Platelet reactivity in comatose survivors of cardiac arrest undergoing percutaneous coronary intervention and hypothermia

Steblovnik, Klemen; Blinc, Aleš; Mijovski, Mojca Božič; Kranjec, Igor; Melkić, Enver; Noč, Marko

doi:10.4244/eijy14m05_02

Cited by 25 publications

(15 citation statements)

References 37 publications

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“…In addition, activation of the coagulation and anticoagulation system as well as simultaneous activation of endogenous fibrinolysis and anti-fibrinolysis may contribute to microcirculatory reperfusion disorders [ 14 , 15 ]. During the post-cardiac arrest phase with ongoing hypothermia, platelet inhibition by clopidogrel is almost nonexistent [ 16 – 18 ]. Unlike clopidogrel, ticagrelor does not require cytochrome p450 (CYP) conversion and there are no genetic polymorphisms known that may result in a loss of function, and therefore be of disadvantage in patients after OHCA [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Efficacy of enteral ticagrelor in hypothermic patients after out-of-hospital cardiac arrest

et al. 2015

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IntroductionDelivery of crushed ticagrelor via a nasogastric tube is a widely spread off-label use in unconscious patients following out-of-hospital cardiac arrest (OHCA). Notwithstanding the importance of a potent dual antiplatelet therapy in these patients, the efficacy of crushed ticagrelor after OHCA has not been established yet.MethodsIn a prospective, single-center, observational trial, 38 consecutive MI patients after OHCA were included. 27 patients (71.1 %) underwent mild induced hypothermia. The primary outcome was platelet inhibition at 24h measured by impedance aggregometry.ResultsThere was sufficient platelet inhibition in most patients after OHCA. In all hypothermic patients, there was an adequate platelet inhibition by ticagrelor at 24 h (p < 0.001). 15 patients (39.5 %) had significant gastroesophageal reflux and one patient with significant reflux had inadequate platelet inhibition at 24 h. There were no stent thrombosis or recurrent atherothrombotic events in these patients.ConclusionAdministration of crushed ticagrelor via a nasogastric tube reliably inhibited platelet function in vitro and in vivo regardless of the presence of hypothermia in MI patients. Thus, platelet inhibition can be reliably achieved in MI patients during neuroprotective hypothermia following OHCA.

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Section: Introductionmentioning

confidence: 99%

Efficacy of enteral ticagrelor in hypothermic patients after out-of-hospital cardiac arrest

et al. 2015

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“…In STEMI patients without CS or after CPR, the pre-hospital administration of ticagrelor was not associated with a better outcome [30]. It is known that In STEMI patients with CS or after CPR the optimal platelet inhibition occurs hours after administration of P2Y12 [1,18,20]. The time delay of P2Y12 administration would be expected to be of lesser importance in these patients since there is a delay of less than one hour in pre-hospital settings in comparison to in-hospital administration.…”

Section: Discussionmentioning

confidence: 99%

“…Prasugrel may inhibit platelets incompletely and seems to have similar pharmacodynamics as clopidogrel in patients with CS and therapeutic hypothermia [13,19]. Ticagrelor (without the need for biotransformation) inhibits platelets significantly earlier than clopidogrel; however, some non-responders were noticed after CPR and therapeutic hypothermia [18,20]. Newer P2Y12 were not yet proven to be clinically superior to clopidogrel in patients with CS and / or after CPR [13].…”

Section: Introductionmentioning

confidence: 99%

Impact of the New P2Y12 Receptor Inhibitors on Mortality in STElevation Myocardial Infarction Patients with Cardiogenic Shock and / or After Cardiopulmonary Resuscitation Undergoing Percutaneous Coronary Intervention

Kanic¹,

Vollrath²,

Naji³

et al. 2016

Cardiovasc Pharm Open Access

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IntroductionST-Elevation Myocardial Infarction (STEMI) represents a highly pro-thrombotic state with platelets being greatly activated [1,2]. The early and strong platelet inhibition seems to be of paramount importance in patients with STEMI undergoing Percutaneous Coronary Intervention (PCI) [3]. Newer P2Y12 receptor inhibitors prasugrel and ticagrelor (newer P2Y12) exhibit more rapid, potent, and consistent platelet inhibition than clopidogrel and reduce the risk for ischemic cardiovascular complications [4][5][6][7][8][9][10]. In STEMI patients, an initial delay in the onset of newer P2Y12 antiplatelet action was observed and ticagrelor did not appear superior to prasugrel [3]. However, patients with Cardiogenic Shock (CS) or after Cardio Pulmonary Resuscitation (CPR) were mostly excluded from randomized studies and data on the clinical efficacy of these drugs comparing to clopidogrel in these patients is sparse [11][12][13].CS has a profound effect on drug absorption and metabolism due to the disturbance of microcirculation, the use of catecholamines and opioids which results in slower platelet inhibition [13][14][15]. The pharmacological properties of the newer P2Y12 are promising in a CS setting since their bioactivation is more rapid and consistent when compared to clopidogrel [2,13].Mild therapeutic hypothermia leads to a pro-thrombotic milieu per se and activation of the P2Y12 receptor inhibitors (P2Y12) may AbstractBackground: Little is known about clinical efficacy of newer P2Y12 receptor inhibitors in ST-elevation myocardial infarction patients presenting with cardiogenic shock or after cardiopulmonary resuscitation. The aim of our study was to establish the possible role of newer P2Y12 receptor inhibitors prasugrel and ticagrelor on survival in comparison to clopidogrel administration in ST-elevation myocardial infarction patients presenting with cardiogenic shock and / or after cardiopulmonary resuscitation.

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“…The challenges of drug administration and the higher risk of stent thrombosis, which may be exacerbated by therapeutic hypothermia (see below), suggest the need for the administration of an intravenous antiplatelet agent to ‘bridge’ the delayed effect of oral P2Y12 inhibitors. There is recent evidence that administration of eptifibatide in this setting results in profound platelet inhibition for at least 22 h 81. Similarly, it has been demonstrated in patients with STEMI and no cardiac arrest that a bolus of abciximab without additional infusion might be sufficient 82.…”

Section: Is Immediate Cag Recommended For All Oohca Survivors?mentioning

confidence: 96%

Out-of-hospital cardiac arrest: contemporary management and future perspectives

Nerla

Webb

MacCarthy

2015

Heart

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Platelet reactivity in comatose survivors of cardiac arrest undergoing percutaneous coronary intervention and hypothermia

Cited by 25 publications

References 37 publications

Efficacy of enteral ticagrelor in hypothermic patients after out-of-hospital cardiac arrest

Efficacy of enteral ticagrelor in hypothermic patients after out-of-hospital cardiac arrest

Impact of the New P2Y12 Receptor Inhibitors on Mortality in STElevation Myocardial Infarction Patients with Cardiogenic Shock and / or After Cardiopulmonary Resuscitation Undergoing Percutaneous Coronary Intervention

Out-of-hospital cardiac arrest: contemporary management and future perspectives

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