Coronary artery disease (CAD) develops gradually through several distinct stages, each representing a progression in the narrowing and damage of the coronary arteries that supply blood to the heart muscle. Understanding these stages helps explain how the disease evolves from a silent condition to one that causes symptoms and serious complications.
The very first stage begins with **damage to the inner lining of the coronary arteries**, called the endothelium. This damage is usually caused by risk factors such as high levels of low-density lipoprotein (LDL) cholesterol, high blood pressure, smoking, diabetes, obesity, sedentary lifestyle, and chronic stress. These factors create tiny injuries or inflammation in the artery walls, making the smooth inner surface rough and vulnerable.
Once the endothelium is damaged, **LDL cholesterol particles penetrate the artery wall** and accumulate beneath the surface. The body’s immune system responds by sending white blood cells called macrophages to engulf the cholesterol. However, these macrophages become overloaded and transform into foam cells filled with fat. The accumulation of foam cells forms the earliest visible lesion called a **fatty streak**. This stage is silent and can begin as early as childhood or adolescence without causing symptoms.
As the fatty streaks grow, the body attempts to contain the damage by forming a protective layer over the fatty deposits. This layer consists of smooth muscle cells and collagen fibers, creating a structure known as an **atherosclerotic plaque**. The plaque has a soft, fatty core covered by a tougher fibrous cap. Over time, the plaque enlarges and starts to narrow the artery’s lumen, reducing blood flow. This narrowing is called **stenosis**.
During this stage, the artery wall may also undergo **calcification**, where calcium deposits build up around the plaque. This calcification stiffens the artery, reducing its elasticity and making it less able to expand and contract with each heartbeat. Although the artery may still allow some blood flow, the reduced flexibility and narrowing can impair oxygen delivery to the heart muscle, especially during increased demand such as exercise or stress.
If the plaque remains stable, symptoms may be minimal or absent. However, plaques can become unstable if the fibrous cap thins or ruptures. When this happens, the fatty core is exposed to the bloodstream, triggering the formation of a blood clot (thrombus). This clot can partially or completely block the artery, leading to **acute coronary events** such as unstable angina or a heart attack (myocardial infarction).
In some cases, the artery may develop **aneurysms** or abnormal dilations due to weakening of the vessel wall from inflammation and damage. This is less common but can complicate the disease.
The progression of coronary artery disease can be summarized in these stages:
1. **Endothelial injury and dysfunction** – Damage to the artery lining caused by risk factors.
2. **Fatty streak formation** – Accumulation of foam cells and early lipid deposits.
3. **Plaque development** – Formation of fibrous plaques with fatty cores covered by fibrous caps.
4. **Plaque progression and calcification** – Enlargement and hardening of plaques, narrowing arteries.
5. **Plaque instability and rupture** – Fibrous cap breaks, exposing plaque contents and causing clot formation.
6. **Acute coronary events** – Partial or complete artery blockage leading to angina or heart attack.
7. **Chronic complications** – Persistent narrowing causing chronic chest pain, heart muscle damage, or heart failure.
Throughout these stages, the disease often remains silent until the narrowing significantly limits blood flow or a plaque rupture triggers a sudden blockage. Early stages are typically asymptomatic, which is why coronary artery disease is sometimes called a “silent” disease. Symptoms such as chest pain, shortness of breath, fatigue, or dizziness usually appear only when the heart muscle is not receiving enough oxygen.
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