Abstract
The majority of resuscitated patients present with underlying cardiac disease, and out of these myocardial infarction is most common. Immediate interventional treatment is recommended and routinely requires dual antiplatelet therapy including aspirin and a P2Y12-inhibitor. Therapeutic hypothermia or target temperature management is also recommended in these patients. Cardiogenic shock as well as reduced body temperature impacts platelet reactivity and its medical inhibition. The study aims to quantify aspirin- and P2Y12-mediated platelet inhibition in patients presenting with myocardial infarction and cardiopulmonary resuscitation. Twenty-five resuscitated patients were enrolled in this prospective, observational, non-randomized single-centre study. These patients were compared to 77 matched controls from the ATLANTIS-ACS database of non-resuscitated patients with myocardial infarction. Platelet function testing was performed by light transmittance aggregometry. Aspirin reactivity was monitored by inducing platelet aggregation with collagen and arachidonic acid, respectively. P2Y12 inhibition was recorded by stimulation of platelet aggregation with adenosine diphosphate. To quantify the overall platelet response, thrombin receptor-activated peptide was used. Aspirin-mediated platelet reactivity decreased significantly in resuscitated patients during the first days and was significantly weaker on day 3 (collagen AUC 253.8 (122.7–352.2) vs. 109.0 (73.0–182.0); p = 0.022). P2Y12-mediated platelet inhibition was also impaired in resuscitated patients on day 3 (mean ADP AUC (IQR): CPR 172.1 (46.7−346.5) vs. control 43.9 (18.9–115.2); p < 0.05). Aspirin- and P2Y12-mediated platelet inhibition is impaired in resuscitated patients treated with therapeutic hypothermia. On day 3, we recorded lowest inhibitory effects of both drug types and patients might be at particular risk at that time. Potentially, intravenous aspirin and P2Y12 inhibitors might still supply a more predictable and stable platelet inhibition.
Highlights
Therapeutic hypothermia as targeted temperature management of 32–36 °C for 24 h is still recommended for patients after cardiopulmonary resuscitation (CPR) to improve neurological outcome [1]
Demographic data were quite similar in both groups (Table 1) and within the group of resuscitated patients divided by the P2Y12 inhibitor used (Additional file 1: Table s1), patients with resuscitation had less
Our study indicates a moderate effect on platelet inhibition by P2Y12 inhibitors, which is, only detectable for ticagrelor and prasugrel
Summary
Therapeutic hypothermia as targeted temperature management of 32–36 °C for 24 h is still recommended for patients after cardiopulmonary resuscitation (CPR) to improve neurological outcome [1]. 60% of all out-of-hospital cardiac arrest patients have suffered acute myocardial infarction (AMI), and the majority of these patients undergo primary percutaneous intervention (PCI) and require dual antithrombotic therapy. Dual inhibition of platelet function with aspirin and a P2Y12 inhibitor is recommended as soon as possible in STEMI patients. Administration of platelet inhibitors is necessary as highest risk of stent thrombosis (ST) is reported within the early phase after stent implantation. There is evidence for an increased risk of stent thrombosis after PCI despite administration of antiplatelet drugs in resuscitated patients treated with therapeutic hypothermia [3, 4]. Underlying mechanisms of bioavailability are still unclear; both reduced gastrointestinal absorption due to cardiogenic shock and delayed metabolism as well as an accelerated platelet turnover due to inflammation might cause altered platelet inhibition and plasmatic coagulation
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