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, AESV, AEDV) 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)-treat-ed 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). AESV, AEDV, 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 y-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-AESV (p = 0.41) and IS-AEDV (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 (pro-portional 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.