Adenosine stress perfusion cardiac magnetic resonance imaging in patients undergoing intracoronary bone marrow cell transfer after ST-elevation myocardial infarction: the BOOST-2 perfusion substudy

Aims In the placebo-controlled, double-blind BOne marrOw transfer to enhance ST-elevation infarct regeneration (BOOST) 2 trial, intracoronary autologous bone marrow cell (BMC) transfer did not improve recovery of left ventricular ejection fraction (LVEF) at 6 months in patients with ST-elevation myo...

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Veröffentlicht in:Clinical research in cardiology 2020-05, Vol.109 (5), p.539-548
Hauptverfasser: Seitz, Andreas, Wollert, Kai C., Meyer, Gerd P., Müller-Ehmsen, Jochen, Tschöpe, Carsten, May, Andreas E., Empen, Klaus, Chorianopoulos, Emmanuel, Ritter, Benedikta, Pirr, Jens, Arseniev, Lubomir, Heuft, Hans-Gert, Ganser, Arnold, Abu-Zaid, Eed, Katus, Hugo A., Felix, Stephan B., Gawaz, Meinrad P., Schultheiss, Heinz-Peter, Ladage, Dennis, Bauersachs, Johann, Mahrholdt, Heiko, Greulich, Simon
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Sprache:eng
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Zusammenfassung:Aims In the placebo-controlled, double-blind BOne marrOw transfer to enhance ST-elevation infarct regeneration (BOOST) 2 trial, intracoronary autologous bone marrow cell (BMC) transfer did not improve recovery of left ventricular ejection fraction (LVEF) at 6 months in patients with ST-elevation myocardial infarction (STEMI) and moderately reduced LVEF. Regional myocardial perfusion as determined by adenosine stress perfusion cardiac magnetic resonance imaging (S-CMR) may be more sensitive than global LVEF in detecting BMC treatment effects. Here, we sought to evaluate (i) the changes of myocardial perfusion in the infarct area over time (ii) the effects of BMC therapy on infarct perfusion, and (iii) the relation of infarct perfusion to LVEF recovery at 6 months. Methods and results In 51 patients from BOOST-2 (placebo, n  = 10; BMC, n  = 41), S-CMR was performed 5.1 ± 2.9 days after PCI (before placebo/BMC treatment) and after 6 months. Infarct perfusion improved from baseline to 6 months in the overall patient cohort as reflected by the semi-quantitative parameters, perfusion defect–infarct size ratio (change from 0.54 ± 0.20 to 0.43 ± 0.22; P  = 0.006) and perfusion defect–upslope ratio (0.54 ± 0.23 to 0.68 ± 0.22; P 
ISSN:1861-0684
1861-0692
DOI:10.1007/s00392-019-01537-4