European heart journal. Cardiovascular Imaging · 2026
Platelet activation and thrombosis in microvascular obstruction.
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Balmforth Craig, Giaj Levra Alessandro, Whittington Beth, Morgan Aidan, Macaskill Mark G, Tzolos Evangelos, Jordan Alex J, Ramtoola Tariq, Clark Tim, Rooney Michelle, Lucatelli Christophe, van Beek Edwin J R, Slomka Piotr J, Sellers Stephanie L, Koglin Norman, Stephens Andrew W, Hardewig Iris, Newby David E, Williams Michelle C, Dweck Marc R
Аннотация
AIMS: Microvascular obstruction (MVO) remains a major complication following coronary reperfusion, but its pathogenesis is poorly defined. We evaluated myocardial platelet activation and thrombosis using fluorine-18-labelled GP1 ([18F]GP1) positron emission tomography (PET) in patients with anterior ST-segment elevation myocardial infarction.
METHODS AND RESULTS: In a single-centre observational cohort study, 100 patients with acute anterior ST-segment elevation myocardial infarction underwent hybrid cardiac [18F]GP1 PET and magnetic resonance (MR) imaging with gadolinium enhancement and repeat imaging at 3-6 months. Myocardial [18F]GP1 uptake was quantified using target-to-background ratio (TBRmax) and percentage myocardial uptake (burden) and compared with MR measures of infarction, MVO and adverse ventricular remodelling. One hundred patients (60 ± 10 years, 91% male) underwent [18F]GP1 PET/MR imaging at a median of 13 days following index presentation. Increased myocardial [18F]GP1 uptake was observed in 44% of participants (TBRmax 1.89 ± 0.50). All 40 patients with MR-defined MVO demonstrated myocardial [18F]GP1 uptake. Myocardial [18F]GP1 uptake burden correlated with (ρ = 0.84; P < 0.001), and exceeded (by 18%), MR-defined burden of MVO. Myocardial [18F]GP1 uptake was associated with infarct size, lower left ventricular ejection fraction and longer time-to-reperfusion. Angiographic no-reflow was the strongest independent association of MVO (adjusted odds ratio 16.15; P < 0.001). Persistent myocardial [18F]GP1 uptake at follow up (22%, 7/32) was associated with lower left ventricular ejection fraction. Resolution of cardiac MR-defined MVO was observed in 78% of patients at follow-up and was universally concordant with resolution of myocardial [18F]GP1 uptake.
CONCLUSION: MVO following ST-segment elevation myocardial infarction is universally associated with myocardial platelet activation, extending beyond structural abnormalities identified by cardiac MR. These findings are consistent with an important mechanistic contribution of platelet-mediated microvascular thrombosis to no-reflow and MVO, highlighting a potentially targetable biological pathway in a condition for which effective therapies remain elusive.
METHODS AND RESULTS: In a single-centre observational cohort study, 100 patients with acute anterior ST-segment elevation myocardial infarction underwent hybrid cardiac [18F]GP1 PET and magnetic resonance (MR) imaging with gadolinium enhancement and repeat imaging at 3-6 months. Myocardial [18F]GP1 uptake was quantified using target-to-background ratio (TBRmax) and percentage myocardial uptake (burden) and compared with MR measures of infarction, MVO and adverse ventricular remodelling. One hundred patients (60 ± 10 years, 91% male) underwent [18F]GP1 PET/MR imaging at a median of 13 days following index presentation. Increased myocardial [18F]GP1 uptake was observed in 44% of participants (TBRmax 1.89 ± 0.50). All 40 patients with MR-defined MVO demonstrated myocardial [18F]GP1 uptake. Myocardial [18F]GP1 uptake burden correlated with (ρ = 0.84; P < 0.001), and exceeded (by 18%), MR-defined burden of MVO. Myocardial [18F]GP1 uptake was associated with infarct size, lower left ventricular ejection fraction and longer time-to-reperfusion. Angiographic no-reflow was the strongest independent association of MVO (adjusted odds ratio 16.15; P < 0.001). Persistent myocardial [18F]GP1 uptake at follow up (22%, 7/32) was associated with lower left ventricular ejection fraction. Resolution of cardiac MR-defined MVO was observed in 78% of patients at follow-up and was universally concordant with resolution of myocardial [18F]GP1 uptake.
CONCLUSION: MVO following ST-segment elevation myocardial infarction is universally associated with myocardial platelet activation, extending beyond structural abnormalities identified by cardiac MR. These findings are consistent with an important mechanistic contribution of platelet-mediated microvascular thrombosis to no-reflow and MVO, highlighting a potentially targetable biological pathway in a condition for which effective therapies remain elusive.