eISSN: 1897-4295
ISSN: 1734-9338
Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej
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4/2022
vol. 18
 
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abstract:
Original paper

Infarct size and long-term left ventricular remodelling in acute myocardial infarction patients subjected to transcoronary delivery of progenitor cells

Łukasz Czyż
1
,
Łukasz Tekieli
1, 2
,
Tomasz Miszalski-Jamka
3
,
R. Paweł Banyś
3
,
Wojciech Szot
4
,
Wojciech Mazur
5
,
Jakub Chmiel
1
,
Adam Mazurek
1
,
Maciej Skubera
1
,
Władysław Dąbrowski
2
,
Danuta Jarocha
6
,
Piotr Podolec
1
,
Marcin Majka
7
,
Piotr Musiałek
1

  1. Department of Cardiac and Vascular Diseases, Jagiellonian University Medical College, John Paul II Hospital, Krakow, Poland
  2. Department of Interventional Cardiology, Jagiellonian University Medical College, John Paul II Hospital, Krakow, Poland
  3. Department of Radiology, John Paul II Hospital, Krakow, Poland
  4. Nuclear Imaging Laboratory, John Paul II Hospital, Krakow, Poland
  5. Division of Cardiology, The Christ Hospital Health Network, Cincinnati, United States of America
  6. Division of Hematology, Children’s Hospital of Philadelphia, Philadelphia, United States of America
  7. Department of Transplantation, Faculty of Medicine, Institute of Pediatrics, Jagiellonian University Medical College, Krakow, Poland
Adv Interv Cardiol 2022; 18, 4 (70): 465–471
Online publish date: 2023/02/06
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Introduction:
Infarct size (IS) is a fundamental determinant of left-ventricular (LV) remodelling (end-systolic and end-diastolic volume change, ESV, EDV) and adverse clinical outcomes after myocardial infarction (MI). Our prior work found that myocardial uptake of transcoronary-delivered progenitor cells is governed by IS.

Aim:
To evaluate the relationship between IS, stem cell uptake, and the magnitude of LV remodelling in patients receiving transcoronary administration of progenitor cells shortly after MI.

Material and methods:
Thirty-one subjects (age 36–69 years) with primary percutaneous coronary intervention (pPCI)-treated anterior ST-elevation MI (peak CK-MB 584 [181–962] U/l, median [range]) and sustained left ventricle ejection fraction (LVEF) ≤ 45% were studied. On day 10 (median) 4.3 x 106 (median) autologous CD34+ cells (50% labelled with 99mTc-extametazime) were administered via the infarct-related artery (left anterior descending). ΔESV, ΔEDV, and mid circumferential myocardial strain (mCS) were evaluated at 24 months.

Results:
Infarct mass (cMRI) was 57 [11–112] g. Cell label myocardial uptake (whole-body γ-scans) was proportional to IS (r = 0.62), with a median 2.9% uptake in IS 1st tercile (≤ 45 g), 5.2% in 2nd (46–76 g), and 6.7% in 3rd (> 76 g) (p = 0.0006). Cell uptake in proportion to IS attenuated the IS-ΔESV (p = 0.41) and IS-ΔEDV (p = 0.09) relationship. At 24 months, mCS improved in IS 2nd tercile (p = 0.028) while it showed no significant change in smaller (p = 0.87) or larger infarcts (p = 0.58).

Conclusions:
This largest human study with labelled CD34+ cell transplantation shortly after MI suggests that cell uptake (proportional to IS) may attenuate the effect of IS on LV adverse remodelling. To boost this effect, further strategies should involve cell types and delivery techniques to maximize myocardial uptake.

keywords:

cell therapy, infarct size, circumferential strain, myocardial infarction, left ventricular remodelling

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