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Commentary |
1 Department of Radiology, University of Washington School of Medicine and Harborview Medical Center, 325 Ninth Ave., Seattle, WA 98104-2489.
Received September 19, 2005; accepted after revision September 19, 2005.
Address correspondence to T. J. Dubinsky.
More than 600,000 patients in the United States will die each year from acute coronary events, with nearly half presenting with sudden death as the first indication of their underlying coronary artery disease. Therefore, prevention has become the cornerstone of dealing with coronary artery disease. Every physician emphasizes the importance of either not smoking or ceasing to smoke, losing weight through diet and exercise, controlling hypertension, and decreasing serum cholesterol levels as the keys to preventing cardiac disease. The literature has shown that the risk of sudden death from coronary artery atherosclerotic disease is diminished if these factors are controlled.
However, once a patient either survives an acute event or develops more chronic symptoms, then diagnostic methods are used to determine his or her future risk of death from disease progression. These assessments include serology, ECG, radionuclide studies with and without stress testing, electron beam tomography, intravascular sonography, and angiography. Recently, MRI and MDCT coronary angiography have become available as part of the diagnostic armamentarium for evaluating cardiac disease. All of these studies not only determine current levels of cardiac function at rest, under stress, and with exercise, they also determine the need for acute therapeutic intervention, including bypass surgery, stent-graft placement, angioplasty, and thrombolysis for coronary artery stenoses and occlusions.
For decades, one of the most commonly seen findings in patients with coronary artery disease has been calcification within atherosclerotic plaques. Before the development of MDCT, the temporal resolution of CT was not high enough to freeze motion sufficiently to accurately measure the amount of calcification in the coronary arteries, so electron beam tomography, with temporal resolution in the range of 100 msec, became the primary tomographic method for making these measurements. Studies subsequently determined that the presence of calcifications in the coronary arteries increased the risk of future acute myocardial infarctions perhaps as much, if not more than, any other risk factor. Not only did the presence of calcifications increase the risk, but the more heavily calcified the arteries were, the greater the risk for future events. Therefore, scoring methods were developed to measure the amount of calcification present, with the Agatston and volumetric scores being the two methods used currently.
In the Agatston method, a score is produced by measuring an area of plaque and then multiplying that area by a coefficient based on the highest attenuation within the area. In volumetric scoring, an isotropic data set is used to calculate a volume of calcified plaque within an artery [3]. With both methods, a score is rendered, and the patient is given an age-related risk. Risks increase exponentially with increasing calcium in the coronary arteries, with no calcification being normal, small amounts increasing the risk mildly, and then just a little bit more increasing the risk significantly.
The development of MDCT, with temporal resolution in the range of 200 msec or less, has given CT the ability to measure coronary artery calcifications. Although these measurements are dependent of technical factors such as collimation, peak kilovoltage, focal spot size, reconstruction algorithm, and heart rate, several articles, including the one in this issue by Daniell et al. [1], indicate that MDCT can be substituted for EBT. Serially monitoring patients for worsening plaque formation is also valuable, as indicated by Sevrukov et al. [2]. Because the signal-to-noise ratio is higher for any given radiation dose with MDCT than with electron beam tomography, MDCT is more useful for imaging structures other than coronary artery calcifications, including the coronary arteries themselves, using contrast material, and structures outside the heart, such as the aorta and the pulmonary arteries.
The use of CT to produce images of the coronary arteries, and substantial data from intravascular sonography, have shown that the plaque that forms in the coronary arteries is not all the same. In fact, recent studies have indicated that calcification in plaque is an indicator of stable plaque, and that it is the so-called vulnerable plaque that breaks off and causes most acute cardiovascular events [4, 5]. The presence of calcification in a plaque has now been associated with remodeling of the coronary vessel to maintain its luminal diameter. Vulnerable plaque is characterized by fat centrally within the plaque, a thin fibrous capsule surrounded peripherally by macrophages. In fact, recent data indicate that atherosclerotic plaque formation is an inflammatory response to extremely small endothelial injuries of the coronary arteries, and serum C-reactive protein has become a marker for potential coronary artery disease [6]. The data now indicate that these vulnerable plaques break off as a result of an inflammatory mediated response to some unknown trigger, and this then either acutely occludes the coronary arteries or results in spasm that causes an acute myocardial infarction; if a large enough area of myocardium is affected, sudden death occurs. The situation is only worsened by the presence of stenoses in the coronary arteries. Conventional angiography yields information about luminal diameter only, not about plaque characterization; therefore, there may be a real niche for MDCT coronary angiography in patients presenting to the emergency department with acute symptoms of cardiac disease as well as patients at low and intermediate risk for coronary artery disease.
The measurement of coronary artery calcification appears to define a different cohort of patients than those with vulnerable plaque in their coronary arteries, although some patients probably have both, which is why the older literature indicates increased risk based on calcium scores. Although a patient with heavily calcified vessels may show progressive symptoms related to worsening myocardial ischemia, angina, or congestive heart failure, it is the presence of fatty plaque that really increases the risk for acute infarctions in patients, whether they have calcified plaque in their vessels or not. The notion that a patient presenting to the emergency department with chest pain can undergo a calcium scoring study that will then appropriately triage the patient to angiographic therapy versus bypass surgery is no longer thought to be correct. Angiography must be performed to determine whether a vessel has been acutely occluded and if areas of stenosis are present. MDCT can do all of this, as well as show other sites of vulnerable plaque that may lead to future cardiac events if left untreated.
The effect of medical therapy for fatty plaque is being investigated at numerous medical centers throughout the world, and determining the proper therapy for patients with vulnerable plaque that is not producing significant stenosis will occupy much of the future literature. Determining which patients develop stable calcified plaque versus unstable vulnerable plaque, as well as delineating the inflammatory mechanisms that lead to acute events, may lead to currently unknown therapies. The ultimate goals are to determine who will best benefit from what treatment and whether the disease-specific mortality from acute myocardial infarcts can be reduced. Calcium scoring is an important part of this process, but by no means does a calcium score yield all the information needed to completely assess a patient's future risk for myocardial infarcts.
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