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

INTRODUCTION

Infarct size (IS) is a fundamental determinant of left-ventricular (LV) remodelling (end-systolic and end-diastolic volume change, ΔESV, ΔEDV) 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 × 10 (median) autologous CD34+ cells (50% labelled with Tc-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 ( = 0.62), with a median 2.9% uptake in IS 1 tercile (≤ 45 g), 5.2% in 2 (46-76 g), and 6.7% in 3 (> 76 g) ( = 0.0006). Cell uptake in proportion to IS attenuated the IS-ΔESV ( = 0.41) and IS-ΔEDV ( = 0.09) relationship. At 24 months, mCS improved in IS 2 tercile ( = 0.028) while it showed no significant change in smaller ( = 0.87) or larger infarcts ( = 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.