providers use various imaging techniques. A CT coronary calcium scan measures the amount of calcified plaque in the heart’s arteries. A carotid ultrasound uses sound waves to create images of the carotid arteries in the neck, detecting narrowing. An angiogram may be performed for a more detailed view, where contrast dye highlights blockages on an X-ray.
Management of atherosclerosis focuses on slowing plaque progression and preventing complications. Lifestyle modifications are a foundational component of treatment, including adopting a heart-healthy diet, regular physical activity, and smoking cessation. These changes help manage risk factors like high blood pressure and cholesterol.
Medical treatments are often used with lifestyle changes. Medications such as statins are prescribed to lower LDL cholesterol levels, while antiplatelet drugs like aspirin help prevent blood clots. For individuals with hypertension, medications to control blood pressure are also a standard part of treatment.
In cases where plaque has caused significant narrowing or an acute blockage, more invasive procedures may be necessary. Angioplasty involves inserting a catheter with a balloon to the blockage site, where it is inflated to compress the plaque and widen the artery; a stent is often left to keep the artery open. Atherectomy is a procedure that uses a catheter with a specialized tool to physically remove plaque. For extensive blockages, coronary artery bypass surgery creates a new route for blood by grafting a healthy blood vessel around the blocked segment.