Atherosclerosis and Heart Attacks
Atherosclerosis is a disease caused by the build up of plaque along the walls of the arteries. Plaque is a sticky substance composed of fat, cholesterol, calcium and other substances in the blood. As it builds up along the arterial walls, the passageway through the vessels narrows. In some cases, the plaque can build enough to significantly impede the flow of blood, like a clog in a drainpipe. When that happens in a coronary artery, part of the heart muscle doesn’t get enough oxygen, leading to angina (chest pain). If the area is completely deprived of oxygenated blood, that part of the heart muscle dies (a heart attack).

In the past, doctors believed that most heart attacks occurred when the arteries become blocked by plaque. However, scientists have learned that a significant number of heart attacks are caused when the cap, or crust on top of the plaque, is weak. This type of plaque is known as vulnerable, or soft, plaque. If the cap ruptures or cracks, the cholesterol, fats and other chemicals inside the plaque deposit are released into the bloodstream. The body senses an “injury” and sends platelets to seal the site. The platelets adhere to the sticky plaque cells, causing clumps of cells and the formation of a clot. That clot can become large enough to block the artery, leading to a heart attack.

The American Heart Association estimates 16.8 million Americans have coronary artery disease. It’s the leading cause of disease-related death in the U.S. This year, 1.25 million men and women in this country will have a heart attack.

Vulnerable Plaque and Heart Attack Risk
Vulnerable plaque often lies hidden on the walls of the artery. Often, the deposits don’t bulge out, so they may not be detected with standard imaging or diagnostic tests. And since they are so small, patients often don’t have any symptoms until the plaque ruptures, causing a sudden, unexpected heart attack.

Vulnerable plaque appears to be associated with inflammation. Researchers at Beth Israel Deaconess Medical Center in Boston have been studying the combined use of PET/CT scans to screen patients for these areas of “hot” plaque. Prior to a scan, the patient is given an injection of glucose with a radioactive tracer (called 18F-FDG). The glucose is taken up by active cells (like areas of inflammation), carrying the tracer with it. The CT part of the imaging shows the anatomy of the heart. The PET portion detects the location and concentration of the radioactive tracer. But the scientists found the active heart muscle cells took in so much of the radioactive glucose plaque “hot spots” could not be seen.

To overcome the imaging obstacle, the researchers give patients a high-fat drink three hours before the scan. The radioactive glucose injection is given two hours later (one hour before the scan). Nuclear Medicine Specialist, Gerald Kolodny, M.D., explains the heart muscle takes up the fat for its energy needs rather than the glucose. This enables the inflammatory cells in vulnerable plaque to take up more of the radioactive glucose, creating a better picture of those “hot spots.”

In a study published in the April 2009 issue of The Journal of Nuclear Medicine, the researchers report the technique can effectively detect vulnerable plaque in coronary arteries. Further research needs to be done to confirm the efficacy of the technique and determine who may benefit most from the testing. Kolodny says if 18F-FDG PET/CT proves to correctly identify areas of vulnerable plaque, the technique may be useful for screening high-risk patients and monitoring the effects of therapy.

AUDIENCE INQUIRY
For general information on heart attacks:
American Heart Association, http://www.americanheart.org
National Heart, Lung and Blood Institute, http://www.nhlbi.nih.gov

BIBLIOGRAPHY
Ben-Haim, Simona, M.D., D.Sc., et al., “Evaluation of 18F-FDG Uptake and Arterial Wall Calcifications Using 18F-FDG PET/CT,” The Journal of Nuclear Medicine, November 2004, Vol. 45, No. 11, pp. 1816-1821.

Lee, Su Jin, et al., “Reversal of Vascular 18F-FDG Uptake with Plasma High-Density Lipoprotein Elevation by Atherogenic Risk Reduction,” The Journal of Nuclear Medicine, August 2008, Vol. 49, No. 8, pp. 1277-1282.

Rudd, James, et al., “Atherosclerosis Inflammation Imaging with 18F-FDG PET,” The Journal of Nuclear Medicine, June 2008, Vol. 49, No. 6, pp. 871-878.

Williams, Gethin, and Gerald Kolodny, “Suppression of Myocardial 18F-FDG Uptake by Preparing Patients with a High-Fat, Low-Carbohydrate Diet,” AJR: American Journal of Roentgenology, February 2008, Vol. 190, No. 2, pp. W151-W156.

Wykrzykowska, Joanna, et al., “Imaging of Inflamed and Vulnerable Plaque in Coronary Arteries with 18F-FDG PET/CT in Patients with Suppression of Myocardial Uptake Using a Low-Carbohydrate, High-Fat Preparation,” The Journal of Nuclear Medicine, April 2009, Vol. 50, No. 4, pp. 563-568.