ArticleJournal of the American Heart Association2018
GLP-1 Is a Coronary Artery Vasodilator in Humans.
Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Effect of Hemoglobin A1c Reduction or Weight Reduction on Blood Pressure in Glucagon-Like Peptide-1 Receptor Agonist and Sodium-Glucose Cotransporter-2 Inhibitor Treatment in Type 2 Diabetes Mellitus: A Meta-Analysis.Journal of the American Heart Association · 2020Pooled it
- GLP-1 vasodilatation in humans with coronary artery disease is not adenosine mediated.BMC cardiovascular disorders · 2021Trial
- Mechanisms of GLP-1 Receptor Agonists in HFpEF: Exploring Weight-Dependent and Independent Drivers of Therapeutic Benefit.Circulation. Heart failure · 2026Review
- Acute Contractile Effects of Glucagon-like-Peptide-1 Receptor Agonists in the Human Heart.Pharmaceutics · 2026Review
- Glucagon-like Peptide-1 Receptor Dependent Signaling in Cardiovascular Health and Disease: A Mini-review.Journal of cardiovascular translational research · 2026Review
- Coronary microvascular dysfunction in systemic inflammatory diseases: From pathophysiology and prevalence to diagnosis and management.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2025Review
- Immune and Vascular Function in Cardiometabolic Disorders: Interplay With Sex Differences and Impact on Incretin Therapy.Acta physiologica (Oxford, England) · 2025Review
- Current Evidence-Based Treatment of Angina With Nonobstructive Coronary Arteries (ANOCA).Journal of the Society for Cardiovascular Angiography & Interventions · 2025Review
- GLP-1 Receptor Agonists and Myocardial Perfusion: Bridging Mechanisms to Clinical Outcomes.International journal of molecular sciences · 2025Review
- Mechanisms of ferroptosis and glucagon-like peptide-1 receptor agonist in post-percutaneous coronary intervention restenosis.Molecular and cellular biochemistry · 2025Review
- Semaglutide Improves Myocardial Perfusion and Performance in a Large Animal Model of Coronary Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- G Protein-Coupled Receptors: A Century of Research and Discovery.Circulation research · 2024Review
- Transforming Diabetes Care: The Molecular Pathways through Which GLP1-RAs Impact the Kidneys in Diabetic Kidney Disease.Biomedicines · 2024Review
- Glucagon-like peptide 1 receptor agonists: cardiovascular benefits and mechanisms of action.Nature reviews. Cardiology · 2023Review
- Glucagon-Like Peptide-1 Receptor Agonist Protects Against Diabetic Cardiomyopathy by Modulating microRNA-29b-3p/SLMAP.Drug design, development and therapy · 2023Article
- Coronary Microvascular Dysfunction in Diabetes Mellitus: Pathogenetic Mechanisms and Potential Therapeutic Options.Biomedicines · 2022Review
- A single dose of exenatide had no effect on blood flow velocity in the middle cerebral artery in elderly healthy volunteers: Randomized, placebo-controlled, double-blind clinical trial.Frontiers in aging neuroscience · 2022Article
- GLP-1 Receptor Agonists and Coronary Arteries: From Mechanisms to Events.Frontiers in pharmacology · 2022Review
- Revisiting the Complexity of GLP-1 Action from Sites of Synthesis to Receptor Activation.Endocrine reviews · 2021Review
- Cardiovascular effects of antiobesity drugs: are the new medicines all the same?International journal of obesity supplements · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Background The mechanism underlying the beneficial cardiovascular effects of the incretin GLP-1 (glucagon-like peptide 1) and its analogues in humans is elusive. We hypothesized that activating receptors located on vascular smooth muscle cells to induce either peripheral or coronary vasodilatation mediates the cardiovascular effect of GLP -1. Methods and Results Ten stable patients with angina awaiting left anterior descending artery stenting underwent forearm blood flow measurement using forearm plethysmography and post-percutaneous coronary intervention coronary blood flow measurement using a pressure-flow wire before and after peripheral GLP -1 administration. Coronary sinus and artery bloods were sampled for GLP -1 levels. A further 11 control patients received saline rather than GLP -1 in the coronary blood flow protocol. GLP -1 receptor (GLP-1R) expression was assessed by immunohistochemistry using a specific GLP -1R monoclonal antibody in human tissue to inform the physiological studies. There was no effect of GLP -1 on absolute forearm blood flow or forearm blood flow ratio after GLP -1, systemic hemodynamics were not affected, and no binding of GLP -1R monoclonal antibody was detected in vascular tissue. GLP -1 reduced resting coronary transit time (mean [ SD ], 0.87 [0.39] versus 0.63 [0.27] seconds; P=0.02) and basal microcirculatory resistance (mean [ SD ], 76.3 [37.9] versus 55.4 [30.4] mm Hg/s; P=0.02), whereas in controls, there was an increase in transit time (mean [SD], 0.48 [0.24] versus 0.83 [0.41] seconds; P<0.001) and basal microcirculatory resistance (mean [SD], 45.9 [34.7] versus 66.7 [37.2] mm Hg/s; P=0.02). GLP -1R monoclonal antibody binding was confirmed in ventricular tissue but not in vascular tissue, and transmyocardial GLP -1 extraction was observed. Conclusions GLP -1 causes coronary microvascular dilation and increased flow but does not influence peripheral tone. GLP -1R immunohistochemistry suggests that GLP -1 coronary vasodilatation is indirectly mediated by ventricular-coronary cross talk.
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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 Socratic graph.