Atherosclerosis is a condition characterized by the hardening and narrowing of arteries, driven by the gradual accumulation of plaque on the inner walls of these blood vessels. This slow, progressive disease can begin developing as early as childhood, often without noticeable symptoms for years. Over time, this buildup can interfere with blood flow, leading to various health problems.
The Process of Plaque Buildup
The development of plaque begins with damage to the endothelium, the thin layer of cells lining the arteries. This injury makes the artery wall more permeable, allowing particles like low-density lipoproteins (LDL), known as “bad” cholesterol, to pass through. Once LDL particles cross the damaged endothelium, they can become trapped and modified within the artery wall’s inner layer.
This LDL accumulation triggers an inflammatory response from the immune system. White blood cells called monocytes are recruited to the site and enter the artery wall. These monocytes transform into larger cells known as macrophages, which consume the trapped LDL particles. This process forms “foam cells,” which are macrophages filled with fatty substances.
As more foam cells gather, they form a fatty streak, the earliest visible sign of atherosclerosis. Over time, these fatty streaks grow into more complex plaques. Smooth muscle cells from the artery’s middle layer migrate into the inner layer, where they multiply and produce a connective tissue matrix. This activity, with the accumulation of foam cells, debris, and calcium, builds a mature plaque.
The plaque develops a hard, fibrous cap of smooth muscle cells and collagen, which covers a soft, lipid-rich core. This structure protrudes into the artery’s channel, or lumen, progressively narrowing the space for blood flow. The artery may attempt to remodel itself by expanding, but this is often insufficient to prevent narrowing.
Factors That Accelerate Atherosclerosis
Several factors can initiate endothelial damage or accelerate plaque formation. Modifiable factors are related to lifestyle and health conditions that can be managed. Non-modifiable factors, such as age and genetic predisposition, cannot be changed.
High levels of LDL cholesterol contribute to plaque growth by increasing the lipid that can enter the artery wall. High blood pressure, or hypertension, exerts mechanical stress on the endothelium, creating injury sites prone to plaque development. Chemicals in tobacco smoke injure endothelial cells, reduce protective nitric oxide, and promote inflammation, which hastens the process.
Diabetes mellitus also contributes to the disease, as elevated blood sugar levels can harm the endothelium by increasing inflammation and oxidative stress. Obesity promotes a state of chronic, low-grade inflammation that supports plaque formation. Non-modifiable factors include advancing age and a family history, which can indicate a genetic susceptibility.
Associated Health Complications
Advanced atherosclerosis leads to health problems through two primary mechanisms: extreme narrowing of an artery or the sudden rupture of a plaque. When a plaque grows large enough, it restricts blood flow, depriving tissues and organs of oxygen. This reduction in blood flow can cause symptoms during physical exertion when oxygen demand is highest.
A more immediate danger comes from plaque rupture. Some plaques with a thin fibrous cap over a large lipid core are unstable. If this cap breaks, the material inside is exposed to the bloodstream, triggering the rapid formation of a blood clot, or thrombus. This clot can expand and completely block the artery, leading to a sudden medical event.
These events manifest as specific diseases depending on the location of the affected artery:
- In the arteries supplying the heart, it causes coronary artery disease, which can lead to chest pain (angina) or a heart attack.
- In the arteries leading to the brain, it is known as carotid artery disease and can cause a stroke or transient ischemic attack (TIA).
- In the arteries of the limbs, it results in peripheral artery disease, causing pain and potentially tissue death.
- In the arteries leading to the kidneys, it can contribute to chronic kidney disease.
Diagnosis and Medical Management
Diagnosis begins with a physical exam and a review of a patient’s medical and family history to assess risk factors. A doctor might listen for a “bruit,” a whooshing sound indicating turbulent blood flow through a narrowed artery. Blood tests are used to measure cholesterol and blood sugar levels, which are indicators of risk.
To visualize the arteries and assess plaque buildup, healthcare professionals use various imaging techniques. An ultrasound can create images of the arteries and measure blood flow. A computed tomography (CT) angiogram provides detailed pictures of the blood vessels, and an electrocardiogram (ECG) can detect heart problems related to reduced blood flow.
Management of atherosclerosis focuses on slowing its progression and preventing complications. Lifestyle modifications are foundational, including a diet low in saturated fats, regular physical exercise, and quitting smoking. Medications are used to control risk factors such as high cholesterol and blood pressure, and antiplatelet agents like low-dose aspirin may be recommended to prevent blood clots.
For severe blockages, more invasive procedures may be necessary. Angioplasty involves inserting a balloon-tipped catheter into the narrowed artery, which is inflated to widen the vessel. A small mesh tube called a stent is often placed during angioplasty to help keep the artery open. In cases of extensive blockages, coronary artery bypass surgery can reroute blood flow around diseased artery sections.