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J Am Coll Cardiol, 2007; 49:1740-1749, doi:10.1016/j.jacc.2006.11.050 (Published online 3 April 2007).
© 2007 by the American College of Cardiology Foundation
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The Year in Atherothrombosis

Javier Sanz, MD, Pedro R. Moreno, MD, FACC and Valentin Fuster, MD, PhD, FACC*

The Zena and Michael A. Wiener Cardiovascular Institute/Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, Mount Sinai School of Medicine, New York, New York.


Figure 1
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  		Figure 1 Worldwide Causes of Death Secondary to Chronic Diseases

Reprinted with permission from Fuster V, Voute J. MDGs: chronic diseases are not on the agenda. Lancet 2005;366:1512–14. AIDS = acquired immunodeficiency syndrome; HIV = human immunodeficiency virus.

 

Figure 2
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  		Figure 2 Predictive Value of H-FABP After an Acute Coronary Syndrome

Rates of death, myocardial infarction (MI), or congestive heart failure (CHF) stratified by baseline concentration of brain natriuretic peptide (BNP), troponin I (Tn), or heart-type fatty acid binding protein (H-FABP) in the OPUS-TIMI 16 study. BNP + = BNP >80 pg/ml; Tn + = troponin I >1.5 ng/ml. Reproduced with permission from O’Donoghue et al. (20).

 

Figure 3
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  		Figure 3 Plaque Inflammation and Haptoglobin Variants

Color illustrations and bar graphs comparing macrophage content in atherosclerotic plaques of apolipoprotein E knockout mice with the haptoglobin (Hp) 1-1 or Hp 2-2 genotype. Increased macrophage infiltration (black arrows) is noted in the Hp 2-2 plaques. Adapted with permission from Levy et al. (31).

 

Figure 4
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  		Figure 4 LDL Cholesterol and Coronary Disease Progression

Relationship between plasmatic low-density lipoprotein (LDL) cholesterol levels and progression/regression of disease (quantified as median change in percent atheroma volume) as derived from several intravascular ultrasound trials. Reproduced from Nissen et al. (65). (JAMA, April 5, 2006, Vol. 295, page 1563; Copyright © [2006], American Medical Association. All rights reserved.)

 

Figure 5
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  		Figure 5 Diagnostic Performance of Coronary Angiography With MRI and MDCT

Weighted sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of coronary angiography with multidetector computed tomography (MDCT) and magnetic resonance imaging (MRI) after inclusion of unassessable segments. Data from Schuijf et al. (41).

 

Figure 6
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  		Figure 6 Combined PET and MRI Detection of Plaque Inflammation

Transaxial cervical images obtained with high-resolution magnetic resonance imaging (HRMRI), 18fluorodeoxyglucose (FDG) positron emission tomography (PET), and fused images (FUSED) in a patient with transient right visual disturbance. (Row A) The magnetic resonance imaging (MRI) shows a large stenotic plaque in the right internal carotid artery (green arrow), which only shows mild radiotracer uptake on the FDG-PET and fused images (blue and red arrows). (Row B) At a different position, MRI shows the vertebral arteries (yellow arrows), whereas the FDG-PET and fused images show a highly inflamed right vertebral artery plaque (white and black arrows) that could be the cause of the patient’s symptoms. Reproduced with permission from Davies et al. (48).

 

Figure 7
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  		Figure 7 Coronary Atheroma Regression Associated With High-Intensity Statin Therapy

(Top) Baseline and follow-up intravascular ultrasound images of a single coronary cross section after 24 months of rosuvastatin treatment. (Bottom) Measurements superimposed on the same cross sections, showing the reduction in atheroma area. EEM = external elastic membrane. Reproduced with permission from Nissen et al. (65). (JAMA, April 5, 2006, Vol. 295, page 1563; Copyright © [2006], American Medical Association. All rights reserved.)

 




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Copyright © 2007 by the American College of Cardiology Foundation.