Plaque rupture is intimately connected to the formation of plaque deposits on the inside walls of arteries. Plaque deposits on artery walls are a central feature in atherosclerosis, or the hardening and narrowing of arteries. 

Although researchers are still working to find the causes of atherosclerosis, the process of plaque buildup is closely connected to LDL “bad” cholesterol, which penetrates the lining of the artery, or endothelium. Once inside the arterial wall, the LDL cholesterol stimulates an immune response that sends white blood cells to the site of the injury. These white blood cells, along with the LDL, release toxins in the arterial wall that increase the damage. Over time, the white blood cells, cholesterol and cell byproducts combine to form a lipid foam that extends from the interior of the artery wall to coat the inside wall of the artery itself. At this point, the person may not be experiencing symptoms related to their disease, but the atherosclerotic process has already begun in earnest.

Exposed to the bloodstream, the growing plaque deposit continues to attract cholesterol, white blood cells and other fats found circulating in the blood. As the plaque continues to build up, some of the plaque formations develop a relatively thick covering, due to either fibrosis (scarring) or calcification. These types of plaque are considered to be stable plaques. Other types of plaque are known as unstable plaques, which (in comparison to stable plaques) have the following:

If the coating of an unstable plaque is stripped off, this is known as a plaque rupture. The exact trigger of a plaque rupture is unknown. However, it can occur as a result of a strong, fast blood flow, especially during heavy exertion or emotional stress, when the coating is thin and the core of fat/white blood cells is particularly full. 

If the coating of the unstable plaque is torn off, the fatty core will be exposed. Small fatty particles are then released, traveling through the bloodstream until they become lodged in an artery (embolism). Furthermore, the site of the plaque rupture may rapidly seal over as blood platelets congregate at the site of the injury and initiate the blood clotting process, creating an even larger blockage (thrombosis) in that part of the artery. Depending on where the embolism or the thrombosis is located, this situation may lead to one of the following:

• If the embolism or the thrombosis is lodged in a coronary artery and blocks the blood flow to the heart, it could trigger a heart attack.
  
  
• If the embolism or the thrombosis is lodged in a cerebral artery, or one of the smaller arteries within the brain, and blocks the blood flow to the brain, it could trigger a transient ischemic attack (TIA) or a stroke.
  
  
• If the embolism becomes lodged in a non-major artery, it could cause an arterial embolism, resulting in pain, tissue damage and/or other symptoms in the area that is deprived of blood.

According to the American Heart Association, atherosclerosis patients with an inactive lifestyle and high cholesterol levels have a higher risk of plaque rupture if they suddenly begin strenuous activity. Not only does strenuous activity include overexerting oneself during exercise, but it also includes:

• Having sex
• Certain household chores (e.g., vacuuming)
• Mowing the lawn
• Working outside (e.g., mowing the lawn, shoveling snow)