What Is Vulnerable Plaque?

Plaque Prone to Rupture

According to current thinking, the most common type of vulnerable plaque is characterized by a thin fibrous cap and large necrotic core. In other words, this is a soft plaque that is "vulnerable" to sudden rupture. In addition, this type of vulnerable plaque is hidden within the arterial wall, not visibly blocking the artery.

The rupture of this type of vulnerable plaque causes the release of the plaque's contents, ­ a liquid pool of fat, cholesterol, and other debris into the blood stream, where they cause a blood clot to form that can block blood flow to the heart and cause a heart attack. In fact, recent data published in Forbes magazine has shown that vulnerable plaque rupture causes as many as 85% of all heart attacks.

Besides the plaque prone to rupture described above, two other types of plaques are suspected to be vulnerable plaques: plaque prone to erosion, and plaque with a calcified nodule.

What Causes Vulnerable Plaque?

The Role of Chronic Inflammation

Cardiologists have come to recognize the pivotal role that the immune system plays in the process of plaque formation (atherosclerosis) and in the prevalence of Coronary Heart Disease and heart attacks. It is now becoming clear that chronic, inflammatory processes driven by the immune system cause atherosclerosis and the resulting transformation of cholesterol and debris into hard and soft plaque.

It is important to note that these immune system processes are believed to contribute significantly to vulnerable plaque rupture, as well as the coagulation cascade that rapidly creates a blood clot and causes a heart attack. Researchers are finding that the activity of various immune system cells and agents lead to the formation of plaque in the arterial wall (see diagram) and the deterioration of the thin fibrous caps that cover vulnerable plaques.

It is ironic that the body's own protection mechanism, the immune system, triggers plaque rupture and subsequent heart attack.

As cholesterols are absorbed by the artery, proteins called "cytokines" are released. The cytokines cause inflammation and make the arterial wall sticky, resulting in the attraction of immune-system cells to the area. The immune-system cells are called "monocytes."

When the monocytes enter the arterial wall, they differentiate into "macrophage" cells and begin to absorb fat droplets. Over time, these fat-filled cells form a plaque – what researchers now call "vulnerable plaque."