Platelet activation and thrombosis in microvascular obstruction
Abstract
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.
Related
- CO087 | PLATELET ACTIVATION AND THROMBOSIS IN PATIENTS WITH FACTOR V LEIDEN MUTATION: A CROSS-SECTIONAL STUDY
- Strategies to reduce microvascular obstruction and infarct size in patients with ST-elevation myocardial infarction
- Exploratory predictive value of novel inflammatory biomarkers for microvascular obstruction after emergency revascularization in STEMI patients
- PO150 | FACTOR XII DEFICIENCY IN THE SETTING OF RECURRENT THROMBOSIS AND EXTENDED VENOUS OBSTRUCTION: A CASE ANALYSIS
- Activation of Platelet Caspase-1 and P-Selectin Over-Expression in Sickle Cell Disease Patients: An Involvement of NLRP3 Inflammasome?
BibTeX
@article{balmforth2026platelet,
title = {{Platelet activation and thrombosis in microvascular obstruction}},
author = {Craig Balmforth and Alessandro Giaj Levra and Beth Whittington and Aidan Morgan and Mark G Macaskill and Evangelos Tzolos and Alex J Jordan and Tariq Ramtoola and Tim Clark and Michelle Rooney and Christophe Lucatelli and Edwin J R van Beek and Piotr J Slomka and Stephanie L Sellers and Norman Koglin and Andrew W Stephens and Iris Hardewig and David E Newby and Michelle C Williams and Marc R Dweck},
journal = {European Heart Journal Cardiovascular Imaging},
year = {2026},
month = aug,
doi = {10.1093/ehjci/jeag225},
url = {https://doi.org/10.1093/ehjci/jeag225},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Platelet activation and thrombosis in microvascular obstruction
AU - Craig Balmforth
AU - Alessandro Giaj Levra
AU - Beth Whittington
AU - Aidan Morgan
AU - Mark G Macaskill
AU - Evangelos Tzolos
AU - Alex J Jordan
AU - Tariq Ramtoola
AU - Tim Clark
AU - Michelle Rooney
AU - Christophe Lucatelli
AU - Edwin J R van Beek
AU - Piotr J Slomka
AU - Stephanie L Sellers
AU - Norman Koglin
AU - Andrew W Stephens
AU - Iris Hardewig
AU - David E Newby
AU - Michelle C Williams
AU - Marc R Dweck
PY - 2026
DA - 2026/08/30
JO - European Heart Journal Cardiovascular Imaging
DO - 10.1093/ehjci/jeag225
UR - https://doi.org/10.1093/ehjci/jeag225
AB - 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.
SN - 2047-2404
SN - 2047-2412
ER -