For many years, it has been thought that the main cause of a heart attack was the buildup of the type of plaque that causes coronary artery disease. However, these types of blockages only cause 3 of 10 heart attacks. Researchers found that many people who have heart attacks seem to have plaque-free arteries, so they began to look at how inflammation affects the arteries. They are finding that inflammation, in fact, can lead to a heart attack.
What is Vulnerable Plaque?
Inflammation leads to the development of a soft or “vulnerable” plaque in the coronary (and all) arteries. This type of plaque does not bulge out and block blood flow through the artery; it is found inside the artery wall. Vulnerable plaque has a greater number of inflammatory cells, is prone to rupture, and leads to acute coronary events, such as heart attack or stroke. Vulnerable plaque is filled with a complex of different types of blood clotting cells, and this is what makes it particularly dangerous. Additionally, not all vulnerable plaque ruptures, so researchers are trying to determine why.
What Causes Vulnerable Plaque?
Fat droplets circulate in the blood and are absorbed by an artery. When the artery absorbs the fat, it releases inflammation-causing proteins called cytokines. The cytokines make the artery wall sticky. The sticky artery walls attract immune system cells called monocytes. The monocytes squeeze into the artery wall and absorb or “eat” the fat. This inflammatory process forms the plaque.
When this inflammation is combined with other stresses (e.g., high blood pressure), the thin covering over the plaque cracks and bleeds, spilling the contents of the vulnerable plaque into the bloodstream. The sticky cytokines on the artery wall capture the blood cells (mainly platelets) that rush to the “injury.” When these cells clump together, they can form a clot large enough to block the artery.
Who is at Risk?
The major factors that promote plaque formation — cigarette smoking, high blood pressure, a high fat diet, and diabetes — are well established. These risk factors give rise to a variety of noxious stimuli that release chemicals and activate the inflammatory process. This leads not only to the formation of plaque, but it may also contribute to its disruption and the blood clot formation.
Patients with chronic inflammation may also be at risk for vulnerable plaque formation. A 2007 Mayo Clinic study found that rheumatoid arthritis patients with cardiovascular disease had significantly more vulnerable plaques than patients who had only cardiovascular disease (48% versus 22%).
Early detection of high-risk plaque is critical, but vulnerable plaque is not detectable with current diagnostic methods. If such plaques could be detected and treated, a major advance in healthcare would be achieved.
A possibility that did not exist ten years ago is Optical Coherence Tomography (OCT), an emerging technology that can detect the cellular features or components of vulnerable plaque. Additionally, ultrasound imaging has recently been used to identify dangerous levels of vulnerable plaque. In a study published in the September 2008 issue of Radiology, the authors noted in their findings that vulnerable plaque found in the carotid artery indicated an increased risk of stroke and was linked to cardiovascular disease progressing elsewhere in the patient. While more studies are needed, it was hypothesized that serial ultrasound examinations may be a noninvasive way to identify whether vulnerable plaques exist and improve the effectiveness of various therapies.
Patients with vulnerable plaque may not feel symptoms. Cardiologists have found that measuring the level of a substance called C-reactive protein (CRP) in the bloodstream can help predict the risk of heart attack or stroke. The CRP level corresponds to the level of inflammation activity in the body. Two large studies showed that the higher the CRP levels in the blood, the greater the risk of a heart attack. Many doctors are adding this test to their patients’ cholesterol screening, especially for patients with an intermediate or high cardiovascular risk score.
Patients can lower their CRP levels in the same ways that they can cut their heart attack risk: take aspirin, eat a proper diet, quit smoking, and begin an exercise program. Researchers also think that obesity and diabetes may be tied to high levels of CRP.
Medicines like ACE inhibitors and aspirin appear to reduce inflammation, which may prevent heart attacks in patients with high CRP levels. Cholesterol-lowering medicines have also been found to lower CRP levels, and researchers are investigating their use to prevent heart attacks in people with normal cholesterol levels.
Recent studies have shown that smoking is very dangerous for people with vulnerable plaque. The nicotine in cigarettes directly affects the inflammatory response, causing the release of more cytokines. Researchers are also studying how family history and genetic factors contribute to the inflammation process. Most doctors agree that heart-healthy habits still play the most important role in reducing the risk of heart attack.
In the News
The death of NBC political analyst Tim Russert surprised many because Russert had taken steps to control his cardiovascular risk factors. He took blood pressure medication, cholesterol medication, and aspirin. He had yearly stress tests and checkups and exercised regularly in an attempt to control his weight. But while much can be done to reduce cardiovascular risk, coronary events cannot be predicted with 100 percent accuracy. Russert died after a plaque in one of his coronary arteries ruptured and blocked blood flow to his heart. The event led to an abnormal heart rhythm that caused cardiac arrest. According to a 2008 feature in the New York Times, the challenge for cardiologists is determining which patients have “vulnerable plaques,” which are more prone to rupture. “It’s the real dilemma we have in cardiology today,” former AHA President Dr. Sidney Smith told the New York Times. “Is it possible to identify the group at higher short-term risk?” Some advocate for more testing, while many researchers are focusing on identifying biomarkers, substances in the blood that could indicate a higher probability of plaque rupture. “You want to be sure your blood pressure and lipids are controlled, that you’re not smoking, and that you have the right waist circumference, but there are other things we need to understand. There’s tremendous promise, but we still have a long way to go,” added Smith.
Texas Heart Institute www.texasheartinstitute.com/HIC/Topics/Cond/vulplaq.cfm
Center for the Integration of Medicine and Innovative Technology www.cimit.org/vplaque.html
American Heart Association www.americanheart.org/presenter.jhtml?identifier=3057860