Author + information
- Received June 16, 2005
- Accepted June 27, 2005
- Published online April 18, 2006.
- ↵⁎Reprint requests and correspondence:
Dr. Jagat Narula, University of California, Irvine, Division of Cardiology, 101 The City Drive, Building 53, Route 81, Room 100, Orange, California 92868-4080.
Whatever we may have observed, perceived, or believed over the course of many years of our clinical practice and pathology research pertaining to atherosclerotic coronary disease, we have paid undivided attention to the luminal stenosis. The characteristics of the vascular wall have not received enough attention. Although the demonstration of luminal obstruction or consequent reduction in blood flow may explain symptomatic status of coronary disease, it does not accurately determine the likelihood of acute coronary events. Luminal interrogation does not offer detection of vulnerable plaques.
We have inherited, imbibed, and communicated not-so-accurate notions about vulnerable plaques. We have tacitly believed that even trivial plaques may rupture and that the arterial tree may have such plaques in abundance. Such a notion is primarily based on the fact that the culprit lesions resulting in acute coronary events often have not shown significant angiographic luminal obstruction. However, pathological studies have demonstrated that lesions likely to be vulnerable to rupture usually are not multiple, occur more often in the proximal and middle part of major arteries and, in a large proportion of cases, are fairly sizable. These lesions involve at least 50% of cross-sectional vascular area in more than 80% of instances, and the necrotic cores often occupy >60° of vessel circumferentially and 10% to 25% of plaque area. Such lesions longitudinally span as long as up to 2 cm and assume vulnerability wherever the necrotic cores surface. The vulnerable sites are not necessarily confined to plaque shoulders. Such lesions may only display minimal encroachment on the lumen because of positive remodeling. The vulnerable lesions often occur in proximal or middle parts of coronary arteries. Relative proximity of these sizable lesions renders them amenable to imaging modalities.
The detection of vulnerable atherosclerotic plaques will be dependent upon demonstration of thin fibrous caps and large necrotic cores. Such techniques may involve noninvasive imaging by computed tomography or magnetic resonance imaging in the future. Invasive techniques could involve intravascular ultrasound, optical coherence, and intravascular magnetic resonance imaging, or near-infrared and thermographic measurements. Only optical coherence tomography may allow evaluation of fibrous cap thickness.
The necrotic cores are perpetuated by intraplaque hemorrhages, which often are secondary to exaggerated plaque neovascularization. Vascularization and intraplaque hemorrhage may provide additional targets for imaging. An oxidized lipid state is associated with plaque and systemic inflammation. Whereas 18F-deoxyglucose positron emission tomographic imaging could become a noninvasive indicator of plaque inflammation, C-reactive protein and other biomarkers will continue to allow the detection of a systemic inflammatory state.
Although the recognition of systemic inflammation describes the patients at high risk of developing acute events (vulnerable patients), imaging modalities will need to identify the lesions at imminent risk of inducing events (vulnerable plaques). With a unique objective of stimulating discussion targeted at development of imaging techniques, Amersham Healthcare (now GE Healthcare) organized a “Vulnerable Plaque Symposium” in Boston in October 2003. Widely acclaimed investigators from all over the world participated in the symposium. All participants contributed to this supplement supported by GE Healthcare and Astellas Healthcare. The emphasis of this volume is on identification of vulnerable plaques. The consensus reaffirms that we need the attention of cardiologists, who should equally be committed to evaluating the arterial lumen and the plaques themselves, especially in noncritically obstructed arteries.
The editors sincerely thank Dr. Johan Verjans for his assistance during the editorial process. They also thank James A. Kaufman, Dr. Claudio Marelli, Paul Cload (GE Healthcare), and Jerry Olszeweski (Astellas Healthcare) for their support in the publication of this supplement.
- Received June 16, 2005.
- Accepted June 27, 2005.
- American College of Cardiology Foundation