Abstract
Transcoronary stem cell transfer and evolution of infarct-related artery atherosclerosis: evaluation with conventional and novel imaging techniques including Quantitative Virtual Histology (qVH)
- Department of Interventional Cardiology, Jagiellonian University Institute of Cardiology, Krakow, Poland
- John Paul II Hospital, Krakow, Poland
- Department of Cardiac and Vascular Diseases, Jagiellonian University, Institute of Cardiology, John Paul II Hospital, Krakow, Poland
- St. Adalbert’s Hospital, Poznan, Poland
- Department of Radiology, John Paul II Hospital, Krakow, Poland
- Jagiellonian University Department of Transplantation, Krakow, Poland
- Division of Cardiology and Structural Heart Diseases, Medical University of Silesia, Katowice, Poland
Introduction:
It has been suggested that infarct-related artery (IRA) atherosclerosis progression after stem cell transcoronary administration might represent a stem-cell mediated adverse effect.
Aim:
To evaluate, using conventional (quantitative coronary angiography, QCA, intravascular ultrasound – IVUS) and novel (quantitative virtual histology – qVH) tools, evolution of IRA atherosclerosis following transcoronary stem cell transfer.
Material and methods:
QCA, IVUS, VH-IVUS and qVH were performed in 22 consecutive patients (4 women) aged 59 years (data provided as median) undergoing a distal-to-stent infusion of 2.21 × 106 CD34+CXCR4+ autologous bone marrow cells via a cell delivery-dedicated perfusion catheter at anterior AMI day 7. Imaging was repeated at 12 months. This was a substudy of Myocardial Regeneration by Intracoronary Infusion of Selected Population of Stem Cells in Acute Myocardial Infarction (REGENT) Trial (NCT00316381).
Results:
18.2% subjects showed absence of distal-to-stent angiographic/IVUS atherosclerotic lesion(s) at baseline and no new lesion(s) at 12-months. In the remaining cohort, there were 28 lesions by QCA (32 by IVUS) at baseline and no new lesion(s) at follow-up. Three fibroatheromas evolved (2 to calcified fibroatheroma and 1 to a fibrocalcific lesion); other plaques maintained their stable (low-risk) phenotypes. Diameter stenosis of QCA-identified lesions was 29.5 vs. 26.5% (p = 0.012, baseline vs. 12-months). Gray-scale IVUS showed reduction in area stenosis (33.8 vs. 31.0%, p = 0.004) and plaque burden (66.27 vs. 64.56%, p = 0.009) at 12-months. Peak fibrotic plaque content increased from 70.41% to 75.0% (p = 0.004). qVH peak confluent necrotic core area and minimal fibrous cap thickness remained stable (0.64 vs. 0.59 mm2, p = 0.290, and 0.15 vs. 0.16 mm, p = 0.646).
Conclusions:
This study, using a range of classic and novel imaging techniques, indicates lack of any stimulatory effect of transcoronary stem cell transfer on coronary atherosclerosis. Whether, and to what extent, a moderate reduction in plaque burden and stenosis severity at 12-months results from optimized pharmacotherapy and/or stem cell transfer requires further elucidation.
Keywords
stem cells, progenitor cells, transcoronary administration, atherosclerosis
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