ArticleCirculation. Cardiovascular imaging2018
Molecular Imaging of VWF (von Willebrand Factor) and Platelet Adhesion in Postischemic Impaired Microvascular Reflow.
Article in Circulation. Cardiovascular imaging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 40 citations in OpenAlex.
- Mouse models to study von Willebrand factor in thrombosis: a scoping review.Research and practice in thrombosis and haemostasis · 2026Article
- Inflammasome inhibition in myocardial infarction reduces early reperfusion injury and suppresses systemic plaque activation.Atherosclerosis · 2026Article
- Periprocedural Assessment of Coronary Microcirculatory Function to Predict Clinical Outcomes After Elective Percutaneous Coronary Intervention.Journal of the American Heart Association · 2025Article
- Removal of endothelial surface-associated von villebrand factor suppresses accelerate datherosclerosis after myocardial infarction.Journal of translational medicine · 2024Article
- Article
- Biomedical Imaging in Experimental Models of Cardiovascular Disease.Circulation research · 2022Review
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- Plasma and rhADAMTS13 reduce trauma-induced organ failure by restoring the ADAMTS13-VWF axis.Blood advances · 2021Observational
- Echocardiographic Molecular Imaging of the Effect of Anticytokine Therapy for Atherosclerosis.Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography · 2021Article
- Overexpression of Activating Transcription Factor 3 Alleviates Cardiac Microvascular Ischemia/Reperfusion Injury in Rats.Frontiers in pharmacology · 2021Article
- Microvascular Impairment After Myocardial Infarction: It Is Not Just About Obstruction.Circulation. Cardiovascular imaging · 2020Article
- Ultrasound molecular imaging: insights into cardiovascular pathology.Journal of echocardiography · 2020Review
- Noninvasive Evaluation of No-Reflow Phenomenon.Circulation. Cardiovascular imaging · 2018Article
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9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundComplete mechanistic understanding of impaired microvascular reflow after myocardial infarction will likely lead to new therapies for reducing infarct size. Myocardial contrast echocardiography perfusion imaging and molecular imaging were used to evaluate the contribution of microvascular endothelial-associated VWF (von Willebrand factor) and platelet adhesion to microvascular no-reflow. METHODS AND
resultsMyocardial infarction was produced by transient LAD ligation in WT (wild type) mice, WT mice treated with the VWF proteolytic enzyme ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin type 1 motif, member 13), and ADAMTS13-deficient (ADAMTS13-/-) mice. Myocardial contrast echocardiography perfusion imaging and molecular imaging of VWF and platelet GP (glycoprotein) Ibα were performed 30 minutes after ischemia-reperfusion. Infarct size was measured at 3 days. Mortality during ischemia-reperfusion incrementally increased in WT+ADAMTS13, WT, and ADAMTS13-/- mice (14%, 43%, and 63%, respectively; P<0.05). For WT mice, molecular imaging signal for platelets and VWF in the postischemic risk area was 4- to 5-fold higher ( P<0.05) compared with both the remote nonischemic regions or to sham-treated mice. Signal enhancement in the risk area was completely abolished by ADAMTS13 treatment for both platelets (12.8±3.3 versus -1.0±4.4 IU; P<0.05) and VWF (13.9±4.0 versus -1.0±3.0 IU; P<0.05). ADAMTS13-/- compared with WT mice had 2- to 3-fold higher risk area signal for platelets (33.1±8.5 IU) and VWF (30.9±1.9 IU). Microvascular reflow in the risk area incrementally decreased for WT+ADAMTS13, WT, and ADAMTS13-/- mice ( P<0.05), whereas infarct size incrementally increased ( P<0.05).
conclusionsMechanistic information on microvascular no-reflow is possible by combining perfusion and molecular imaging. In reperfused myocardial infarction, excess endothelial-associated VWF and secondary platelet adhesion in the risk area microcirculation contribute to impaired reflow and are modifiable.
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