All of the following discussion is taken from an excellent review paper: The Role of Inflammation in Cardiovascular Disease. It is not easy reading, so I’m going translate it into language that’s simpler for non-physicians to understand.

The cells that line the arteries in the body, including the arteries in the heart are called the vascular endothelium. In normal people, the endothelium has anti-inflammatory and antithrombotic (anti-clot forming) properties. It controls which molecules can cross it and which cannot. The endothelium also controls the smooth muscle contraction and relaxation which dilates or constricts the arteries. This takes place through the balance between the release of substances which dilate the arteries, such as nitric oxide (NO), and substances that constrict the arteries such as endothelin.

Effects of chronic inflammation on endothelium

Chronic inflammation from any cause reduces nitric oxide and endothelin, resulting in damage to the junctions between the endothelial cells. This allows larger molecules, like cholesterol to cross into the endothelial cells. When chronic inflammation is present, LDL (bad cholesterol) metabolism is shifted from large- and medium-size LDL particles towards small and dense LDL particles. These particles cause more atherosclerosis than larger ones because they are not cleared as well by the liver LDL receptors. They thus tend to persist in the circulation. These small dense LDL particles accumulate underneath the endothelium. These particles induce a local inflammatory response. White blood cells called macrophages engulf the LDL particles and release inflammatory cytokines. Many of these macrophages die forming a necrotic core. This stimulates the the formation of a fibrous collagen cap in the wall of the arteries over the LDL particles and dead macrophages.

From systemic inflammation to focal atherosclerosis

Even though inflammation is systemic, atheromatous plaques are focal. They tend to occur where arteries branch or on side branches because these areas are exposed to disturbed blood flow.

Stable vs unstable plaques

The plaques with the fibrous collagen caps when initially formed are stable. If chronic inflammation stops, then they remain stable and do not cause narrowing of the coronary arteries. If chronic inflammation persists then more macrophages continue to release inflammatory cytokines. These inflammatory molecules start to thin some of the fibrous caps making them unstable and prone to rupture.

What happens when a plaque ruptures?

When a plaque ruptures it exposes the interior of the plaque to the bloodstream. This activates the blood clotting system and a clot forms that can obstruct the artery. If it completely obstructs the artery it causes a classic heart attack, also called a STEMI (ST elevation myocardial infarction). The ST refers to a part of an electrocardiogram called the ST segment. In a classic heart attack there is elevation of the ST segments on the electrocardiogram. The elevation makes the electrocardiogram look like firemen’s hats. Here is an example of an electrocardiogram with marked elevation of the ST segments.

If the clot does not completely obstruct the artery the ST segments do not show elevation, but some damage to the heart muscle still happens. The symptoms of this kind of heart attack are similar to a classic heart attack with chest pain radiating to the arm or neck. This kind of heart attack is called an NSTEMI (Non-ST Elevation MI. It is usually detected by measuring enzymes that are released by the injured heart muscle.

Plaques that partially obstruct arteries

Even plaques that are stable and not in danger of rupture can get large enough to partially obstruct arteries in the heart. When these plaques obstruct more than 50% of the diameter of the artery they can cause symptoms. When a person exercises the heart muscle needs more blood and the obstruction limits the blood flow. In this case a person may get chest pain with exercise (angina) that goes away when they sit down and rest.

Strokes

Chronic inflammation causes exactly the same kind of changes in the carotid arteries and other arteries in the brain. Rupture of a plaque in these vessels can cause a stroke. Sometimes platelets adhere to a ruptured plaque in an artery that causes a transient obstruction of the artery that is then washed away by the blood stream. That results in temporary stroke symptoms that resolve in 5-10 minutes. This is called a TIA (Transient Ischemic Attack). A TIA can be a warning signal of risk of a bigger stroke. People who have TIA’s should be immediately evaluated for risk of a bigger stroke.

Treatment of vascular inflammation

Statins are a class of medicine that we used to think work primarily by lowering LDL cholesterol. It was later found that statins have a powerful anti-inflammatory effect. This may well be the major reason that statins reduce the risk of heart attack and stroke.

Bottom Line

Chronic inflammation results in changes in the endothelium of arteries in the heart and brain. These changes allow LDL cholesterol to accumulate in the endothelium causing fibrous plaques. Continued inflammation causes these plaques to become unstable and prone to rupture. Ruptured plaques cause blood clots to form which can lead to heart attacks and strokes. Statins have a powerful anti-inflammatory effect which may be the main reason they reduce the risk of heart attacks and strokes.