ArticleMolecular medicine (Cambridge, Mass.)
Thrombin receptor and ventricular arrhythmias after acute myocardial infarction.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 17 citations in OpenAlex.
- TRAP-induced PAR1 expression with its mechanism during AMI in a rat model.BMC cardiovascular disorders · 2023Article
- Impact of Pre-Revascularization and Post-Revascularization Cardiac Arrest on Survival Prognosis in Patients With Acute Myocardial Infarction and Following Emergency Percutaneous Coronary Intervention.Frontiers in cardiovascular medicine · 2021Article
- Straight to the heart: Pleiotropic antiarrhythmic actions of oral anticoagulants.Pharmacological research · 2019Review
- Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction.Journal of geriatric cardiology : JGC · 2016Review
- Effects of thrombin and thrombin receptor activation on cardiac function after acute myocardial infarction.American journal of translational research · 2015Article
- Reduction in dynamin-2 is implicated in ischaemic cardiac arrhythmias.Journal of cellular and molecular medicine · 2014Article
- Thrombin and its receptor enhance ST-segment elevation in acute myocardial infarction by activating the KATP channel.Molecular medicine (Cambridge, Mass.)Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism mediating the development of ventricular arrhythmia (VA) after acute myocardial infarction (AMI) is still uncertain. Thrombin receptor (TR) activation has been proven to be arrhythmogenic in many other situations, and we hypothesize that it may participate in the genesis of post-AMI VA. Using a left coronary artery ligation rat model of AMI, we found that a local injection of hirudin into the left ventricle (LV) significantly reduced the ratio of VA durations to infarction sizing, whereas injection of thrombin receptor-activating peptide (TRAP) increased the ratios of VA duration to infarction sizing. The effects of TR activation on whole-cell currents were investigated in isolated myocytes. TRAP increased a glibenclamide-sensitive outward current. Pretreatment of rats with glibenclamide (4 mg/kg intraperitoneally) eliminated the effects of a local injection of TRAP on the ratios of VA durations to infarction sizing. TR mRNA and protein expression in the ischemic left ventricle had reached its peak by 20 min postligation in the rat AMI model (P < 0.05). TR-immunoreactive myocytes were observed in infarcted LV but were seldom seen in the right ventricle or in the normal heart. By 60 min, TR transcript levels had returned to control levels. We conclude that increased TR activation and expression in the infarcted LV after AMI may contribute to VA through a mechanism involving glibenclamide-sensitive potassium channels.
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