Ticagrelor-Related Severe Dyspnoea: Mechanisms, Characteristic Features, Differential Diagnosis and Treatment

Krakowiak, Alicja; Kuleta, Jakub; Plech, Iwona; Zarębiński, Maciej; Wojciechowska, Małgorzata; Wretowski, Dominik; Cudnoch-Jędrzejewska, Agnieszka

doi:10.1177/1179547620956634

Cited by 9 publications

(11 citation statements)

References 43 publications

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“…The incidence of ticagrelor-related dyspnea was the same in both patients with chronic heart failure or chronic obstructive pulmonary disease and those without these diseases [31]. Up to date, the two most plausible hypotheses explaining the potential mechanisms of ticagrelor-induced dyspnea have been debated [10,32]. In the literature, the greatest attention is paid to a structural similarity between ticagrelor and adenosine, activation of adenosine receptors (A1R), and stimulation of vagal C fibers via receptors.…”

Section: Introductionmentioning

confidence: 99%

“…Other authors state that ticagrelor can induce dyspnea via P2Y12 receptors present on vagal C fibers themselves. Some literature sources mention the third cause of dyspnea, i.e., ticagrelor-induced release of adenosine triphosphate (ATP) from erythrocytes; however, this hypothesis is less plausible (Figure 1) [10,32]. The most plausible hypotheses explaining the causes for the occurrence of ticagrelorrelated dyspnea are as follows [10,32]:…”

Section: Introductionmentioning

confidence: 99%

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Factors Determining Ticagrelor-Induced Dyspnea in Patients with Acute Coronary Syndrome

et al. 2022

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(1) Background: The aim of this study was to determine clinical and genetic factors predicting the development of dyspnea in patients receiving ticagrelor. (2) Methods: A total of 277 patients with acute myocardial infarction (with and without ST-segment elevation), who underwent coronary angiography and PTCA with stent implantation and treated with antiplatelet drugs (ticagrelor and aspirin), were enrolled in this study. Platelet aggregation (induction with high-sensitivity ADP, ADP HS) testing was performed using a MULTIPLATE analyzer and reagents for the determination of P2Y12 receptor activity. Venous blood samples were collected for genotyping. (3) Results: Patients experiencing ticagrelor-related dyspnea had lower ADP HS. ROC curve analysis showed that an ADP HS cut-off of ≤19.5 U was associated with the development of dyspnea. The ADP HS value of ≤19.5 U and any dose of atorvastatin lower than 80 mg (or no atorvastatin) increased the risk of dyspnea by more than 4 and 2 times, respectively (OR = 4.07, p ≤ 0.001 and OR = 2.25; p = 0.008). (4) Conclusion: A lower ADP HS value possibly indicates greater ticagrelor activity and a higher plasma concentration of this drug. Atorvastatin might have an impact on the occurrence of ticagrelor-related dyspnea by affecting ticagrelor metabolism. No impact of any genetic variant on the development of dyspnea was determined.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Factors Determining Ticagrelor-Induced Dyspnea in Patients with Acute Coronary Syndrome

et al. 2022

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“…Across the lungs, there are no pathological auscultatory characteristics, although severe bronchial spasms with a reduction in blood oxygen may be found. Dyspnea attacks frequently recur over the course of a few hours or even days [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

“…Bradycardia and blocks in the conduction system arise approximately two hours after taking the medication, last for a short time, and then disappear; in most cases, they do not manifest clinically [ 9 ]. The most frequent type of bradyarrhythmia is sinus bradycardia (39.6%), followed by dropped beats (31.2%) and then ventricular pauses (5.8%) predominantly due to AV node pauses and secondarily due to AV blocks [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Pathophysiological and Molecular Basis of the Side Effects of Ticagrelor: Lessons from a Case Report

Cesarini¹,

Muraca²,

Berteotti

et al. 2023

IJMS

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Ticagrelor is currently considered a first-line choice in dual antiplatelet therapy (DAPT) following revascularization of acute coronary syndrome (ACS). However, its use is correlated with an increased incidence of two side effects, dyspnea and bradyarrhythmias, whose molecular mechanisms have not yet been defined with certainty and, consequently, neither of the therapeutic decisions they imply. We report the case of a patient with acute myocardial infarction treated with ticagrelor and aspirin as oral antithrombotic therapy after primary percutaneous coronary intervention (PCI), manifesting in a significant bradyarrhythmic episode that required a switch of antiplatelet therapy. Starting from this case report, this article aims to gather the currently available evidence regarding the molecular mechanisms underlying these side effects and propose possible decision-making algorithms regarding their management in clinical practice.

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“…Although ticagrelor is generally well tolerated [ 41 ], dyspnea which is mild to moderate in severity was observed in premarketing studies [ 42 , 43 ]. Dyspnea, related to ticagrelor therapy mainly develops shortly after the first days of treatment and has been linked to the increased extracellular level of adenosine [ 44 ]. In the present trial, early onset of dyspnea cases was reported only in the brand Brilique®.…”

Section: Discussionmentioning

confidence: 99%

Testing P2Y12 platelet inhibitors generics beyond bioequivalence: a parallel single-blinded randomized trial

et al. 2022

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Cardiovascular diseases are the leading cause of death worldwide. Ticagrelor is an oral antiplatelet drug used in acute coronary syndrome. Although generic drugs are approved for their bioequivalence to the original product, they are not necessarily to be therapeutically equivalent. This study was conducted to prove the efficacy and safety of ticagrelor generically named Ticaloguard® compared to its brand Brilique® in healthy volunteers. A loading dose of 180 mg ticagrelor named Brilique® or Ticaloguard® followed by a 90 mg twice daily regimen as maintenance dose was given to 14 and 15 volunteers in Tica and Brili groups, respectively. The platelet aggregation on the ADP agonist was assessed at baseline and repeated 1 h and 3 h after the loading dose, on day 4 (after reaching steady-state), 12 and 24 h after discontinuation of the antiplatelet drug. Adverse effects from trial medications were noted by direct questions. It was shown that generic Ticaloguard® provides a similar therapeutic effect and safety as its branded Brilique® (p > 0.05). This will permit safe and trusted use of the generic Ticaloguard® when treating it in the same manner as Brilique®. Testing generic drug effects rather than simple bioequivalency, especially for drugs that are used in critical life-threatening situations, is crucial. We advocate applying this form of a clinical trial to test surrogate clinical efficacy for generics used in critical indications before having real-world data whenever possible.

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Ticagrelor-Related Severe Dyspnoea: Mechanisms, Characteristic Features, Differential Diagnosis and Treatment

Cited by 9 publications

References 43 publications

Factors Determining Ticagrelor-Induced Dyspnea in Patients with Acute Coronary Syndrome

Factors Determining Ticagrelor-Induced Dyspnea in Patients with Acute Coronary Syndrome

Pathophysiological and Molecular Basis of the Side Effects of Ticagrelor: Lessons from a Case Report

Testing P2Y12 platelet inhibitors generics beyond bioequivalence: a parallel single-blinded randomized trial

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