Culprit Plaque in Myocardial InfarctionGoing Beyond Angiography*
Aloke V. Finn, MD ,
Gaku Nakazawa, MD ,
Jagat Narula, MD, PhD, FACC and
Renu Virmani, MD, FACC ,*
Emory University School of Medicine, Atlanta, Georgia
CVPath Institute, Inc., Gaithersburg, Maryland
University of California, Irvine, California.

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Figure 1 Thrombus Propagation in Plaque Rupture
(A) Composite of a longitudinal section of proximal left anterior descending (LAD) and left diagonal (LD) coronary arteries with plaque rupture in the LAD. Note propagation of the thrombus upstream from the site of plaque rupture (arrowheads) extending up to the first major sidebranch (LD). (B) The same longitudinal section with Carstairs stain for detection of fibrin (dark red) and platelets (blue-gray). The proximal and distal propagated thrombus consists predominantly of fibrin and red cells, whereas the rupture site has platelet-rich thrombus. Modified with permission from Virmani et al., editors. The Vulnerable Plaque: Strategies for Diagnosis and Management. Malden, MA: Blackwell Publishing, 2007.
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Figure 2 Two Cases of Sudden Coronary Death
(A) Proximal section shows severe narrowing of the lumen with a relatively large necrotic core area (NC) in the absence of plaque rupture, whereas the distal nonstenotic section (B) reveals the rupture site (C) with a much smaller NC and an occlusive thrombus (Thr). It is therefore possible that intravascular ultrasound would not be able to detect the distal site of rupture, because the NC is small. (D and E) Section of left anterior descending coronary artery at the site of severest luminal narrowing with a nonocclusive Thr. Note large NC with overlying ruptured thin fibrous cap (box area) and a higher magnification in panel E. Intravascular ultrasound would easily detect the large NC.
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