{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jenkins WS"],"funding":["British Heart Foundation","Medical Research Council","Wellcome Trust","Academy of Medical Sciences"],"pagination":["607-615"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5566089"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["103(8)"],"pubmed_abstract":["

Objective

Maladaptive repair contributes towards the development of heart failure following myocardial infarction (MI). The αvβ3 integrin receptor is a key mediator and determinant of cardiac repair. We aimed to establish whether αvβ3 integrin expression determines myocardial recovery following MI.

Methods

18F-Fluciclatide (a novel αvβ3-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

18F-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 18F-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). 18F-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), 18F-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

18F-Fluciclatide uptake is increased at sites of recent MI acting as a biomarker of cardiac repair and predicting regions of recovery.

Trial registration number

NCT01813045; Post-results."],"journal":["Heart (British Cardiac Society)"],"pubmed_title":["Cardiac α<sub>V</sub>β<sub>3</sub> integrin expression following acute myocardial infarction in humans."],"pmcid":["PMC5566089"],"funding_grant_id":["G0701127","RG/16/10/32375","AMS-SGCL1-Rudd","FS/13/77/30488","FS/12/29/29463","PG/12/8/29371","FS/14/78/31020","PG/09/083/27667","FS/12/84/29814","RM/13/2/30158","FS/16/19/31982"],"pubmed_authors":["Jenkins WS","Pawade T","Vesey AT","Wilson I","Neale A","Rudd JH","Moles C","Vickers A","Newby DE","Connell M","Dweck MR","Lucatelli C","Mirsadraee S","Stirrat C","Fletcher A","van Beek EJ"],"additional_accession":[]},"is_claimable":false,"name":"Cardiac α<sub>V</sub>β<sub>3</sub> integrin expression following acute myocardial infarction in humans.","description":"

Objective

Maladaptive repair contributes towards the development of heart failure following myocardial infarction (MI). The αvβ3 integrin receptor is a key mediator and determinant of cardiac repair. We aimed to establish whether αvβ3 integrin expression determines myocardial recovery following MI.

Methods

18F-Fluciclatide (a novel αvβ3-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

18F-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 18F-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). 18F-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), 18F-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

18F-Fluciclatide uptake is increased at sites of recent MI acting as a biomarker of cardiac repair and predicting regions of recovery.

Trial registration number

NCT01813045; Post-results.","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Apr","modification":"2026-06-16T05:03:03.598Z","creation":"2026-06-16T03:07:42.045Z"},"accession":"S-EPMC5566089","cross_references":{"pubmed":["27927700"],"doi":["10.1136/heartjnl-2016-310115"]}}