Plaque rupture is a dangerous condition in which a formation of plaque within an artery ruptures, releasing fatty particles and other non-soluble material into the bloodstream. There are several dangerous situations that may result from this event. After the rupture, the site of the rupture could seal over with an overlying clot, causing a potentially larger blockage in the artery. Also, the fatty particles may become lodged (as embolisms) further downstream in the artery. In either case, the result may be a heart attack or stroke.

Plaque deposits are created as part of the disease process known as atherosclerosis, sometimes called "hardening of the arteries." During this process, the sensitive interior walls of arteries are compromised, allowing fatty streaks to form inside the artery. Over time, as the injury to the arterial wall worsens, the fatty streaks grow into fat deposits that penetrate into the artery wall. These fat deposits are made up cholesterol, white blood cells and other cell byproducts. Over time, the deposit may be covered with a relatively thick lining. Plaque rupture occurs when the lining develops a crack or tear and in the inner contents erupt into the bloodstream. This prompts formation of blood clots.

Prevention of plaque build–up is the best strategy for avoiding the dangerous effects of a plaque rupture. These preventive strategies are described in this article.

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)

Although people will not feel anything from the plaque rupture itself, they will clearly feel the effects of a plaque rupture if it leads to a heart attack, transient ischemic attack (TIA) or stroke, or arterial embolism. The symptoms of each of these conditions are described below.

Heart attack symptoms

Up to 25 percent of people having a heart attack experience no symptoms at all (a silent heart attack). However, the majority of people experience symptoms such as the following:

TIA and stroke symptoms

Both a TIA and a stroke produce similar symptoms, which are temporary in the TIA and longer-lasting or permanent in the case of a stroke. These symptoms include:

• Weakness, numbness or tingling on one side of the body
• Confusion
• Trouble speaking (e.g., slurred speech)
• Difficulty understanding speech
• Loss of balance or coordination (i.e., vertigo)
• Severe headache

People having a TIA or stroke may also have a variety of visual problems that include:

• Partial loss of vision or complete blindness
• Double vision
• Abnormal eye movements
• Blurred vision
• A gray shading or fogging within the field of vision

Arterial embolism symptoms

An arterial embolism can cause a number of symptoms. The signs and symptoms of an arterial embolism depend on the artery that is blocked and the organs or region it had been supplying. Arterial emboli tend to become lodged at the fork of major arteries, with more than 50 percent affecting vessels in the lower extremities. Blocking an artery in an extremity usually results in symptoms such as:

• Pain, numbness, coldness and/or tingling in the affected extremity
• Lack of pulse in the extremity’s arteries, on the far side of the blockage
• Pallor or mottling of the skin over the affected area
• A heightened sensitivity of the skin (paresthesia) in that area
• Muscular spasms or paralysis of the area

Although atherosclerosis may be diagnosed by a number of tests, detecting unstable plaques that might be ready to rupture has been a more difficult challenge for medical professionals. Usually, these sites are discovered only after the plaque has ruptured. One possible solution is a new, experimental technique called thermography. Because an elevated temperature in the arteries may provide warning of an impending rupture, researchers are studying whether a plaque rupture could be identified by basically taking the temperature of an artery with a heat-sensitive catheter.

Other techniques being researched include those that scan for whether calcification is present. Harder, calcified plaque formations may be less likely to rupture. The ultrafast CT scans for calcium in the arteries as a measurement of calcification, and the experimental intravascular MRI, helps to identify plaque formations that are softer and higher in fat content. However, more research is necessary before either of these procedures is used more regularly for this purpose.

Although a physician can treat the effects of a plaque rupture (e.g., a heart attack or stroke), there is currently no way to remove the fatty particles that are released into the bloodstream. Instead, treatment often focuses on people at high risk of plaque rupture (e.g., those who have been diagnosed with atherosclerosis), to reduce the risk of a plaque rupture in the first place.

Physicians do not typically design treatment to specifically prevent a plaque rupture because it is very hard to measure the stability of plaque deposits. Instead, treatment for atherosclerosis focuses on reducing disease progression. This many include methods to reduce cholesterol, including exercise and dietary changes. In addition to eating a heart-healthy diet, the following general recommendations are offered:

Cholesterol lowering therapy is advised for patients who have other risk factors such as diabetes, hypertension, smoking and a family history of coronary artery disease. Statins have been proven to hold the progression of atherosclerosis and reduce the risk of heart attack in high risk patients. This is presumably due to an anti-inflammatory effect that results in plaque stabilization, in addition to an effect that lowers serum cholesterol.

Medications that may be prescribed for people with atherosclerosis include:

• Antiplatelets (e.g., aspirin or clopidogrel) inhibit the formation of blood clots by decreasing the ability of platelets (the body’s natural blood-clotters) to bind together. In the case of atherosclerosis, antiplatelets prevent a damaged vessel from becoming blocked due to excessive concentration of platelets. Recently, it has been observed that the beneficial effects of aspirin are diminished with the use of nonsteroidal anti-inflammatory drugs (e.g., ibuprofen). Studies have also shown that men and women react differently to aspirin therapy. It appears that aspirin is more effective in preventing heart attacks in men than women, and more effective in preventing stroke in women than men.
  
  
• Anticoagulants also help to minimize the formation of blood clots.

If lifestyle changes and medication are not helpful for people with atherosclerosis, then more invasive interventions may be necessary to prevent plaque rupture. For example, the physician may choose to do a cardiac catheterization. During this procedure, a thin tube (catheter) is inserted through a blood vessel in the body (usually the groin) and fed all the way to the heart. Once in place, the physician may choose to do a balloon angioplasty, which uses a balloon-tipped catheter to press plaque back against the artery walls, increasing the amount of room through which blood can pass through the vessel.

A variant of the balloon angioplasty is the laser angioplasty. This procedure uses a laser-tipped catheter to emit pulsing bursts of light, destroying the built-up plaque in the artery and allowing the flow of blood to resume through the newly widened blood vessel. Because of the effectiveness of balloon angioplasty, laser angioplasties are rarely performed today.

This procedure uses a laser-tipped catheter to emit pulsing bursts of light, destroying the built-up plaque in the artery and allowing the flow of blood to resume through the newly widened blood vessel.

Alternatively, the physician may choose to do an atherectomy, particularly if the plaque in the artery is particularly hardened (calcified). The procedure uses one of three catheters, all of which destroy plaque by cutting it away. Depending on the technique used, the residue is pulverized and allowed to flow harmlessly through the bloodstream, or removed as the catheter is withdrawn, or vacuumed through the catheter and out of the body during the procedure.

In conjunction with an angioplasty or atherectomy, the physician may also choose to perform stenting, in which a wire mesh metal tube called a stent is inserted into the area of a damaged artery. The stent acts as a scaffold, stretching and supporting the artery walls, and permitting blood to flow freely through the previously blocked vessel. Stents now utilized are coated with a drug that reduces the chances of restenosis (re-narrowing). These are called drug eluting stents.

In some cases of severe atherosclerosis in multiple coronary arteries, the patient may be recommended for bypass surgery. During this surgery, bypass grafts (e.g. blood vessels) are harvested from a patient’s body and sewed onto the coronary arteries, thus routing blood around the blockage. This form of open-heart surgery is highly effective in restoring blood flow to the heart muscle.

These techniques (which are considered revascularization) are reserved for patients in whom the atherosclerotic plaque has resulted in obstruction to the coronary arteries (greater than 70 percent stenosis). This is particularly the case in the presence of symptoms or functional heart abnormalities due to such obstructions.

If the atherosclerosis occurs in the carotid arteries, the patient may be recommended for a surgery called carotid endarterectomy. During this procedure, the surgeon opens the arteries in the neck that supply the brain and face with oxygen-rich blood. The plaque deposits are stripped from the inside of the vessel, then the arteries are stitched shut. This can be a highly effective surgery to prevent stroke in some patients. Another approach is carotid angioplasty/stenting, as described above.

Preparing questions in advance can help patients have more meaningful discussions with their physicians about their conditions. Patients may wish to ask their doctors the following questions related to plaque ruptures:

1. How can I tell if I have a plaque rupture?
   
   
2. Is there any way to tell whether the plaque in my blood vessels is stable or unstable? What is the difference?
   
   
3. What sorts of conditions or events does a plaque rupture put me at risk for?
   
   
4. Am I at greater risk from a plaque rupture occurring due to my weight?
   
   
5. How much danger does a plaque rupture put me in?
   
   
6. What should I do if I think a plaque rupture has occurred?
   
   
7. Are there any lifestyle changes I can make to reduce the chances that a plaque rupture will occur?
   
   
8. Do you recommend any medications or therapies to reduce my chances of having a plaque rupture?
   
   
9. Are there any activities that I should avoid?
   
   
10. Am I at increased risk of plaque rupture while I am pregnant?