Heart Block Caused by Ticagrelor Use in a Patient Who Underwent Adenosine Diastolic Fractional Reserve Assessment: A
Asseel Al-Bayati1, Kyle Wiseman1, Ndausung Udongwo1
1Department of Internal Medicine, Jersey Shore University Medical Center, Neptune, NJ, USA.
Insights
Ticagrelor, a P2Y12 receptor antagonist, can cause bradycardia. This case highlights recurrent sinus arrest and ventricular asystole in a patient treated with ticagrelor.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Ticagrelor is a P2Y12 receptor antagonist recommended for acute coronary syndromes.
- It offers superior P2Y12 inhibition compared to clopidogrel.
- Ticagrelor also increases blood adenosine levels, enhancing cardioprotective effects.
Observation:
- A patient pre-treated with ticagrelor experienced recurrent sinus arrest and ventricular asystole.
- Physiological assessment involved fractional flow reserve (FFR) with adenosine infusion.
Findings:
- Ticagrelor's inhibition of adenosine transporters may contribute to adverse effects like bradycardia.
- The case demonstrates a potential link between ticagrelor, adenosine levels, and cardiac arrhythmias.
Implications:
- Clinicians should be aware of ticagrelor's potential to cause significant bradyarrhythmias.
- Further research may explore the role of adenosine in ticagrelor-associated cardiac events.
Abstract:
Ticagrelor is a direct and rapid-acting antagonist of the P2Y12-adenosine diphosphate receptor found on platelets. The drug is recommended as a first-line antiplatelet agent in patients with acute coronary syndromes, as evidenced in its superiority compared to clopidogrel according to the Platelet Inhibition and Patient Outcomes study. Specifically, the mechanism of action has been proven to show higher inhibition and less variability in its action on P2Y12 receptors compared to clopidogrel. Additionally, ticagrelor inhibits the equilibrative nucleoside transporter 1 adenosine transporter protein leading to an increased concentration of adenosine in the blood, particularly at sites of ischemia. This effect increases the biological efficacy of ticagrelor in terms of cardioprotection, anticoagulation effects, and anti-inflammatory effects. However, the effects are also thought to be responsible for some of the adverse pharmacological effects reported with ticagrelor, such as bradycardia and ventricular pauses > 3 seconds. Herein, we report a case of recurrent sinus arrest and ventricular asystole in a patient pre-treated with ticagrelor and subsequent physiological assessment of a coronary lesion with fractional flow reserve using intravenous adenosine infusion.
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