doi: 10.1161/01.CIR.0000087480.94275.97
(Circulation. 2003;108:1664.)
© 2003 American Heart Association, Inc.
Review: Current Perspective |
From Vulnerable Plaque to Vulnerable Patient
A Call for New Definitions and Risk Assessment Strategies: Part I
From The Center for Vulnerable Plaque Research, University of Texas—Houston, The Texas Heart Institute, and President Bush Center for Cardiovascular Health, Memorial Hermann Hospital, Houston (M. Naghavi, S.W.C., S.L., M.M., A.Z., J.T.W.); The Leducq Center for Cardiovascular Research, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (P.L., M.A.); Department of Cardiology and Institute of Experimental Clinical Research, Aarhus University, Aarhus, Denmark (E.F.); Experimental Cardiology Laboratory, Vascular Biology of the University Medical Center in Utrecht, the Netherlands (G.P.); Ohio State University (J.R.); the Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai Medical Center, New York, NY (Z.F.); Cardiac Catheterization Laboratory at the VA Medical Center, University of Kentucky, Lexington (P.M.); Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (P.H.S.); Division of Cardiology, New England Medical Center, Boston, Mass (S.W.); Department of Medicine, Section of Cardiology, Tulane University School of Medicine, New Orleans, La (P.R.); Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC (A.B., A.F., R.V.); Department of Radiology, University of Washington, Seattle (C.Y.); Stanford University Medical Center Stanford, Calif (P.J.F.); Cardiovascular Health Research Unit, University of Washington, Seattle (D.S.S.); Department of Cardiology, Athens Medical School, Athens, Greece (C.S.); Catheterization Laboratory, Thorax Center, Erasmus University, Rotterdam, the Netherlands (C.L.d.K.); Division of Cardiology, Department of Medicine, University of Turku, Finland (K.E.J.A.); Institute of Arteriosclerosis Research and the Institute of Clinical Chemistry and Laboratory Medicine, Central Laboratory, Hospital of the University of Münster, Munich, Germany (G.A.); Department of Clinical Radiology, University of Münster, Munich, Germany (C.R.B.); Mayo Clinic Medical School, Jacksonville, Fla (J.H.C.); Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Ga (Z.S.G.); Bristol Heart Institute, Bristol University, Bristol, United Kingdom (C.J.); Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, Mass (I.-K.J.); Department of Internal Medicine II, Cardiology, University of Ulm, Ulm, Germany (W.K.); University of Kentucky, Lexington, Ky (R.A.L.); R.L. Roudebush VA Medical Center, Indianapolis, Ind (K.M.); School of Public Health, University of Texas—Houston, Houston, Texas (J.D.); Division of Cardiology, University of California Los Angeles, Los Angeles, Calif (M. Navab); Fondazione Salvatore Maugeri, University of Pavia, Pavia, Italy (S.G.P.); Department of Cardiovascular Therapeutics, Pfizer Global Research and Development, Ann Arbor Laboratories, Ann Arbor, Mich (M.D.R.); Paul Dudley White Coronary Care System at St. Agnes HealthCare, Baltimore, Md (R.B.); Center for Human Nutrition, University of Texas Health Science Center, Dallas (S.M.G.); Lenox Hill Hospital, New York, NY (R.M.); Catheterization Laboratories, Ospedale San Raffaele and Emo Centro Cuore Columbus, Milan, Italy (A.C.); Human Genetics Center, Institute of Molecular Medicine, Houston, Tex (E.B.); Department of Medicine, Baylor College of Medicine, Houston, Tex (C.B., W.I.); Minneapolis Heart Institute and Foundation, Minneapolis, Minn (R.S.S.); Division of Cardiology, University of Maryland School of Medicine, Baltimore, Md (R.V.); Karolinska Institute, Center for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden (G.K.H.); Section of Cardiology, University of Chicago, Ill (D.P.F.); Vascular Physiology and Thrombosis Research Laboratory of the Atherosclerosis Research Center, Cedars-Sinai Medical Center, Los Angeles, California (S.K.); Cardiology Department, Hannover University, Hannover, Germany (H.D.); Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Ill (P.G.); UCLA School of Medicine and Cedars-Sinai Medical Center, Los Angeles, Calif (P.K.S.); Massachusetts General Hospital, Harvard Medical School and CIMIT (Center for Integration of Medicine and Innovative Technology), Boston, Mass (J.E.M.); Cardiovascular Division, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, Mass (P.M.R.); and Indiana University School of Medicine, Krannert Institute of Cardiology, Indianapolis (D.P.Z.).
Correspondence to Morteza Naghavi, MD, Association for Eradication of Heart Attack, 2472 Bolsover, No. 439, Houston, TX 77005. E-mail mn{at}vp.org
Abstract
Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.
Key Words: coronary disease • plaque • myocardial infarction • atherosclerosis • death, sudden
Cardiovascular disease has long been the leading cause of death in developed countries, and it is rapidly becoming the number one killer in the developing countries.1 According to current estimates, 61 800 000 Americans have one or more types of cardiovascular disease.2
Every year, >1 million people in the United States and >19 million others worldwide experience a sudden cardiac event (acute coronary syndromes and/or sudden cardiac death). A large portion of this population has no prior symptom.3 There is considerable demand for diagnosis and treatment of the pathologic conditions that underlie these sudden cardiac events. This consensus document proposes new directions to prevent infarction and sudden cardiac events.4
Underlying Causes of Sudden Fatal and Nonfatal Cardiac Events
Figure 1 delineates the underlying causes of acute cardiac events. The first branch point of the tree indicates patients who lack significant atherosclerosis or related myocardial damage, that is, those who have no ischemic heart disease (see The Nonischemic Vulnerable Myocardium). This leaves the patients with atherosclerosis, some of whom also have a hypercoagulable state (see Vulnerable Blood).
|
The next branch point involves the presence or absence of an occlusive or subocclusive thrombus. A thrombus identifies a culprit plaque that may be ruptured or nonruptured.
Plaque rupture is the most common type of plaque complication, accounting for 
70% of fatal acute myocardial infarctions and/or sudden coronary deaths (Figure 2). Several retrospective autopsy series and a few cross-sectional clinical studies have suggested that thrombotic coronary death and acute coronary syndromes are caused by the plaque features and associated factors presented in Table 1.5–7 Most techniques for detecting and treating vulnerable plaque are devoted to rupture-prone plaque. This type of plaque has been termed a "thin-cap fibroatheroma."8
|
|
In some cases, a deep plaque injury cannot be identified despite a careful search. The thrombus appears to be superimposed on a de-endothelialized, but otherwise intact, plaque. This type of superficial plaque injury is called "plaque erosion."9 Other types of culprit plaques also exist (Figure 2). In cases involving nonruptured plaques, plaque erosion or nodular calcification usually accompanies the luminal thrombus.5 Other forms of thrombosis in nonruptured plaques may be described in the future. In all cases that involve a superimposed thrombus, the underlying lesion may be stenotic or nonstenotic. However, nonstenotic lesions are far more frequent than stenotic plaques and account for the majority of culprit ruptured plaques.10
|
In cases of sudden cardiac death without thrombosis, we hypothesize that coronary spasm, emboli to the distal intramural vasculature, or myocardial damage related to previous injury may account for a terminal arrhythmic episode.
The Challenge of Terminology: Culprit Plaque Versus Vulnerable Plaque
Culprit Plaque, a Retrospective Terminology
Interventional cardiologists and cardiovascular pathologists retrospectively describe the plaque responsible for coronary occlusion and death as a culprit plaque, regardless of its histopathologic features. For prospective evaluation, clinicians need a similar term for describing such plaques before an event occurs. Plaque rupture was reported sporadically by pathologists in the early 20th century; it became a focus of attention of pioneering scientists in the 1960s (Table 2) and was later documented further by others.11–15
Since the 1970s, scientists have been seeking the mechanisms responsible for converting chronic coronary atherosclerosis to acute coronary artery disease.11–15,17 As insights into this process have evolved, the relevant terminology has been continually updated. In the 1980s, Falk11 and Davies and Thomas15 used "plaque disruption" synonymously with "plaque rupture." Later, Muller and colleagues18,19 used "vulnerable" to describe rupture-prone plaques as the underlying cause of most clinical coronary events. When this functional definition was proposed, the plaque considered responsible for acute coronary events (based on retrospective autopsy studies) had a large lipid pool, a thin cap, and macrophage-dense inflammation on or beneath its surface (Figure 3).
|
Over the past several years, "vulnerable plaque" has been used sometimes to denote this concept and at other times to denote the specific histopathologic appearance of the above-described plaque. This dual usage is confusing, particularly as plaques can have other histologic features (see Figure 2) that may also cause acute coronary events.5
Vulnerable Plaque, a Future Culprit Plaque
The term "vulnerable" is defined by English dictionaries as "susceptible to injury or susceptible to attack,"20 as in "We are vulnerable both by water and land, without either fleet or army" (Alexander Hamilton). It denotes the likelihood of having an event in the future. The term vulnerable has been used in various reports in the medical literature, all of which describe conditions susceptible to injury. In this regard, the term "vulnerable plaque" is most suitable to define plaques susceptible to complications. An alternative term, "high-risk plaque," has been recently proposed.18 The term "high-risk" is often used to describe the high-risk patient groups with acute coronary syndromes. However, our intention is to provide a terminology to identify apparently healthy subjects at risk of future events. Therefore, the term vulnerable seems to be more appropriate. Also, because "vulnerable plaque" has already been widely adopted by investigators and clinicians, we recommend that the existing usage of this term be continued. We advise that the underlying morphological features be described broadly enough to include all dangerous plaques that involve a risk of thrombosis and/or rapid progression.
To provide a uniform language to help standardize the terminology, we recommend "vulnerable plaque" to identify all thrombosis-prone plaques and plaques with a high probability of undergoing rapid progression, thus becoming culprit plaques (Table 3). A proposed histopathologic classification for different types of vulnerable plaque is presented in Figure 2. A list of proposed major and minor criteria for defining vulnerable plaques, based on autopsy studies (culprit plaques), is presented in Table 4.
|
|
A large number of vulnerable plaques are relatively uncalcified, relatively nonstenotic, and similar to type IV atherosclerotic lesions described in the American Heart Association classification.21 However, as depicted in Figure 3, different types of vulnerable plaque exist. Although Table 1 shows the relative distribution of ruptured and nonruptured culprit plaques, the exact prevalence of each type of vulnerable plaque is unknown and can only be determined in prospective studies.
Pan-Coronary Vulnerability
Several investigators have noted the presence of more than one vulnerable plaque in patients at risk of cardiovascular events. Mann and Davies22 and Burke et al23 in cardiac autopsy specimens, Goldstein et al24 in angiography studies, Nissen25 and Rioufol et al26 with intravascular ultrasound, and Buffon et al27 measuring neutrophil myeloperoxidase found multiple rupture-prone or ruptured plaques in a wide range of cardiovascular patient populations. A most recent series of publications on vulnerability reiterated the importance of going beyond a vulnerable plaque and called for evaluating the total arterial tree as a whole.28–30
Silent-Plaque Rupture
Thrombotic complications that arise from rupture or fissure (small rupture) of a vulnerable plaque may be clinically silent yet contribute to the natural history of plaque progression and ultimately luminal stenosis.31,32
Beyond the Atherosclerotic Plaque
It is important to identify patients in whom disruption of a vulnerable plaque is likely to result in a clinical event. In these patients, other factors beyond plaque (ie, thrombogenic blood and electrical instability of myocardium) are responsible for the final outcome (Figure 4). We propose that such patients be referred to as "vulnerable patients." In fact, plaques with similar characteristics may have different clinical presentations because of blood coagulability (vulnerable blood) or myocardial susceptibility to develop fatal arrhythmia (vulnerable myocardium). The latter may depend on a current or previous ischemic condition and/or a nonischemic electrophysiological abnormality.
|
Definition of a Cardiovascular Vulnerable Patient
The term "cardiovascular vulnerable patient" is proposed to define subjects susceptible to an acute coronary syndrome or sudden cardiac death based on plaque, blood, or myocardial vulnerability (for example, 1-year risk 
5%). Extensive efforts are needed to quantify an individual’s risk of an event according to each component of vulnerability (plaque, blood, and myocardium). Such a comprehensive risk-stratification tool capable of predicting acute coronary syndromes as well as sudden cardiac death would be very useful for preventive cardiology (Figure 4).
Diagnosis of Vulnerable Plaque/Artery
A number of issues have hampered establishment of ideal criteria for defining vulnerable plaque: (1) the current body of evidence is largely based on cross-sectional and retrospective studies of culprit plaques; (2) robust prospective outcome studies based on plaque characterization have not been done (due to the lack of a reproducible, validated diagnostic technique); and (3) a lack of a representative animal model of plaque rupture and acute coronary syndrome/sudden death.
On the basis of retrospective evidence, we propose that the criteria listed in Tables 4 and 5
be used to define a vulnerable plaque. The sensitivity, specificity, and overall predictive value of each potential diagnostic technique need to be assessed before entering clinical practice.
|
Major Criteria
The following are proposed as major criteria for detection of a vulnerable plaque. The presence of one or a combination of these factors may warrant higher risk of plaque complication. Techniques for detection of vulnerable plaque based on these criteria are briefly summarized here. A detailed discussion of advantages and disadvantages are reviewed elsewhere.33
1. Active Inflammation
Plaques with active inflammation may be identified by extensive macrophage accumulation.13 Possible intravascular diagnostic techniques34,35 include thermography (measurement of plaque temperature),36,37 contrast-enhanced (CE) MRI,38,39 fluorodeoxyglucose positron emission tomography,33,40 and immunoscintigraphy.41 It has recently been shown that optical coherence tomography reflects the macrophage content of the fibrous cap.42 Noninvasive options include MRI with superparamagnetic iron oxide35,36 and gadolinium fluorine compounds.43–45
2. A Thin Cap With a Large Lipid Core
These plaques have a cap thickness of <100 µm and a lipid core accounting for >40% of the plaque’s total volume.8 Possible intravascular diagnostic techniques include optical coherence tomography (OCT),46,47 intravascular ultrasonography (IVUS),48 high-resolution IVUS,49 elastography (palpography),50,51 MRI,52 angioscopy,53 near infrared (NIR) spectroscopy,54–56 and radiofrequency IVUS analysis.57,58 The only noninvasive options are presently MRI and possibly CT.34,35,59–62
3. Endothelial Denudation with Superficial Platelet Aggregation
These plaques are characterized by superficial erosion and platelet aggregation or fibrin deposition.5 Possible intravascular diagnostic techniques include angioscopy with dye63 and matrix-targeted/fibrin-targeted immune scintigraphy and OCT.46,47 Noninvasive options include fibrin/matrix-targeted contrast enhanced MRI,64 platelet/fibrin-targeted single photon emission computed tomography,41 and MRI.52
4. Fissured/Injured Plaque
Plaques with a fissured cap (most of them involving a recent rupture) that did not result in occlusive thrombi may be prone to subsequent thrombosis, entailing occlusive thrombi or thromboemboli.5 Possible intravascular diagnostic techniques include OCT,46,47 IVUS, high-resolution IVUS,49 angioscopy, and MRI.34,35 A noninvasive option is fibrin-targeted CE-MRI.64,65
5. Severe Stenosis
On the surface of plaques with severe stenosis, shear stress imposes a significant risk of thrombosis and sudden occlusion. Therefore, a stenotic plaque may be a vulnerable plaque regardless of ischemia. Moreover, a stenotic plaque may indicate the presence of many nonstenotic or less stenotic plaques that can be vulnerable to rupture and thrombosis24,66 (Figure 5). The current standard technique is invasive x-ray angiography.32 Noninvasive options include multislice CT,67,68 magnetic resonance angiography with or without a contrast agent, and electron-beam tomography angiography.59,69–71
|
Minor Criteria
For techniques that focus on the plaque level, minor criteria include the following features.
1. Superficial Calcified Nodules
These plaques have a calcified nodule within, or very close to, their cap, and this structure protrudes through and can rupture the cap. This event may or may not be associated with severe coronary calcification and a high calcium score.5 Possible intravascular diagnostic techniques include OCT,46,47 IVUS and elastography (palpography).48 Noninvasive options include electron-beam CT,72 multisection spiral CT,73 and MRI.34,35
2. Yellow Color (on Angioscopy)
Yellow plaques, particularly glistening ones, may indicate a large lipid core and thin fibrous cap, suggesting a high risk of rupture. However, because plaques in different stages can be yellow and because not all lipid-laden plaques are destined to rupture or undergo thrombosis, this criterion may lack sufficient specificity.53,74 Possible intravascular diagnostic techniques include angioscopy73 and transcatheter colorimetry.75 No diagnostic method has yet been developed for noninvasive angioscopy.
3. Intraplaque Hemorrhage
Extravasation of red blood cells, or iron accumulation in plaque, may represent plaque instability.76 Possible intravascular diagnostic techniques include NIR spectroscopy,54,55 tissue Doppler methods,77 and intravascular MRI. A noninvasive option is MRI.34,35,61
4. Endothelial Dysfunction
Impaired endothelial vasodilator function occurs in a variety of acute and chronic disease states. Patients with cardiovascular risk factors have endothelial dysfunction. Endothelial dysfunction predicts CHD and stroke.89,95 Vulnerable plaques have sites of active inflammation and oxidative stress and are likely to be associated with impaired endothelial function. Possible diagnostic techniques are endothelium-dependent coronary artery dilatation (intravascular)78 and measurement of flow-mediated dilatation by brachial artery ultrasonography and other emerging techniques (noninvasive).79
5. Expansive (Positive) Remodeling
Many of the nonstenotic lesions undergo "expansive," "positive," or "outward" remodeling, namely compensatory enlargement before impinging significantly on the vascular lumen. This phenomenon was considered as positive remodeling because the luminal area was not affected and stenosis was the only measure of risk. However, with the emphasis on plaque rupture in nonstenotic lesions, the so-called positive remodeling may not be truly positive and beneficial. Several studies have suggested that such remodeling is a potential surrogate marker of plaque vulnerability.80,81 In these studies, intravascular ultrasound was used to evaluate remodeling in coronary arteries. A recent study by Kim et al82 introduced a noninvasive method for detection of expansive remodeling in coronary arteries by MRI. CT might also provide a noninvasive method for studying arterial remodeling.
Few of the above techniques have been tested in clinical trials showing ability to predict events. MRI and CT-based approaches are being developed. These technologies and strategies must also be evaluated with regard to their cost effectiveness.
Functional Versus Structural Assessment
A growing body of evidence indicates that different types of vulnerable plaque with various histopathology and biology exist. To evaluate plaque vulnerability, it is evident that a combined approach capable of evaluating structural characteristics (morphology) as well as functional properties (activity) of plaque may be more informative and may provide higher predictive value than a single approach. For instance, a combination of IVUS or OCT with thermography80,83 may provide more diagnostic value than each of these techniques alone. Such an arrangement can be useful for both intravascular as well as noninvasive diagnostic methods (Figure 6). Autopsy84 and IVUS studies85 have shown that atherosclerotic lesions are frequently found in young and asymptomatic individuals. It is unclear what percentage of these lesions present morphologies of rupture-prone vulnerable plaques. Moreover, chronic inflammation86 and macrophage/foam cell formation are an intrinsic part of the natural history of atherosclerosis. These data suggest that screening only based on plaque morphology and/ or chronic markers of inflammation may not provide satisfactory predictive value for detection of vulnerable patients.
|
Pan-Arterial Approach
Diagnostic and therapeutic methods may focus on the total burden of coronary artery disease.27 The coronary Calcium Score is a good example of using CT for this purpose.72 The total burden of calcified atherosclerotic plaques in all coronary arteries is identified by ultrafast CT. Extensive efforts are underway to improve image quality, signal processing, and interpretation of detailed components of coronary arteries that lend hope of a new calcium scoring and risk stratification technique based on CT information.87 Like systemic indexes of inflammation (eg, high sensitive CRP), endothelial dysfunction as measured by impaired flow-mediated vasodilation in the brachial artery can aid in the detection of pan-arterial vulnerability and may serve as a screening tool.88,89
Another emerging technique is the measurement of the transcoronary gradient (difference in concentration between coronary ostium and coronary sinus or between proximal and distal segments of each coronary segment) of various factors, including cytokines,90 adhesion molecules,91 temperature, etc.
It will be important in the future to identify plaques that are on a trajectory of evolution toward a vulnerable state, to find out how long they will stay vulnerable, and to be able to target interventions to those plaques most likely to develop thrombosis. Similarly, factors that protect plaques from becoming vulnerable also need to be identified. It is likely that local hemodynamic factors and 3-dimensional morphology may provide insight regarding the temporal course of an evolving plaque.
New studies are unraveling the role of the adventitia and periadventitial connective and adipose tissue in vulnerability of atherosclerotic plaques.92 Further studies are needed to define the importance of these findings in the detection and treatment of vulnerable plaques.
Acknowledgments
We are indebted to Valentin Fuster, MD, and Salim Yusuf, MD, for their insightful reviews and thoughtful comments.
Footnotes
Many of the authors of this work, in addition to their research activities, have served as consultants to and/or employees of pharmaceutical, medical equipment, and other related companies.
Guest editor for this article was Eugene Braunwald, MD, Brigham and Women’s Hospital.
This article is Part I of a 2-part article. Part II will appear in the October 14, 2003 issue of Circulation.
References
1. Yusuf S, Reddy S, Ounpuu S, et al. Global burden of cardiovascular diseases, I: general considerations, the epidemiologic transition, risk factors, and impact of urbanization. Circulation. 2001; 104: 2746–2753.
2. American Heart Association. 2002 Heart and Stroke Statistical Update. Dallas, Tex: American Heart Association; 2002.
3. Myerburg RJ, Interian A Jr, Mitrani RM, et al. Frequency of sudden cardiac death and profiles of risk. Am J Cardiol. 1997; 80: 10F–19F.[CrossRef][Medline] [Order article via Infotrieve]
4. Zipes DP, Wellens HJ. Sudden cardiac death. Circulation. 1998; 98: 2334–2351.
5. Virmani R, Kolodgie FD, Burke AP, et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000; 20: 1262–1275.
6. Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995; 92: 657–671.
7. Davies MJ. A macro and micro view of coronary vascular insult in ischemic heart disease. Circulation. 1990; 82 (suppl II): II-38–II-46.[Medline] [Order article via Infotrieve]
8. Kolodgie FD, Burke AP, Farb A, et al. The thin-cap fibroatheroma: a type of vulnerable plaque: the major precursor lesion to acute coronary syndromes. Curr Opin Cardiol. 2001; 16: 285–292.[CrossRef][Medline] [Order article via Infotrieve]
9. Farb A, Burke AP, Tang AL, et al. Coronary plaque erosion without rupture into a lipid core: a frequent cause of coronary thrombosis in sudden coronary death. Circulation. 1996; 93: 1354–1363.
10. Ambrose JA, Tannenbaum MA, Alexopoulos D, et al. Angiographic progression of coronary artery disease and the development of myocardial infarction. J Am Coll Cardiol. 1988; 12: 56–62.[Abstract]
11. Falk E. Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis: characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. Br Heart J. 1983; 50: 127–134.
12. Friedman M, Van den Bovenkamp GJ. Role of thrombus in plaque formation in the human diseased coronary artery. Br J Exp Pathol. 1966; 47: 550–557.[Medline] [Order article via Infotrieve]
13. Constantinides P. Pathogenesis of cerebral artery thrombosis in man. Arch Pathol. 1967; 83: 422–428.[Medline] [Order article via Infotrieve]
14. Chapman I. Relationships of recent coronary artery occlusion and acute myocardial infarction. J Mt Sinai Hosp N Y. 1968; 35: 149–154.[Medline] [Order article via Infotrieve]
15. Davies MJ, Thomas AC. Plaque fissuring: the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina. Br Heart J. 1985; 53: 363–373.
17. Willerson JT, Campbell WB, Winniford MD, et al. Conversion from chronic to acute coronary artery disease: speculation regarding mechanisms. Am J Cardiol. 1984; 54: 1349–1354.[CrossRef][Medline] [Order article via Infotrieve]
18. Muller J, Tofler G, Stone P. Circadian variation and triggers of onset of acute cardiovascular disease. Circulation. 1989; 79: 733–743.
19. Muller JE, Abela GS, Nesto RW, et al. Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier. J Am Coll Cardiol. 1994; 23: 809–813.[Abstract]
20. Vulnerable. In: Merriam-Webster’s Collegiate Dictionary & Thesaurus. 11th ed (e-book). Springfield, Mass: Merriam-Webster, Inc; 2003.
21. Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis : a report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. 1995; 92: 1355–1374.
22. Mann J, Davies MJ. Mechanisms of progression in native coronary artery disease: role of healed plaque disruption. Heart. 1999; 82: 265–268.
23. Burke AP, Farb A, Malcom GT, et al. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med. 1997; 336: 1276–1282.
24. Goldstein JA, Demetriou D, Grines CL, et al. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med. 2000; 343: 915–922.
25. Nissen SE. Who is at risk for atherosclerotic disease? Lessons from intravascular ultrasound. Am J Med. 2002; 112 (suppl 8A): 27S–33S.[CrossRef][Medline] [Order article via Infotrieve]
26. Rioufol G, Finet G, Ginon I, et al. Multiple atherosclerotic plaque rupture in acute coronary syndrome. Circulation. 2002; 106: 804–808.
27. Buffon A, Biasucci LM, Liuzzo G, et al. Widespread coronary inflammation in unstable angina. N Engl J Med. 2002; 347: 5–12.
28. Casscells W, Naghavi M, Willerson JT. Vulnerable atherosclerotic plaque: a multifocal disease. Circulation. 2003; 107: 2072–2075.
29. Maseri A, Fuster V. Is there a vulnerable plaque? Circulation. 2003; 107: 2068–2071.
30. Kereiakes DJ. The emperor’s clothes: in search of the vulnerable plaque. Circulation. 2003; 107: 2076–2077.
31. Davies MJ. Pathology of arterial thrombosis. Br Med Bull. 1994; 50: 789–802.
32. Burke AP, Kolodgie FD, Farb A, et al. Healed plaque ruptures and sudden coronary death: evidence that subclinical rupture has a role in plaque progression. Circulation. 2001; 103: 934–940.
33. Vallabhajosula S, Fuster V. Atherosclerosis: imaging techniques and the evolving role of nuclear medicine. J Nucl Med. 1997; 38: 1788–1796.
34. Fayad ZA, Fuster V. Clinical imaging of the high-risk or vulnerable atherosclerotic plaque. Circ Res. 2001; 89: 305–316.
35. Naghavi M, Madjid M, Khan MR, et al. New developments in the detection of vulnerable plaque. Curr Atheroscler Rep. 2001; 3: 125–135.[Medline] [Order article via Infotrieve]
36. Stefanadis C, Diamantopoulos L, Vlachopoulos C, et al. Thermal heterogeneity within human atherosclerotic coronary arteries detected in vivo : a new method of detection by application of a special thermography catheter. Circulation. 1999; 99: 1965–1971.
37. Stefanadis C, Toutouzas K, Tsiamis E, et al. Thermal heterogeneity in stable human coronary atherosclerotic plaques is underestimated in vivo: the "cooling effect" of blood flow. J Am Coll Cardiol. 2003; 41: 403–408.
38. Schmitz SA, Coupland SE, Gust R, et al. Superparamagnetic iron oxide-enhanced MRI of atherosclerotic plaques in Watanabe hereditable hyperlipidemic rabbits. Invest Radiol. 2000; 35: 460–471.[CrossRef][Medline] [Order article via Infotrieve]
39. Ruehm SG, Corot C, Vogt P, et al. Magnetic resonance imaging of atherosclerotic plaque with ultrasmall superparamagnetic particles of iron oxide in hyperlipidemic rabbits. Circulation. 2001; 103: 415–422.
40. Lederman RJ, Raylman RR, Fisher SJ, et al. Detection of atherosclerosis using a novel positron-sensitive probe and 18-fluorodeoxyglucose (FDG). Nucl Med Commun. 2001; 22: 747–753.[CrossRef][Medline] [Order article via Infotrieve]
41. Ciavolella M, Tavolaro R, Taurino M, et al. Immunoscintigraphy of atherosclerotic uncomplicated lesions in vivo with a monoclonal antibody against D-dimers of insoluble fibrin. Atherosclerosis. 1999; 143: 171–175.[CrossRef][Medline] [Order article via Infotrieve]
42. Tearney GJ, Yabushita H, Houser SL, et al. Quantification of macrophage content in atherosclerotic plaques by optical coherence tomography. Circulation. 2003; 107: 113–119.
43. Krinsky GA, Freedberg R, Lee VS, et al. Innominate artery atheroma: a lesion seen with gadolinium-enhanced MR angiography and often missed by transesophageal echocardiography. Clin Imaging. 2001; 25: 251–257.[CrossRef][Medline] [Order article via Infotrieve]
44. Bonk RT, Schmiedl UP, Yuan C, et al. Time-of-flight MR angiography with Gd-DTPA hexamethylene diamine co-polymer blood pool contrast agent: comparison of enhanced MRA and conventional angiography for arterial stenosis induced in rabbits. J Magn Reson Imaging. 2000; 11: 638–646.[CrossRef][Medline] [Order article via Infotrieve]
45. Yuan C, Kerwin WS, Ferguson MS, et al. Contrast-enhanced high resolution MRI for atherosclerotic carotid artery tissue characterization. J Magn Reson Imaging. 2002; 15: 62–67.[CrossRef][Medline] [Order article via Infotrieve]
46. Patwari P, Weissman NJ, Boppart SA, et al. Assessment of coronary plaque with optical coherence tomography and high-frequency ultrasound. Am J Cardiol. 2000; 85: 641–644.[CrossRef][Medline] [Order article via Infotrieve]
47. Jang I-K, Bouma BE, Kang D-H, et al. Visualization of coronary atherosclerotic plaques in patients using optical coherence tomography: comparison with intravascular ultrasound. J Am Coll Cardiol. 2002; 39: 604–609.
48. Nissen SE. Clinical images from intravascular ultrasound: coronary disease, plaque rupture, and intervention—the inside view. Am J Cardiol. 2001; 88: 16–18.
49. Nissen SE, Yock P. Intravascular ultrasound : novel pathophysiological insights and current clinical applications. Circulation. 2001; 103: 604–616.
50. de Korte CL, Cespedes EI, van der Steen AF, et al. Intravascular ultrasound elastography: assessment and imaging of elastic properties of diseased arteries and vulnerable plaque. Eur J Ultrasound. 1998; 7: 219–224.[CrossRef][Medline] [Order article via Infotrieve]
51. de Korte CL, Sierevogel MJ, Mastik F, et al. Identification of atherosclerotic plaque components with intravascular ultrasound elastography in vivo: a Yucatan pig study. Circulation. 2002; 105: 1627–1630.
52. Corti R, Osende JI, Fuster V, et al. Artery dissection and arterial thrombus aging: the role of noninvasive magnetic resonance imaging. Circulation. 2001; 103: 2420–2421.
53. Takano M, Mizuno K, Okamatsu K, et al. Mechanical and structural characteristics of vulnerable plaques: analysis by coronary angioscopy and intravascular ultrasound. J Am Coll Cardiol. 2001; 38: 99–104.
54. Cassis LA, Lodder RA. Near-IR imaging of atheromas in living arterial tissue. Anal Chem. 1993; 65: 1247–1256.[Medline] [Order article via Infotrieve]
55. Moreno PR, Lodder RA, Purushothaman KR, et al. Detection of lipid pool, thin fibrous cap, and inflammatory cells in human aortic atherosclerotic plaques by near-infrared spectroscopy. Circulation. 2002; 105: 923–927.
56. Wang J, Geng YJ, Guo B, et al. Near-infrared spectroscopic characterization of human advanced atherosclerotic plaques. J Am Coll Cardiol. 2002; 39: 1305–1313.
57. Jeremias A, Kolz ML, Ikonen TS, et al. Feasibility of in vivo intravascular ultrasound tissue characterization in the detection of early vascular transplant rejection. Circulation. 1999; 100: 2127–2130.
58. Nair A, Kuban BD, Tuzcu EM, et al. Coronary plaque classification with intravascular ultrasound radiofrequency data analysis. Circulation. 2002; 106: 2200–2206.
59. Helft G, Worthley SG, Fuster V, et al. Progression and regression of atherosclerotic lesions: monitoring with serial noninvasive magnetic resonance imaging. Circulation. 2002; 105: 993–998.
60. Hatsukami TS, Ross R, Polissar NL, et al. Visualization of fibrous cap thickness and rupture in human atherosclerotic carotid plaque in vivo with high-resolution magnetic resonance imaging. Circulation. 2000; 102: 959–964.
61. Yuan C, Mitsumori LM, Ferguson MS, et al. In vivo accuracy of multispectral magnetic resonance imaging for identifying lipid-rich necrotic cores and intraplaque hemorrhage in advanced human carotid plaques. Circulation. 2001; 104: 2051–2056.
62. Yuan C, Zhang S-X, Polissar NL, et al. Identification of fibrous cap rupture with magnetic resonance imaging is highly associated with recent transient ischemic attack or stroke. Circulation. 2002; 105: 181–185.
63. Uchida Y, Nakamura F, Tomaru T, et al. Prediction of acute coronary syndromes by percutaneous coronary angioscopy in patients with stable angina. Am Heart J. 1995; 130: 195–203.[CrossRef][Medline] [Order article via Infotrieve]
64. Flacke S, Fischer S, Scott MJ, et al. Novel MRI contrast agent for molecular imaging of fibrin: implications for detecting vulnerable plaques. Circulation. 2001; 104: 1280–1285.
65. Corti R, Osende JI, Fayad ZA, et al. In vivo noninvasive detection and age definition of arterial thrombus by MRI. J Am Coll Cardiol. 2002; 39: 1366–1373.
66. Asakura M, Ueda Y, Yamaguchi O, et al. Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: an angioscopic study. J Am Coll Cardiol. 2001; 37: 1284–1288.
67. Nieman K, Oudkerk M, Rensing BJ, et al. Coronary angiography with multi-slice computed tomography. Lancet. 2001; 357: 599–603.[CrossRef][Medline] [Order article via Infotrieve]
68. Giesler TBU, Ropers D, Ulzheimer S, et al. Noninvasive visualization of coronary arteries using contrast-enhanced multidetector CT: influence of heart rate on image quality and stenosis detection. AJR Am J Roentgenol. 2002; 179: 911–916.
69. Duerinckx AJ. Imaging of coronary artery disease: MR. J Thorac Imaging. 2001; 16: 25–34.[CrossRef][Medline] [Order article via Infotrieve]
70. Hecht HS. New developments in atherosclerosis imaging: electron beam tomography. Curr Atheroscler Rep. 2001; 3: 417–424.[Medline] [Order article via Infotrieve]
71. Corti R, Fayad ZA, Fuster V, et al. Effects of lipid-lowering by simvastatin on human atherosclerotic lesions: a longitudinal study by high-resolution, noninvasive magnetic resonance imaging. Circulation. 2001; 104: 249–252.
72. Rumberger JA. Tomographic (plaque) imaging: state of the art. Am J Cardiol. 2001; 88: 66E–69E.[CrossRef][Medline] [Order article via Infotrieve]
73. Achenbach S, Ropers D, Regenfus M, et al. Noninvasive coronary angiography by magnetic resonance imaging, electron-beam computed tomography, and multislice computed tomography. Am J Cardiol. 2001; 88: 70E–73E.[CrossRef][Medline] [Order article via Infotrieve]
74. Kodama K, Asakura M, Ueda Y, et al. The role of plaque rupture in the development of acute coronary syndrome evaluated by the coronary angioscope. Intern Med. 2000; 39: 333–335.[Medline] [Order article via Infotrieve]
75. Lehmann KG, van Suylen RJ, Stibbe J, et al. Composition of human thrombus assessed by quantitative colorimetric angioscopic analysis. Circulation. 1997; 96: 3030–3041.
76. Moulton KS. Plaque angiogenesis and atherosclerosis. Curr Atheroscler Rep. 2001; 3: 225–233.[Medline] [Order article via Infotrieve]
77. Nasu K, Kawamoto A, Sasaki Y, et al. Measurement of vascular tissue blood flow of the atherosclerotic aorta in Watanabe heritable hypercholesterolemic (WHHL) rabbit by using laser Doppler flowmeter-equipped balloon catheter. Am J Cardiol. 1999; 84: 84P.
78. Drexler H, Zeiher AM, Wollschlager H, et al. Flow-dependent coronary artery dilatation in humans. Circulation. 1989; 80: 466–474.
79. Vogel RA. Brachial artery ultrasound: a noninvasive tool in the assessment of triglyceride-rich lipoproteins. Clin Cardiol. 1999 (6 suppl); 22: II34–II39.[Medline] [Order article via Infotrieve]
80. Varnava AM, Mills PG, Davies MJ. Relationship between coronary artery remodeling and plaque vulnerability. Circulation. 2002; 105: 939–943.
81. Smits PC, Pasterkamp G, Quarles van Ufford MA et al. Coronary artery disease: arterial remodelling and clinical presentation. Heart. 1999; 82: 461–464.
82. Kim WY, Stuber M, Bornert P, et al. Three-dimensional black-blood cardiac magnetic resonance coronary vessel wall imaging detects positive arterial remodeling in patients with nonsignificant coronary artery disease. Circulation. 2002; 106: 296–299.
83. Naghavi M, Madjid M, Gul K, et al. Thermography basket catheter: in vivo measurement of the temperature of atherosclerotic plaques for detection of vulnerable plaques. Catheter Cardiovasc Interv. 2003; 59: 52–59.[CrossRef][Medline] [Order article via Infotrieve]
84. Wissler RW, Strong JP. Risk factors and progression of atherosclerosis in youth. PDAY Research Group. Pathological Determinants of Atherosclerosis in Youth. Am J Pathol. 1998; 153: 1023–1033.
85. Tuzcu EM, Kapadia SR, Tutar E, et al. High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults: evidence from intravascular ultrasound. Circulation. 2001; 103: 2705–2710.
86. Pasterkamp G, Schoneveld AH, van der Wal AC, et al. Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox. J Am Coll Cardiol. 1998; 32: 655–662.
87. Becker CR, Nikolaou K, Muders M, et al. Ex vivo coronary atherosclerotic plaque characterization with multi-detector-row CT. Eur Radiol. 2003; 12: 12.
88. Vogel RA. Heads and hearts: the endothelial connection. Circulation. 2003; 107: 2766–2768.
89. Targonski PV, Bonetti PO, Pumper GM, et al. Coronary endothelial dysfunction is associated with an increased risk of cerebrovascular events. Circulation. 2003; 107: 2805–2809.
90. Cusack MR, Marber MS, Lambiase PD, et al. Systemic inflammation in unstable angina is the result of myocardial necrosis. J Am Coll Cardiol. 2002; 39: 1917–1923.
91. Yamamoto H, Uemura S, Tomoda Y, et al. Transcardiac gradient of soluble adhesion molecules predicts progression of coronary artery disease. Int J Cardiol. 2002; 84: 249–257.[CrossRef][Medline] [Order article via Infotrieve]
92. Moreno PR, Purushothaman KR, Fuster V, et al. Intimomedial interface damage and adventitial inflammation is increased beneath disrupted atherosclerosis in the aorta: implications for plaque vulnerability. Circulation. 2002; 105: 2504–2511.
93. Friedman M, Van den Borenkamp G.J. The pathogenesis of a coronary thrombus. Am J Pathol. 1966; 48: 19–44.[Medline] [Order article via Infotrieve]
94. Friedman M. The pathogenesis of coronary plaques, thromboses, and hemorrhages: an evaluative review. Circulation. 1975; 52 (suppl III): III34–III40.[Medline] [Order article via Infotrieve]
95. Halcox JP, Schenke WH, Zalos G, et al. Prognostic value of coronary vascular endothelial function. Circulation. 2002; 106: 653–658.
This article has been cited by other articles:
 |
|
 |
|
  J. Herrmann, D. Mannheim, C. Wohlert, D. Versari, F. B. Meyer, J. P. McConnell, M. Gossl, L. O. Lerman, and A. Lerman Expression of lipoprotein-associated phospholipase A2 in carotid artery plaques predicts long-term cardiac outcome Eur. Heart J., December 1, 2009; 30(23): 2930 - 2938. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. A. Parikh and M. A. Costa Secondary Prevention, the Interventional Way: Prophylactic Drug-Eluting Stents for Nonobstructive Saphenous Vein Graft Disease Circulation, November 17, 2009; 120(20): 1940 - 1942. [Full Text] [PDF]
|
|
|
|
 |
|
 G. Bastarrika, Y. S. Lee, W. Huda, B. Ruzsics, P. Costello, and U. J. Schoepf CT of Coronary Artery Disease Radiology, November 1, 2009; 253(2): 317 - 338. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Wischgoll, J. S. Choy, and G. S. Kassab Extraction of morphometry and branching angles of porcine coronary arterial tree from CT images Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1949 - H1955. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Kumar and C. P. Cannon Acute Coronary Syndromes: Diagnosis and Management, Part I Mayo Clin. Proc., October 1, 2009; 84(10): 917 - 938. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V O Puntmann How-to guide on biomarkers: biomarker definitions, validation and applications with examples from cardiovascular disease Postgrad. Med. J., October 1, 2009; 85(1008): 538 - 545. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S Lavi, J-H Bae, C S Rihal, A Prasad, G W Barsness, R J Lennon, D R Holmes Jr, and A Lerman Segmental coronary endothelial dysfunction in patients with minimal atherosclerosis is associated with necrotic core plaques Heart, September 15, 2009; 95(18): 1525 - 1530. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Schouten, E. Boersma, S. E. Hoeks, R. Benner, H. van Urk, M. R.H.M. van Sambeek, H. J.M. Verhagen, N. A. Khan, M. Dunkelgrun, J. J. Bax, et al. Fluvastatin and Perioperative Events in Patients Undergoing Vascular Surgery N. Engl. J. Med., September 3, 2009; 361(10): 980 - 989. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M Ni, W Q Chen, and Y Zhang Animal models and potential mechanisms of plaque destabilisation and disruption Heart, September 1, 2009; 95(17): 1393 - 1398. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Nozaki, S. Sugiyama, H. Koga, K. Sugamura, K. Ohba, Y. Matsuzawa, H. Sumida, K. Matsui, H. Jinnouchi, and H. Ogawa Significance of a multiple biomarkers strategy including endothelial dysfunction to improve risk stratification for cardiovascular events in patients at high risk for coronary heart disease. J. Am. Coll. Cardiol., August 11, 2009; 54(7): 601 - 608. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.-K. Hong, D.-W. Park, C.-W. Lee, S.-W. Lee, Y.-H. Kim, D.-H. Kang, J.-K. Song, J.-J. Kim, S.-W. Park, and S.-J. Park Effects of Statin Treatments on Coronary Plaques Assessed by Volumetric Virtual Histology Intravascular Ultrasound Analysis J. Am. Coll. Cardiol. Intv., July 1, 2009; 2(7): 679 - 688. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Wagenknecht, B. Wasserman, L. Chambless, J. Coresh, A. Folsom, T. Mosley, C. Ballantyne, R. Sharrett, and E. Boerwinkle Correlates of Carotid Plaque Presence and Composition as Measured by MRI: The Atherosclerosis Risk in Communities Study Circ Cardiovasc Imaging, July 1, 2009; 2(4): 314 - 322. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Laitinen, A. Saraste, E. Weidl, T. Poethko, A. W. Weber, S. G. Nekolla, P. Leppanen, S. Yla-Herttuala, G. Holzlwimmer, A. Walch, et al. Evaluation of {alpha}v{beta}3 Integrin-Targeted Positron Emission Tomography Tracer 18F-Galacto-RGD for Imaging of Vascular Inflammation in Atherosclerotic Mice Circ Cardiovasc Imaging, July 1, 2009; 2(4): 331 - 338. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. A. Jaffer, P. Libby, and R. Weissleder Optical and Multimodality Molecular Imaging: Insights Into Atherosclerosis Arterioscler Thromb Vasc Biol, July 1, 2009; 29(7): 1017 - 1024. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Suzuki, A. C. Yeung, and F. Ikeno The Pre-Clinical Animal Model in the Translational Research of Interventional Cardiology J. Am. Coll. Cardiol. Intv., May 1, 2009; 2(5): 373 - 383. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Xiong, Y.-B. Deng, Y. Zhu, Y.-N. Liu, and X.-J. Bi Correlation of Carotid Plaque Neovascularization Detected by Using Contrast-enhanced US with Clinical Symptoms Radiology, May 1, 2009; 251(2): 583 - 589. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Pellegrin, F. Alonso, J.-F. Aubert, K. Bouzourene, V. Braunersreuther, F. Mach, J.-A. Haefliger, D. Hayoz, A. Berthelot, J. Nussberger, et al. Swimming Prevents Vulnerable Atherosclerotic Plaque Development in Hypertensive 2-Kidney, 1-Clip Mice by Modulating Angiotensin II Type 1 Receptor Expression Independently From Hemodynamic Changes Hypertension, May 1, 2009; 53(5): 782 - 789. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. T. de Weert, S. Cretier, H. C. Groen, P. Homburg, H. Cakir, J. J. Wentzel, D. W.J. Dippel, and A. van der Lugt Atherosclerotic Plaque Surface Morphology in the Carotid Bifurcation Assessed With Multidetector Computed Tomography Angiography Stroke, April 1, 2009; 40(4): 1334 - 1340. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Seimon and I. Tabas Mechanisms and consequences of macrophage apoptosis in atherosclerosis J. Lipid Res., April 1, 2009; 50(Supplement): S382 - S387. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. U Farooq, A. Khasnis, A. Majid, and M. Y Kassab The role of optical coherence tomography in vascular medicine Vascular Medicine, February 1, 2009; 14(1): 63 - 71. [Abstract] [PDF]
|
|
|
|
 |
|
 L. Saba, R. Sanfilippo, L. Pascalis, R. Montisci, and G. Mallarini Carotid Artery Abnormalities and Leukoaraiosis in Elderly Patients: Evaluation with MDCT Am. J. Roentgenol., February 1, 2009; 192(2): W63 - W70. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. A. Osborn and F. A. Jaffer The year in molecular imaging. J. Am. Coll. Cardiol. Img., January 1, 2009; 2(1): 97 - 113. [Full Text] [PDF]
|
|
|
|
|
|
W. Peeters, W.E. Hellings, D.P.V. de Kleijn, J.P.P.M. de Vries, F.L. Moll, A. Vink, and G. Pasterkamp Carotid Atherosclerotic Plaques Stabilize After Stroke: Insights Into the Natural Process of Atherosclerotic Plaque Stabilization Arterioscler Thromb Vasc Biol, January 1, 2009; 29(1): 128 - 133. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. W. Hamm, H. Möllmann, J.-P. Bassand, and F. van de Werf CHAPTER 16 Acute Coronary Syndromes ESC Textbook of Cardiovascular Medicine, January 1, 2009; 2(1): med-9780199566990-chapter - med-9780199566990-chapter. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. A. Jaffer, C. Vinegoni, M. C. John, E. Aikawa, H. K. Gold, A. V. Finn, V. Ntziachristos, P. Libby, and R. Weissleder Real-Time Catheter Molecular Sensing of Inflammation in Proteolytically Active Atherosclerosis Circulation, October 28, 2008; 118(18): 1802 - 1809. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Beaussier, I. Masson, C. Collin, E. Bozec, B. Laloux, D. Calvet, M. Zidi, P. Boutouyrie, and S. Laurent Carotid Plaque, Arterial Stiffness Gradient, and Remodeling in Hypertension Hypertension, October 1, 2008; 52(4): 729 - 736. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. Goldberger, M. E. Cain, S. H. Hohnloser, A. H. Kadish, B. P. Knight, M. S. Lauer, B. J. Maron, R. L. Page, R. S. Passman, D. Siscovick, et al. American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Scientific Statement on Noninvasive Risk Stratification Techniques for Identifying Patients at Risk for Sudden Cardiac Death: A Scientific Statement From the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention J. Am. Coll. Cardiol., September 30, 2008; 52(14): 1179 - 1199. [Full Text] [PDF]
|
|
|
|
|
|
J. J. Goldberger, M. E. Cain, S. H. Hohnloser, A. H. Kadish, B. P. Knight, M. S. Lauer, B. J. Maron, R. L. Page, R. S. Passman, D. Siscovick, et al. American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Scientific Statement on Noninvasive Risk Stratification Techniques for Identifying Patients at Risk for Sudden Cardiac Death: A Scientific Statement From the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention Circulation, September 30, 2008; 118(14): 1497 - 1518. [Full Text] [PDF]
|
|
|
|
|
|
D. G. Katritsis and B. Meier Percutaneous Coronary Intervention for Stable Coronary Artery Disease J. Am. Coll. Cardiol., September 9, 2008; 52(11): 889 - 893. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Fujii, M. Masutani, T. Okumura, D. Kawasaki, T. Akagami, A. Ezumi, T. Sakoda, T. Masuyama, and M. Ohyanagi Frequency and Predictor of Coronary Thin-Cap Fibroatheroma in Patients With Acute Myocardial Infarction and Stable Angina Pectoris: A 3-Vessel Optical Coherence Tomography Study J. Am. Coll. Cardiol., August 26, 2008; 52(9): 787 - 788. [Full Text] [PDF]
|
|
|
|
|
|
J. Ohayon, G. Finet, A. M. Gharib, D. A. Herzka, P. Tracqui, J. Heroux, G. Rioufol, M. S. Kotys, A. Elagha, and R. I. Pettigrew Necrotic core thickness and positive arterial remodeling index: emergent biomechanical factors for evaluating the risk of plaque rupture Am J Physiol Heart Circ Physiol, August 1, 2008; 295(2): H717 - H727. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. A. Bluemke, S. Achenbach, M. Budoff, T. C. Gerber, B. Gersh, L. D. Hillis, W. G. Hundley, W. J. Manning, B. F. Printz, M. Stuber, et al. Noninvasive Coronary Artery Imaging: Magnetic Resonance Angiography and Multidetector Computed Tomography Angiography: A Scientific Statement From the American Heart Association Committee on Cardiovascular Imaging and Intervention of the Council on Cardiovascular Radiology and Intervention, and the Councils on Clinical Cardiology and Cardiovascular Disease in the Young Circulation, July 29, 2008; 118(5): 586 - 606. [Full Text] [PDF]
|
|
|
|
|
|
F. Alfonso The "vulnerable" stent why so dreadful? J. Am. Coll. Cardiol., June 24, 2008; 51(25): 2403 - 2406. [Full Text] [PDF]
|
|
|
|
|
|
J. N. Redgrave, P. Gallagher, J. K. Lovett, and P. M. Rothwell Critical Cap Thickness and Rupture in Symptomatic Carotid Plaques: The Oxford Plaque Study Stroke, June 1, 2008; 39(6): 1722 - 1729. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Wintermark, S.S. Jawadi, J.H. Rapp, T. Tihan, E. Tong, D.V. Glidden, S. Abedin, S. Schaeffer, G. Acevedo-Bolton, B. Boudignon, et al. High-Resolution CT Imaging of Carotid Artery Atherosclerotic Plaques AJNR Am. J. Neuroradiol., May 1, 2008; 29(5): 875 - 882. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Yoshida, O. Narumi, M. Chin, K. Inoue, T. Tabuchi, K. Oda, M. Nagayama, N. Egawa, M. Hojo, Y. Goto, et al. Characterization of Carotid Atherosclerosis and Detection of Soft Plaque with Use of Black-Blood MR Imaging AJNR Am. J. Neuroradiol., May 1, 2008; 29(5): 868 - 874. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Nussberger, J.-F. Aubert, K. Bouzourene, M. Pellegrin, D. Hayoz, and L. Mazzolai Renin Inhibition by Aliskiren Prevents Atherosclerosis Progression: Comparison With Irbesartan, Atenolol, and Amlodipine Hypertension, May 1, 2008; 51(5): 1306 - 1311. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Ambrose In Search of the "vulnerable plaque": can it be localized and will focal regional therapy ever be an option for cardiac prevention? J. Am. Coll. Cardiol., April 22, 2008; 51(16): 1539 - 1542. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Rundek, H. Arif, B. Boden-Albala, M. S. Elkind, M. C. Paik, and R. L. Sacco Carotid plaque, a subclinical precursor of vascular events: The Northern Manhattan Study Neurology, April 1, 2008; 70(14): 1200 - 1207. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. von Lukowicz, P. O. Hassa, C. Lohmann, J. Boren, V. Braunersreuther, F. Mach, B. Odermatt, M. Gersbach, G. G. Camici, B. E. Stahli, et al. PARP1 is required for adhesion molecule expression in atherogenesis Cardiovasc Res, April 1, 2008; 78(1): 158 - 166. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Rossi, A. Nuzzo, G. Origliani, and M. G. Modena Prognostic role of flow-mediated dilation and cardiac risk factors in post-menopausal women. J. Am. Coll. Cardiol., March 11, 2008; 51(10): 997 - 1002. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Saam, H. R. Underhill, B. Chu, N. Takaya, J. Cai, N. L. Polissar, C. Yuan, and T. S. Hatsukami Prevalence of American Heart Association type VI carotid atherosclerotic lesions identified by magnetic resonance imaging for different levels of stenosis as measured by duplex ultrasound. J. Am. Coll. Cardiol., March 11, 2008; 51(10): 1014 - 1021. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Gottlieb and J. A.C. Lima Screening High-Risk Patients With Computed Tomography Angiography Circulation, March 11, 2008; 117(10): 1318 - 1332. [Full Text] [PDF]
|
|
|
|
|
|
A. Fougerat, S. Gayral, P. Gourdy, A. Schambourg, T. Ruckle, M. K. Schwarz, C. Rommel, E. Hirsch, J.-F. Arnal, J.-P. Salles, et al. Genetic and Pharmacological Targeting of Phosphoinositide 3-Kinase-{gamma} Reduces Atherosclerosis and Favors Plaque Stability by Modulating Inflammatory Processes Circulation, March 11, 2008; 117(10): 1310 - 1317. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. H. Laughlin, S. C. Newcomer, and S. B. Bender Importance of hemodynamic forces as signals for exercise-induced changes in endothelial cell phenotype J Appl Physiol, March 1, 2008; 104(3): 588 - 600. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. M. Heikkila, S. Latti, M. J. Leskinen, J. K. Hakala, P. T. Kovanen, and K. A. Lindstedt Activated Mast Cells Induce Endothelial Cell Apoptosis by a Combined Action of Chymase and Tumor Necrosis Factor-{alpha} Arterioscler Thromb Vasc Biol, February 1, 2008; 28(2): 309 - 314. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. A. Wasserman, A. R. Sharrett, S. Lai, A. S. Gomes, M. Cushman, A. R. Folsom, D. E. Bild, R. A. Kronmal, S. Sinha, and D. A. Bluemke Risk Factor Associations With the Presence of a Lipid Core in Carotid Plaque of Asymptomatic Individuals Using High-Resolution MRI: The Multi-Ethnic Study of Atherosclerosis (MESA) Stroke, February 1, 2008; 39(2): 329 - 335. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Vidula, L. Tian, K. Liu, M. H. Criqui, L. Ferrucci, W. H. Pearce, P. Greenland, D. Green, J. Tan, D. B. Garside, et al. Biomarkers of Inflammation and Thrombosis as Predictors of Near-Term Mortality in Patients with Peripheral Arterial Disease: A Cohort Study Ann Intern Med, January 15, 2008; 148(2): 85 - 93. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. V. Raman, M. W. Winner III, T. Tran, M. Velayutham, O. P. Simonetti, P. B. Baker, J. Olesik, B. McCarthy, A. K. Ferketich, and J. L. Zweier In vivo atherosclerotic plaque characterization using magnetic susceptibility distinguishes symptom-producing plaques. J. Am. Coll. Cardiol. Img., January 1, 2008; 1(1): 49 - 57. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. R. S. Packard and P. Libby Inflammation in Atherosclerosis: From Vascular Biology to Biomarker Discovery and Risk Prediction Clin. Chem., January 1, 2008; 54(1): 24 - 38. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Saba and G. Mallarini MDCTA of Carotid Plaque Degree of Stenosis: Evaluation of Interobserver Agreement Am. J. Roentgenol., January 1, 2008; 190(1): W41 - W46. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Takumi, S. Lee, S. Hamasaki, K. Toyonaga, D. Kanda, K. Kusumoto, H. Toda, T. Takenaka, M. Miyata, R. Anan, et al. Limitation of Angiography to Identify the Culprit Plaque in Acute Myocardial Infarction With Coronary Total Occlusion: Utility of Coronary Plaque Temperature Measurement to Identify the Culprit Plaque J. Am. Coll. Cardiol., December 4, 2007; 50(23): 2197 - 2203. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Hausleiter, T. Meyer, M. Hadamitzky, M. Zankl, P. Gerein, K. Dorrler, A. Kastrati, S. Martinoff, and A. Schomig Non-invasive coronary computed tomographic angiography for patients with suspected coronary artery disease: the Coronary Angiography by Computed Tomography with the Use of a Submillimeter resolution (CACTUS) trial Eur. Heart J., December 2, 2007; 28(24): 3034 - 3041. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Simon, G. Chironi, and J. Levenson Comparative performance of subclinical atherosclerosis tests in predicting coronary heart disease in asymptomatic individuals Eur. Heart J., December 2, 2007; 28(24): 2967 - 2971. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Shah, P. Balan, M. Weinberg, V. Reddy, R. Neems, M. Feinstein, J. Dainauskas, P. Meyer, M. Goldin, and S. B. Feinstein Contrast-enhanced ultrasound imaging of atherosclerotic carotid plaque neovascularization: a new surrogate marker of atherosclerosis? Vascular Medicine, November 1, 2007; 12(4): 291 - 297. [Abstract] [PDF]
|
|
|
|
 |
|
 D. Cui, E. Thorp, Y. Li, N. Wang, L. Yvan-Charvet, A. R. Tall, and I. Tabas Pivotal Advance: Macrophages become resistant to cholesterol-induced death after phagocytosis of apoptotic cells J. Leukoc. Biol., November 1, 2007; 82(5): 1040 - 1050. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Q. Chen, L. Zhang, Y. F. Liu, L. Chen, X. P. Ji, M. Zhang, Y. X. Zhao, G. H. Yao, C. Zhang, X. L. Wang, et al. Prediction of atherosclerotic plaque ruptures with high-frequency ultrasound imaging and serum inflammatory markers Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H2836 - H2844. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Sabeti, O. Schlager, M. Exner, W. Mlekusch, J. Amighi, P. Dick, G. Maurer, K. Huber, R. Koppensteiner, O. Wagner, et al. Progression of Carotid Stenosis Detected by Duplex Ultrasonography Predicts Adverse Outcomes in Cardiovascular High-Risk Patients Stroke, November 1, 2007; 38(11): 2887 - 2894. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A Blumenthal, A. Sherwood, S. D. Rogers, M. A. Babyak, P. Murali Doraiswamy, L. Watkins, B. M. Hoffman, C. O'Connell, J. J. Johnson, S. M. Patidar, et al. Understanding prognostic benefits of exercise and antidepressant therapy for persons with depression and heart disease: the UPBEAT study rationale, design, and methodological issues Clinical Trials, October 1, 2007; 4(5): 548 - 559. [Abstract] [PDF]
|
|
|
|
|
|
J. Horiguchi, C. Fujioka, M. Kiguchi, Y. Shen, C. E. Althoff, H. Yamamoto, and K. Ito Soft and Intermediate Plaques in Coronary Arteries: How Accurately Can We Measure CT Attenuation Using 64-MDCT? Am. J. Roentgenol., October 1, 2007; 189(4): 981 - 988. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Angelini, M. Della Barbera, and G. Thiene Interventional procedures for atherothrombosis: pathology of retrieved material Heart, October 1, 2007; 93(10): 1301 - 1308. [Full Text] [PDF]
|
|
|
|
|
|
C. Ebeling Barbier, T. Bjerner, T. Hansen, J. Andersson, L. Lind, J. Hulthe, L. Johansson, and H. Ahlstrom Clinically Unrecognized Myocardial Infarction Detected at MR Imaging May Not Be Associated with Atherosclerosis Radiology, October 1, 2007; 245(1): 103 - 110. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P.-G. Chassot, A. Delabays, and D. R. Spahn Perioperative antiplatelet therapy: the case for continuing therapy in patients at risk of myocardial infarction Br. J. Anaesth., September 1, 2007; 99(3): 316 - 328. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. White, S. J. Duffy, A. S. Walton, J. F. Ng, G. E. Rice, S. Mukherjee, J. A. Shaw, G. L. Jennings, A. M. Dart, and B. A. Kingwell Matrix metalloproteinase-3 and coronary remodelling: Implications for unstable coronary disease Cardiovasc Res, September 1, 2007; 75(4): 813 - 820. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. A. Jaffer, P. Libby, and R. Weissleder Molecular Imaging of Cardiovascular Disease Circulation, August 28, 2007; 116(9): 1052 - 1061. [Full Text] [PDF]
|
|
|
|
|
|
Y. Wang, Y. Zheng, W. Zhang, H. Yu, K. Lou, Y. Zhang, Q. Qin, B. Zhao, Y. Yang, and R. Hui Polymorphisms of KDR Gene Are Associated With Coronary Heart Disease J. Am. Coll. Cardiol., August 21, 2007; 50(8): 760 - 767. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. L. Anderson, C. D. Adams, E. M. Antman, C. R. Bridges, R. M. Califf, D. E. Casey Jr, W. E. Chavey II, F. M. Fesmire, J. S. Hochman, T. N. Levin, et al. ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) Developed in Collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine J. Am. Coll. Cardiol., August 14, 2007; 50(7): e1 - e157. [Full Text] [PDF]
|
|
|
|
 |
|
 P. Raggi and A. Bellasi Review: Imaging to assess effect of medical therapy in patients with diabetes mellitus The British Journal of Diabetes & Vascular Disease, July 1, 2007; 7(4): 157 - 164. [Abstract] [PDF]
|
|
|
|
|
|
Authors/Task Force Members, J.-P. Bassand, C. W. Hamm, D. Ardissino, E. Boersma, A. Budaj, F. Fernandez-Aviles, K. A.A. Fox, D. Hasdai, E. M. Ohman, et al. Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology Eur. Heart J., July 1, 2007; 28(13): 1598 - 1660. [Full Text] [PDF]
|
|
|
|
|
|
T. Saam, T. S. Hatsukami, N. Takaya, B. Chu, H. Underhill, W. S. Kerwin, J. Cai, M. S. Ferguson, and C. Yuan The Vulnerable, or High-Risk, Atherosclerotic Plaque: Noninvasive MR Imaging for Characterization and Assessment Radiology, July 1, 2007; 244(1): 64 - 77. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Ostling, B. Hedblad, G. Berglund, and I. Goncalves Increased Echolucency of Carotid Plaques in Patients With Type 2 Diabetes Stroke, July 1, 2007; 38(7): 2074 - 2078. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. S. Chatzizisis, A. U. Coskun, M. Jonas, E. R. Edelman, C. L. Feldman, and P. H. Stone Role of Endothelial Shear Stress in the Natural History of Coronary Atherosclerosis and Vascular Remodeling: Molecular, Cellular, and Vascular Behavior J. Am. Coll. Cardiol., June 26, 2007; 49(25): 2379 - 2393. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Saba, G. Caddeo, R. Sanfilippo, R. Montisci, and G. Mallarini CT and Ultrasound in the Study of Ulcerated Carotid Plaque Compared with Surgical Results: Potentialities and Advantages of Multidetector Row CT Angiography AJNR Am. J. Neuroradiol., June 1, 2007; 28(6): 1061 - 1066. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A.D. Hardie, C.M. Kramer, P. Raghavan, E. Baskurt, and K.R. Nandalur The Impact of Expansive Arterial Remodeling on Clinical Presentation in Carotid Artery Disease: A Multidetector CT Angiography Study AJNR Am. J. Neuroradiol., June 1, 2007; 28(6): 1067 - 1070. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. N. Tziakas, J. C. Kaski, G. K. Chalikias, C. Romero, S. Fredericks, I. K. Tentes, A. X. Kortsaris, D. I. Hatseras, and D. W. Holt Total Cholesterol Content of Erythrocyte Membranes Is Increased in Patients With Acute Coronary Syndrome: A New Marker of Clinical Instability? J. Am. Coll. Cardiol., May 29, 2007; 49(21): 2081 - 2089. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Wierman and W. M. Kohrt Review Article: Vascular and Metabolic Effects of Sex Steroids: New Insights Into Clinical Trials Reproductive Sciences, May 1, 2007; 14(4): 300 - 314. [Abstract] [PDF]
|
|
|
|
|
|
F. A. Jaffer, D.-E. Kim, L. Quinti, C.-H. Tung, E. Aikawa, A. N. Pande, R. H. Kohler, G.-P. Shi, P. Libby, and R. Weissleder Optical Visualization of Cathepsin K Activity in Atherosclerosis With a Novel, Protease-Activatable Fluorescence Sensor Circulation, May 1, 2007; 115(17): 2292 - 2298. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Hochman and P. G. Steg Does Preventive PCI Work? N. Engl. J. Med., April 12, 2007; 356(15): 1572 - 1574. [Full Text] [PDF]
|
|
|
|
|
|
W. E. Boden, R. A. O'Rourke, K. K. Teo, P. M. Hartigan, D. J. Maron, W. J. Kostuk, M. Knudtson, M. Dada, P. Casperson, C. L. Harris, et al. Optimal Medical Therapy with or without PCI for Stable Coronary Disease N. Engl. J. Med., April 12, 2007; 356(15): 1503 - 1516. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Schlager, M. Exner, W. Mlekusch, S. Sabeti, J. Amighi, P. Dick, O. Wagner, R. Koppensteiner, E. Minar, and M. Schillinger C-Reactive Protein Predicts Future Cardiovascular Events in Patients With Carotid Stenosis Stroke, April 1, 2007; 38(4): 1263 - 1268. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. R. Nandalur, A. D. Hardie, P. Raghavan, M. J. Schipper, E. Baskurt, and C. M. Kramer Composition of the Stable Carotid Plaque: Insights From a Multidetector Computed Tomography Study of Plaque Volume Stroke, March 1, 2007; 38(3): 935 - 940. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Segers, F. Helderman, C. Cheng, L. C.A. van Damme, D. Tempel, E. Boersma, P. W. Serruys, R. de Crom, A. F.W. van der Steen, P. Holvoet, et al. Gelatinolytic Activity in Atherosclerotic Plaques Is Highly Localized and Is Associated With Both Macrophages and Smooth Muscle Cells In Vivo Circulation, February 6, 2007; 115(5): 609 - 616. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Fayad Endarterectomy and Stenting for Asymptomatic Carotid Stenosis: A Race at Breakneck Speed Stroke, February 1, 2007; 38(2): 707 - 714. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Namba, A. Tanaka, K. Shimada, Y. Ozeki, S. Uehata, T. Sakamoto, Y. Nishida, S. Nomura, and J. Yoshikawa Circulating Platelet-Derived Microparticles Are Associated With Atherothrombotic Events Arterioscler Thromb Vasc Biol, January 1, 2007; 27(1): 255 - 256. [Full Text] [PDF]
|
|
|
|
 |
|
 L. G. Spagnoli, S. Pucci, E. Bonanno, A. Cassone, F. Sesti, A. Ciervo, and A. Mauriello Persistent Chlamydia pneumoniae Infection of Cardiomyocytes Is Correlated with Fatal Myocardial Infarction Am. J. Pathol., January 1, 2007; 170(1): 33 - 42. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||