Strategies to reduce microvascular obstruction and infarct size in patients with ST-elevation myocardial infarction
- 1Department of Medicine, Division of Cardiology, University of Verona
- 2Department of Clinical and Molecular Medicine, Sapienza University
Abstract
Microvascular obstruction (MVO) remains a major challenge in patients with ST-segment elevation myocardial infarction (STEMI), as adequate myocardial reperfusion may not be achieved despite successful epicardial recanalization with primary percutaneous coronary intervention (pPCI). MVO results from multiple interacting mechanisms, including distal embolization, ischemia–reperfusion injury, inflammation, oxidative stress, and microvascular dysfunction, and is associated with larger infarct size and worse clinical outcomes. This review summarizes current and emerging strategies for the diagnosis, prevention, and treatment of MVO in STEMI. Advances in cardiac imaging and invasive or angiography-derived assessment of the coronary microcirculation may improve early identification and risk stratification. Therapeutic approaches include pharmacological and device-based strategies targeting thrombotic burden and distal embolization, reperfusion injury, inflammation, and oxidative stress. However, despite encouraging results for selected interventions, available evidence remains heterogeneous and no specific therapy has become standard of care for MVO. These findings highlight the need to move beyond a uniform approach to MVO. Integration of early diagnosis with identification of the predominant pathophysiological mechanism may provide a framework for future phenotype- and endotype-guided therapeutic strategies delivered within the appropriate therapeutic window. Whether such an approach can improve myocardial reperfusion and clinical outcomes after STEMI requires evaluation in adequately powered prospective trials.
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BibTeX
@article{rossignoli2026strategies,
title = {{Strategies to reduce microvascular obstruction and infarct size in patients with ST-elevation myocardial infarction}},
author = {Carlotta Rossignoli and Leonardo Portolan and Gabriele Pesarini and Simone Fezzi and Verdiana Galli and Andrea Pacchioni and Domenico Tavella and Flavio Ribichini and Roberto Scarsini and Martina Magistri},
journal = {Frontiers in Cardiovascular Medicine},
year = {2026},
month = oct,
doi = {10.3389/fcvm.2026.1981540},
url = {https://www.frontiersin.org/articles/10.3389/fcvm.2026.1981540/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Strategies to reduce microvascular obstruction and infarct size in patients with ST-elevation myocardial infarction
AU - Carlotta Rossignoli
AU - Leonardo Portolan
AU - Gabriele Pesarini
AU - Simone Fezzi
AU - Verdiana Galli
AU - Andrea Pacchioni
AU - Domenico Tavella
AU - Flavio Ribichini
AU - Roberto Scarsini
AU - Martina Magistri
PY - 2026
DA - 2026/10/19
JO - Frontiers in Cardiovascular Medicine
DO - 10.3389/fcvm.2026.1981540
UR - https://www.frontiersin.org/articles/10.3389/fcvm.2026.1981540/full
AB - Microvascular obstruction (MVO) remains a major challenge in patients with ST-segment elevation myocardial infarction (STEMI), as adequate myocardial reperfusion may not be achieved despite successful epicardial recanalization with primary percutaneous coronary intervention (pPCI). MVO results from multiple interacting mechanisms, including distal embolization, ischemia–reperfusion injury, inflammation, oxidative stress, and microvascular dysfunction, and is associated with larger infarct size and worse clinical outcomes. This review summarizes current and emerging strategies for the diagnosis, prevention, and treatment of MVO in STEMI. Advances in cardiac imaging and invasive or angiography-derived assessment of the coronary microcirculation may improve early identification and risk stratification. Therapeutic approaches include pharmacological and device-based strategies targeting thrombotic burden and distal embolization, reperfusion injury, inflammation, and oxidative stress. However, despite encouraging results for selected interventions, available evidence remains heterogeneous and no specific therapy has become standard of care for MVO. These findings highlight the need to move beyond a uniform approach to MVO. Integration of early diagnosis with identification of the predominant pathophysiological mechanism may provide a framework for future phenotype- and endotype-guided therapeutic strategies delivered within the appropriate therapeutic window. Whether such an approach can improve myocardial reperfusion and clinical outcomes after STEMI requires evaluation in adequately powered prospective trials.
SN - 2297-055X
ER -