biostudies-literatureJenkins WSBritish Heart FoundationMedical Research CouncilWellcome TrustAcademy of Medical Sciences607-615https://www.ebi.ac.uk/biostudies/studies/S-EPMC5566089biostudies-literatureUnknown103(8)<h4>Objective</h4>Maladaptive repair contributes towards the development of heart failure following myocardial infarction (MI). The α_vβ₃ integrin receptor is a key mediator and determinant of cardiac repair. We aimed to establish whether α_vβ₃ integrin expression determines myocardial recovery following MI.<h4>Methods</h4>¹⁸F-Fluciclatide (a novel α_vβ₃-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.<h4>Results</h4>¹⁸F-Fluciclatide uptake was increased at sites of acute infarction compared with remote myocardium (tissue-to-background ratio (TBR_mean) 1.34±0.22 vs 0.85±0.17; p<0.001) and myocardium of healthy volunteers (TBR_mean 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 (TBR_mean 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; TBR_mean 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 (TBR_mean 0.95±0.33 vs 0.81±0.27, p=0.002) and associated with increase in probability of regional recovery.<h4>Conclusion</h4>¹⁸F-Fluciclatide uptake is increased at sites of recent MI acting as a biomarker of cardiac repair and predicting regions of recovery.<h4>Trial registration number</h4>NCT01813045; Post-results.Heart (British Cardiac Society)Cardiac α&lt;sub&gt;V&lt;/sub&gt;β&lt;sub&gt;3&lt;/sub&gt; integrin expression following acute myocardial infarction in humans.PMC5566089G0701127RG/16/10/32375AMS-SGCL1-RuddFS/13/77/30488FS/12/29/29463PG/12/8/29371FS/14/78/31020PG/09/083/27667FS/12/84/29814RM/13/2/30158FS/16/19/31982Jenkins WSPawade TVesey ATWilson INeale ARudd JHMoles CVickers ANewby DEConnell MDweck MRLucatelli CMirsadraee SStirrat CFletcher Avan Beek EJfalseCardiac α&lt;sub&gt;V&lt;/sub&gt;β&lt;sub&gt;3&lt;/sub&gt; integrin expression following acute myocardial infarction in humans.<h4>Objective</h4>Maladaptive repair contributes towards the development of heart failure following myocardial infarction (MI). The α_vβ₃ integrin receptor is a key mediator and determinant of cardiac repair. We aimed to establish whether α_vβ₃ integrin expression determines myocardial recovery following MI.<h4>Methods</h4>¹⁸F-Fluciclatide (a novel α_vβ₃-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.<h4>Results</h4>¹⁸F-Fluciclatide uptake was increased at sites of acute infarction compared with remote myocardium (tissue-to-background ratio (TBR_mean) 1.34±0.22 vs 0.85±0.17; p<0.001) and myocardium of healthy volunteers (TBR_mean 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 (TBR_mean 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; TBR_mean 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 (TBR_mean 0.95±0.33 vs 0.81±0.27, p=0.002) and associated with increase in probability of regional recovery.<h4>Conclusion</h4>¹⁸F-Fluciclatide uptake is increased at sites of recent MI acting as a biomarker of cardiac repair and predicting regions of recovery.<h4>Trial registration number</h4>NCT01813045; Post-results.2017-01-01T00:00:00Z2017 Apr2026-06-16T05:03:03.598Z2026-06-16T03:07:42.045ZS-EPMC55660892792770010.1136/heartjnl-2016-310115