ArticleFrontiers in physiology2021
Acute Heart Failure After Reperfused Ischemic Stroke: Association With Systemic and Cardiac Inflammatory Responses.
Article in Frontiers in physiology, 2021. 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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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- APOM-associated inflammation and apoptosis in stroke-exacerbated myocardial infarction: implications for brain-heart interactions.Apoptosis : an international journal on programmed cell death · 2026Article
- Clinical correlates of early post-PCI left ventricular ejection fraction in patients with STEMI: a single-center retrospective study.BMC cardiovascular disorders · 2026Article
- Bidirectional brain-heart interactions in health and disease.Nature reviews. Neurology · 2026Review
- NF-Frontiers in cardiovascular medicine · 2026Article
- Article
- The Heart-Brain Axis: Key Concepts in Neurocardiology.Cardiology discovery · 2025Review
- Cardiometabolic Dysregulation and Heart Failure.Reviews in cardiovascular medicine · 2025Review
- Identification of risk factors for myocardial injury in acute ischemic stroke with diabetes mellitus: a retrospective cohort study on stroke-heart syndrome.Frontiers in stroke · 2025Article
- Stroke-heart syndrome: current progress and future outlook.Journal of neurology · 2024Review
- Post-stroke arrhythmia could be a potential predictor for post-stroke depression.Scientific reports · 2024Article
- Stroke Related Brain-Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Mechanisms of inflammation after ischemic stroke in brain-peripheral crosstalk.Frontiers in molecular neuroscience · 2024Review
- Stroke-Heart Syndrome: Recent Advances and Challenges.Journal of the American Heart Association · 2022Review
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with acute ischemic stroke (AIS) present an increased incidence of systemic inflammatory response syndrome and release of Troponin T coinciding with cardiac dysfunction. The nature of the cardiocirculatory alterations remains obscure as models to investigate systemic interferences of the brain-heart-axis following AIS are sparse. Thus, this study aims to investigate acute cardiocirculatory dysfunction and myocardial injury in mice after reperfused AIS. Ischemic stroke was induced in mice by transient right-sided middle cerebral artery occlusion (tMCAO). Cardiac effects were investigated by electrocardiograms, 3D-echocardiography, magnetic resonance imaging (MRI), invasive conductance catheter measurements, histology, flow-cytometry, and determination of high-sensitive Troponin T (hsTnT). Systemic hemodynamics were recorded and catecholamines and inflammatory markers in circulating blood and myocardial tissue were determined by immuno-assay and flow-cytometry. Twenty-four hours following tMCAO hsTnT was elevated 4-fold compared to controls and predicted long-term survival. In parallel, systolic left ventricular dysfunction occurred with impaired global longitudinal strain, lower blood pressure, reduced stroke volume, and severe bradycardia leading to reduced cardiac output. This was accompanied by a systemic inflammatory response characterized by granulocytosis, lymphopenia, and increased levels of serum-amyloid P and interleukin-6. Within myocardial tissue, MRI relaxometry indicated expansion of extracellular space, most likely due to inflammatory edema and a reduced fluid volume. Accordingly, we found an increased abundance of granulocytes, apoptotic cells, and upregulation of pro-inflammatory cytokines within myocardial tissue following tMCAO. Therefore, reperfused ischemic stroke leads to specific cardiocirculatory alterations that are characterized by acute heart failure with reduced stroke volume, bradycardia, and changes in cardiac tissue and accompanied by systemic and local inflammatory responses.
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