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CAP Home > CAP Reference Resources and Publications > cap_today/cap_today_index.html > CAP Today Archive 2000 > Separating myocardial infarction from ACS
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Separating myocardial infarction from ACS

July 2000
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Diagnosing and treating acute coronary syndromes (ACS) is unlike diagnosing and treating frank myocardial infarction (MI) because the underlying pathophysiology of the two conditions differs.

Dr. Hal Chadow, director of the Division of Cardiology at the Brookdale Hospital and Medical Center and assistant professor of medicine at SUNY Brooklyn, explains that atherosclerotic plaque is more complicated than just an accumulation of low-density lipoprotein. It also contains smooth muscle cells and fat-rich macro-phages called foam cells. The finding in the Physicians Health Study that men with higher levels of C-reactive protein, a marker of inflammation, had a higher risk of myocardial infarction demonstrated the importance of the inflammatory component to atherosclerotic plaque.

In a standard MI, plaque grows large enough to occlude a major coronary artery, cutting off blood flow and oxygen to myocardium and resulting in extensive ischemia and muscle death. This generally occurs when arterial stenosis reaches 90 percent. In ACS the ischemic process occurs through a different mechanism. Structurally, atherosclerotic plaque essentially consists of a lipid core covered by a fibrous cap. When some hypothesized "trigger" makes the plaque unstable, the fibrous cap ruptures and exposes blood flowing through the coronary arterial circulation to a very thrombogenic core. Simultaneous activation of the coagulation cascade and endothelial injury activates platelets, producing a thrombus that is carried downstream and clogs smaller vessels. What triggers an atherosclerotic plaque to rupture is unclear, Dr. Chadow says.

Support for this model, says Dr. Chadow, comes from the observation that if you do an angiogram and find an artery with a 30 percent stenosis and another artery with a 90 percent stenosis, and that patient has an MI in six to 24 months, two-thirds of the time the artery with the 30 percent lesion was the culprit infarct-related vessel. "And that is the lesion that you would do nothing about," he points out. Since myocardial damage from a thrombus is not as sudden and extensive as with occlusion, CK-MB might not rise enough to turn positive and the ECG might not show ST-segment elevation. But substantial necrosis of heart muscle cells occurs nonetheless, though perhaps at a slower rate.

Dr. Paul Heidenreich, assistant professor of medicine at Stanford University School of Medicine and director of echocardiography at the Palo Alto VA Health Care System, calls ST elevation a marker of occlusive thrombus, where the myocardium is dying as each minute goes by. In ACS, there may be an intermittently obstructive thrombus, which is usually platelet-rich and nonocclusive and doesn't produce ST elevation.

Treatment for the two conditions also differs. In frank MI, the goal is to open the artery. Fibrinolytic therapy, such as thrombolysis with tPA or streptokinase, is ideal in this context. In ACS, on the other hand, tPA may actually worsen outcomes. In these patients the goal is to dissolve the platelet-rich thrombus with anti-platelet agents, such as glycoprotein IIb/IIIa inhibitors.

To prevent MIs, it would be useful to be able to identify so-called vulnerable plaques, those with a high propensity for rupture. Research has shown that a plaque with a thin fibrous cap is more likely to rupture, and smooth muscle cells produce degradative proteins called metalloproteinases that digest the fibrous cap and make it more vulnerable to rupture. In addition, lipid-lowering therapy with statins can convert a vulnerable plaque to a stable plaque. Attempts to distinguish vulnerable from stable plaques with magnetic resonance imaging and other imaging modalities are underway, but they are in their "infancy," in Dr. Chadow's view.

William Check, PhD

   
 

 

 

   
 
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