ArticleJournal of cachexia, sarcopenia and muscle2019
Experimental ischaemic stroke induces transient cardiac atrophy and dysfunction.
Article in Journal of cachexia, sarcopenia and muscle, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Brain-Heart Axis and Biomarkers of Cardiac Damage and Dysfunction after Stroke: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2020Pooled it
- Sympathetic nervous system-mediated fibro-adipogenic progenitor mobilization drives stroke-related sarcopenia.Cell discovery · 2026Article
- Article
- Bidirectional brain-heart interactions in health and disease.Nature reviews. Neurology · 2026Review
- Role of beta-blocker therapy on the sympathetic effects in stroke heart syndrome.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Article
- Astragali Radix-Carthami Flos alleviate brain-heart injury after cerebral ischemia/reperfusion via regulating TSPO signaling.NPJ science of food · 2025Article
- Article
- The Heart-Brain Axis: Key Concepts in Neurocardiology.Cardiology discovery · 2025Review
- A temperature-ultrasound sensitive nanoparticle delivery system for exploring central neuroinflammation mechanism in stroke-heart syndrome.Journal of nanobiotechnology · 2024Article
- Increased Myocardial MAO-A, Atrogin-1, and IL-1β Expression in Transgenic Mice with Pancreatic Carcinoma-Benefit of MAO-A Inhibition for Cardiac Cachexia.Biomedicines · 2024Article
- Stroke-heart syndrome: current progress and future outlook.Journal of neurology · 2024Review
- Stroke Related Brain-Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Immunological characterization of stroke-heart syndrome and identification of inflammatory therapeutic targets.Frontiers in immunology · 2023Article
- Systemic inflammation after stroke: implications for post-stroke comorbidities.EMBO molecular medicine · 2022Review
- Stroke-Heart Syndrome: Recent Advances and Challenges.Journal of the American Heart Association · 2022Review
- Iron deficiency is related to low functional outcome in patients at early rehabilitation after acute stroke.Journal of cachexia, sarcopenia and muscle · 2022Observational
- Advances in brain-heart syndrome: Attention to cardiac complications after ischemic stroke.Frontiers in molecular neuroscience · 2022Review
- Ischemic stroke induces cardiac dysfunction and alters transcriptome profile in mice.BMC genomics · 2021Article
- Neurological update: use of cardiac troponin in patients with stroke.Journal of neurology · 2021Review
- The Authors reply: Comment on: "Experimental ischaemic stroke induces transient cardiac atrophy" by Veltkamp et al.Journal of cachexia, sarcopenia and muscle · 2021Article
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStroke can lead to cardiac dysfunction in patients, but the mechanisms underlying the interaction between the injured brain and the heart are poorly understood. The objective of the study is to investigate the effects of experimental murine stroke on cardiac function and molecular signalling in the heart. METHODS AND
resultsMice were subjected to filament-induced left middle cerebral artery occlusion for 30 or 60 min or sham surgery and underwent repetitive micro-echocardiography. Left ventricular contractility was reduced early (24-72 h) but not late (2 months) after brain ischaemia. Cardiac dysfunction was accompanied by a release of high-sensitive cardiac troponin (hsTNT (ng/ml): d1: 7.0 ± 1.0 vs. 25.0 ± 3.2*; d3: 7.3 ± 1.1 vs. 52.2 ± 16.7*; d14: 5.7 ± 0.8 vs. 5.2 ± 0.3; sham vs. 60 min. MCAO; mean ± SEM; *p < 0.05); reduced heart weight (heart weight/tibia length ratio: d1: 6.9 ± 0.2 vs. 6.4 ± 0.1*; d3: 6.7 ± 0.2 vs. 5.8 ± 0.1*; d14: 6.7 ± 0.2 vs. 6.4 ± 03; sham vs. 60 min. MCAO; mean ± SEM; *p < 0.05); resulting from cardiomyocyte atrophy (cardiomyocyte size: d1: 12.8% ± 0.002**; d3: 13.5% ± 0.002**; 14d: 6.3% ± 0.003*; 60 min. MCAO vs. sham; mean ± SEM; **p < 0.01; *p < 0.05), accompanied by increased atrogin-1 and the E3 ubiquitin ligase murf-1. Net norepinephrine but not synthesis was increased, suggesting a reduced norepinephrine release or an increase of norepinephrine re-uptake, resulting in a functional denervation. Transcriptome analysis in cardiac tissue identified the transcription factor peroxisome proliferator-activated receptor gamma as a potential mediator of stroke-induced transcriptional dysregulation involved in cardiac atrophy.
conclusionsStroke induces a complex molecular response in the heart muscle with immediate but transient cardiac atrophy and dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.