Vulnerable plaque

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Vulnerable plaque

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor: Cafer Zorkun, M.D., Ph.D. [2]


A vulnerable plaque is an atheromatous plaque which is particularly prone to produce sudden major problems, such as a heart attack or stroke.

Generally an atheroma becomes vulnerable if it grows more rapidly and has a thin cover separating it from the bloodstream inside the arterial lumen. Tearing of the cover is called plaque rupture.

Criteria for defining vulnerable plaque

Major criteria

  • Active inflammation (monocyte/macrophage/T-cell infiltration)
  • Thin cap with large lipid core
  • Endothelial denudation with superficial platelet aggregation
  • Fissured plaque
  • Stenosis greater than 90%

Minor criteria

  • Superficial calcified nodule
  • Glistening yellow in color
  • Intraplaque hemorrhage
  • Endothelial dysfunction
  • Outward (positive) remodeling


Because artery walls typically enlarge in response to enlarging plaques, these plaques do not usually produce much stenosis of the artery lumen. Therefore, they are not detected by cardiac stress tests or angiography, the tests most commonly performed clinically with the goal of predicting susceptibility to future heart attack. In fact these lesions are not considered as "critical" and/or interventionable by an interventional cardiologist.

In many cases, a vulnerable plaque has a thin fibrous cap and a large and soft lipid pool underlying the cap. These characteristics together with the usual hemodynamic pulsating expansion during systole and elastic recoil contraction during diastole contribute to a high mechanical stress zone on the fibrous cap of the atheroma, making it prone to rupture. Increased hemodynamic stress correlates with increased rates of major cardiovascular events associated with exercise, especially exercise beyond levels the individual does routinely.

Diagnostic Modalities



Clinical Importance

The most frequent cause of a cardiac event following rupture of a vulnerable plaque is blood clotting on top of the site of the ruptured plaque that blocks the lumen of the artery, thereby stopping blood flow to the tissues the artery supplies.

Upon rupture, atheroma tissue debris may spill into the blood stream; these debris are often too large (over 5 micrometers) to pass on through the capillaries downstream. In this, the usual situation, the debris obstruct smaller downstream branches of the artery resulting in temporary to permanent end artery/capillary closure with loss of blood supply to, and death of the previously supplied tissues. A severe case of this can be seen during angioplasty in the slow clearance of injected contrast down the artery lumen. This situation is often termed non-reflow.

Additionally, atheroma rupture may allow bleeding from the lumen into the inner tissue of the atheroma making the atheroma size suddenly increase and protrude into the lumen of the artery producing lumen narrowing or even total obstruction.

Because vulnerable plaques are not revealed by either cardiac stress testing or coronary angiography, the tests most commonly performed clinically with the goal of testing susceptibility to future heart attack, several medical research efforts, starting in the early to mid-1990s, have worked on using intravascular ultrasound IVUS), thermography,(near-infrared spectroscopy) careful clinical follow-up and other methods, to predict these lesions and the individuals most prone to future heart attacks. These efforts remain largely research with no useful clinical methods to date (2006).

However, another approach to detecting and understanding plaque behavior, used in research and by a few clinicians, is to use ultrasound to non-invasively measure wall thickness, usually abbreviated IMT in portions of larger arteries closest to the skin, such as the carotid or femoral arteries. While stability vs. vulnerability cannot be readily distinguished in this way, it is possible to perform careful quantitative baseline measurements of the thickest portions of the arterial wall (locations with the most plaque accumulation), measurements generally termed IMT (intimal medial thickness). While tedious, with care, documenting the (a) IMT, (b) location of each measurement and (c) the apparent plaque size, a basis for tracking and partially verifying the effects of medical treatments on the progression, stability or potential regression of plaque, within a given individual over time, can be achieved.

Repeated atheroma rupture and healing is one of the mechanisms, perhaps the dominant one, which creates artery stenosis.

Management of Patients with Vulnerable Plaque

Newer clinical trial results (2007), e.g. the COURAGE trial[1], have demonstrated that aggressively treating some of the physiologic behavioral factors which promote atheromas with "Optimal Medical Therapy" (not opening stenoses, per-se) produced the most effective results in terms of improving human survival and quality of life for those who have been identified as having already developed advanced cardiovascular disease with many vulnerable plaques.


  1. William E. Boden, M.D., Robert A. O'Rourke, M.D., Koon K. Teo, M.B., B.Ch., Ph.D., Pamela M. Hartigan, Ph.D., David J. Maron, M.D., William J. Kostuk, M.D., Merril Knudtson, M.D., Marcin Dada, M.D., Paul Casperson, Ph.D., Crystal L. Harris, Pharm.D., Bernard R. Chaitman, M.D., Leslee Shaw, Ph.D., Gilbert Gosselin, M.D., Shah Nawaz, M.D., Lawrence M. Title, M.D., Gerald Gau, M.D., Alvin S. Blaustein, M.D., David C. Booth, M.D., Eric R. Bates, M.D., John A. Spertus, M.D., M.P.H., Daniel S. Berman, M.D., G.B. John Mancini, M.D., William S. Weintraub, M.D., for the COURAGE Trial Research Group; Optimal Medical Therapy with or without PCI for Stable Coronary Disease: the COURAGE trial. url= NEJM Volume 356:1503-1516 April 12, 2007 Number 15

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