TY - JOUR
AU - Feuchtner, Gudrun, M
AB - A 52-year-old woman with a history of HIV infection, cigarette smoking, atypical chest pain, and elevated low-density lipoprotein cholesterol (LDL-c) (101 mg/dL) was examined with coronary computed tomography angiography (CCTA). CCTA showed multiple high-risk plaques with signs of plaque inflammation in the left anterior descending artery (LAD) and circumflex artery (CX) (Panel). During 5 years of antiretroviral therapy, biomarkers of inflammation (CD4 cells, neopterin) improved significantly: CD4+ cells increased from 4 to 177 cells/µL and neopterin decreased from 82.3 nmol/L to 10.8 nmol/L. Open in new tabDownload slide Open in new tabDownload slide The patient was prescribed rosuvastatin 10 mg, but she did not take the medication, hence LDL-c remained unchanged after 5 years. After 5 years, coronary calcium score increased mildly from 245.7 Agatston Units (AU) to 381.9 AU. CCTA revealed an impressive regression of multiple high-risk non-calcified lesions in the mid LAD and the proximal CX and a complete transformation into stable calcified lesions. The perivascular fat attenuation index (FAI) increased from being positive for perivascular oedema (−33 HU) in 2014 to above −70 HU (−86 HU) after 5 years, indicating reduced cardiovascular risk. We report full regression of non-calcified ‘high-risk’ plaque by CCTA, which transformed to stable calcified lesions after 5 years of anti-inflammatory (but not statin) treatment. While statins and novel PCSK94 inhibitors are known to induce non-calcified fibroatheroma regression, our case shows that not only statins but also anti-inflammatory mechanisms are important drivers of ‘high-risk’ lesions. CCTA allows for monitoring of therapy success in patients with inflammatory ‘high-risk plaque’. CCTA showed mild increase in coronary calcium from 2014 until 2019, with two new calcified nodules in the mid LAD and one in the proximal CX (arrows, right upper panel). Three-dimensional volume rendering technique (upper panel) and curved multiplanar reformation (lower panels). Transformation of non-calcified lesion (plaque density, 91 HU) in the mid LAD (arrow, left lower panel) into two calcified nodules 2019) with 582 HU (arrow, right lower panel) after 5 years. Similarly, in the proximal CX (arrow, lower panel), a non-calcified high-risk lesion (left) with positive remodelling metamorphosed into a stable calcified lesion with 483 HU (right) and perivascular fat index increased (lowest panel). Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
TI - The magic transformation of high-risk plaque to a calcified after 5 years: monitoring by computed tomography angiography: is inflammation the holy grail?
JO - European Heart Journal - Cardiovascular Imaging
DO - 10.1093/ehjci/jez130
DA - 2019-11-01
UR - https://www.deepdyve.com/lp/oxford-university-press/the-magic-transformation-of-high-risk-plaque-to-a-calcified-after-5-C921doOJVv
SP - 1315
VL - 20
IS - 11
DP - DeepDyve
ER -