| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2001;103:3142.)
© 2001 American Heart Association, Inc.
Clinical Cardiology: New Frontiers |
Evaluation of the Culprit Plaque and the Physiological Significance of Coronary Atherosclerotic Narrowings
From the Department of Internal Medicine, Division of Cardiology, Saint Louis University Health Sciences Center, Saint Louis, Mo (M.J.K.), and the Division of Cardiology, Swiss Cardiovascular Center Bern, University Hospital, Bern, Switzerland (B.M.).
Correspondence to Morton J. Kern, MD, Director, J.G. Mudd Cardiac Catheterization Laboratory, Saint Louis University Health Sciences Center, 3635 Vista Avenue at Grand Blvd, St. Louis, MO 63110. E-mail kernm@slu.edu
Key Words: plaque • atherosclerosis • imaging
 |
Introduction |
|---|
Clues to the identification of a plaque as dangerous (ie, vulnerable to sudden activation and/or rupture) before it becomes the culprit of a major, potentially life-threatening event currently must be gleaned from studies examining plaques after the fact.1 2 Although the risk of a given plaque causing a cardiac event, in particular a myocardial infarction, is closely related to the severity of luminal narrowing (complete occlusions excepted), it is incorrect to focus exclusively on the most conspicuous stenoses, that is, the angiographically significant (>70% diameter narrowing) lesions that compete with a larger number of nonsignificant (<50% diameter narrowing) and, at times, inapparent lesions. Because the aggregate risk of rupture associated with many nonsignificant lesions (each with an admittedly lower individual potential) exceeds that of the fewer significant lesions, a myocardial infarction will more likely originate from a nonsignificant lesion.3
In addressing atherosclerotic plaques, coronary interventionists strive to achieve the following 2 primary therapeutic goals: (1) the elimination of angina and (2) the prevention of myocardial infarction and death. The first goal may be readily achieved with revascularization, either by percutaneous coronary interventions (PCI) or coronary bypass surgery. Methods to identify and neutralize a vulnerable plaque before it produces a coronary occlusion are new and as-yet unproven, and the therapeutic approaches in some cases are highly controversial.4
To these ends, the interventionist is handicapped when
relying solely on contrast angiography to identify fine details of
coronary artery disease because lumenology has an inherent
inability to evaluate the vessel wall, atherosclerotic plaque
dimensions,
This article has been cited by other articles:
 |
|
 |
|
  P. Meimoun, T. Benali, F. Elmkies, S. Sayah, A. Luycx-Bore, L. Doutrelan, Z. Hamdane, J. Boulanger, and C. Tribouilloy Prognostic value of transthoracic coronary flow reserve in medically treated patients with proximal left anterior descending artery stenosis of intermediate severity Eur J Echocardiogr, January 1, 2009; 10(1): 127 - 132. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Rumberger Coronary Computed Tomography Angiography: Our Time Has Come, But There Are Miles to Go Before We Sleep J. Am. Coll. Cardiol., November 18, 2008; 52(21): 1733 - 1735. [Full Text] [PDF]
|
|
|
|
|
|
G. S. Mintz Diabetic Coronary Artery Disease: How Little We Know and How Little Intravascular Ultrasound Has Taught Us J. Am. Coll. Cardiol., July 22, 2008; 52(4): 263 - 265. [Full Text] [PDF]
|
|
|
|
|
|
O. Honda, S. Sugiyama, K. Kugiyama, H. Fukushima, S. Nakamura, S. Koide, S. Kojima, N. Hirai, H. Kawano, H. Soejima, et al. Echolucent carotid plaques predict future coronary events in patients with coronary artery disease J. Am. Coll. Cardiol., April 7, 2004; 43(7): 1177 - 1184. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. J. Gomes, O. Giannotti-Filho, R. P. Paez, N. A. Hossne Jr, R. Catani, and E. Buffolo Coronary artery and myocardial inflammatory reaction induced by intracoronary stent Ann. Thorac. Surg., November 1, 2003; 76(5): 1528 - 1532. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N Mercado, W Maier, E Boersma, C Bucher, V de Valk, W.W O'Neill, B.J Gersh, B Meier, P.W Serruys, and W Wijns Clinical and angiographic outcome of patients with mild coronary lesions treated with balloon angioplasty or coronary stenting: Implications for mechanical plaque sealing Eur. Heart J., March 2, 2003; 24(6): 541 - 551. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. J. Schoen and R. F. Padera Jr. Cardiac Surgical Pathology Card. Surg. Adult, January 1, 2003; 2(2003): 119 - 185. [Full Text]
|
|
|
|
 |
|
 D.S. Celermajer Understanding the pathophysiology of the arterial wall: which method should we choose? Eur. Heart J. Suppl., September 1, 2002; 4(suppl_F): F24 - F28. [Abstract] [PDF]
|
|
|
|
 |
|
 M. J. Quinn, E. F. Plow, and E. J. Topol Platelet Glycoprotein IIb/IIIa Inhibitors: Recognition of a Two-Edged Sword? Circulation, July 16, 2002; 106(3): 379 - 385. [Full Text] [PDF]
|
|
|
|
|
|
D. D. Miller Coronary flow studies for risk stratification in multivessel disease: A physiologic bridge too far? J. Am. Coll. Cardiol., March 6, 2002; 39(5): 859 - 863. [Full Text] [PDF]
|
|
|
|
|
|
C. Di Mario Vulnerable plaques: let's stop sinking on submerged icebergs? Eur. Heart J., March 1, 2002; 23(5): 349 - 351. [Full Text] [PDF]
|
|
|
|
|
|
S. Verheye, G. R.Y. De Meyer, G. Van Langenhove, M. W.M. Knaapen, and M. M. Kockx In Vivo Temperature Heterogeneity of Atherosclerotic Plaques Is Determined by Plaque Composition Circulation, April 2, 2002; 105(13): 1596 - 1601. [Abstract] [Full Text] [PDF]
|
|