Cardiac α V β 3 integrin expression following acute myocardial infarction in humans.

Objective Maladaptive repair contributes towards the development of heart failure following myocardial infarction(MI). The alpha(v)beta(3) integrin receptor is a key mediator and determinant of cardiac repair. We aimed to establish whether alpha(v)beta(3) integrin expression determines myocardial recovery following MI. Methods F-18-Fluciclatide(a novel alpha(v)beta(3)-selective radiotracer) positron emission tomography(PET) and CT imaging and gadolinium-enhanced MRI(CMR) were performed in 21 patients 2 weeks after ST-segment elevation MI(anterior, n= 16; lateral, n= 4; inferior, n= 1). CMR was repeated 9 months after MI. 7 stable patients with chronic total occlusion(CTO) of a major coronary vessel and nine healthy volunteers underwent a single PET/CT and CMR. Results F-18-Fluciclatide uptake was increased at sites of acute infarction compared with remote myocardium (tissue-to-background ratio(TBRmean) 1.34 +/- 0.22 vs 0.85 +/- 0.17; p<0.001) and myocardium of healthy volunteers(TBRmean 1.34 +/- 0.22 vs 0.70 +/- 0.03; p<0.001). There was no F-18-fluciclatide uptake at sites of established prior infarction in patients with CTO, with activity similar to the myocardium of healthy volunteers (TBRmean 0.71 +/- 0.06 vs 0.70 +/- 0.03, p=0.83). F-18-Fluciclatide uptake occurred at sites of regional wall hypokinesia(wall motion index >= 1 vs 0; TBRmean 0.93 +/- 0.31 vs 0.80 +/- 0.26 respectively, p< 0.001) and subendocardial infarction. Importantly, although there was no correlation with infarct size(r=0.03, p=0.90) or inflammation(C reactive protein, r=-0.20, p=0.38), F-18-fluciclatide uptake was increased in segments displaying functional recovery(TBRmean 0.95 +/- 0.33 vs 0.81 +/- 0.27, p=0.002) and associated with increase in probability of regional recovery. Conclusion F-18-Fluciclatide uptake is increased at sites of recent MI acting as a biomarker of cardiac repair and predicting regions of recovery.