Impact of lipid abnormalities in development and progression of transplant coronary disease: a serial intravascular ultrasound study
Samir R. Kapadia, MDa,
Steven E. Nissen, MD, FACCa,
Khaled M. Ziada, MDa,
Gustavo Rincon, MD, FACCa,
Timothy D. Crowe, BSa,
Navdeep Boparai, MSa,
James B. Young, MD, FACCa and
E. Murat Tuzcu, MD, FACCa
a Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
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Figure 1 Identical site in the left anterior descending artery from a baseline (A) and one-year follow-up (B) study. The lesion in the baseline image is from atherosclerosis transmitted from donor with maximum plaque thickness of 0.5 mm. The branch vessel (arrow) along with angiographic landmarks help to identify the same site from the follow-up study. This is an example of donor lesion progression where the maximum plaque thickness is increased by 0.4 mm at follow-up study.
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Figure 2 Identical site in the left circumflex artery from a baseline (A) and one-year follow-up (B) study. There is no intimal thickening at baseline. However, when the same site is identified using pericardium and a branch vessel as a landmark, significant intimal thickening (0.6 mm) is identified at the same site. This is an example of de novo lesion of transplant vasculopathy.
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