scholarly journals Platelet reactivity during mild therapeutic hypothermia in patients with acute myocardial infarction treated with ticagrelor: study protocol of a single-centre study

2017 ◽  
Vol 1 (4) ◽  
pp. 115-119
Author(s):  
Julia Maria Umińska ◽  
Marek Koziński ◽  
Krzysztof Pstrągowski ◽  
Przemysław Paciorek ◽  
Tomasz Fabiszak ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Therapeutic Hypothermia ◽  
Study Protocol ◽  
Platelet Reactivity ◽  
Mild Therapeutic Hypothermia ◽  
Single Centre ◽  
Centre Study ◽  
Single Centre Study

Impact of diabetes on fibrinogen levels and its relationship with platelet reactivity and coronary artery disease: A single-centre study

2015 ◽  
Vol 109 (3) ◽  
pp. 541-550 ◽  
Author(s):  
Gabriella Di Giovine ◽  
Monica Verdoia ◽  
Lucia Barbieri ◽  
Alon Schaffer ◽  
Gianluca Aimaretti ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Reactivity ◽  
Single Centre ◽  
Centre Study ◽  
Single Centre Study ◽  
Artery Disease

Platelet inhibition with prasugrel in patients with acute myocardial infarction undergoing therapeutic hypothermia after cardiopulmonary resuscitation

2016 ◽  
Vol 115 (05) ◽  
pp. 960-968 ◽  
Author(s):  
Ulrike Flierl ◽  
Philipp Röntgen ◽  
Zauner Florian ◽  
Tongers Jörn ◽  
Berliner Dominik ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Therapeutic Hypothermia ◽  
Gastric Tube ◽  
Therapeutic Strategy ◽  
Platelet Reactivity ◽  
Platelet Inhibition ◽  
Reactivity Index ◽  
Vasopressor Use ◽  
Hospital Cardiac Arrest

SummaryAcute myocardial infarction (AMI) is the leading cause for out-of-hospital cardiac arrest. Therapeutic hypothermia improves neurological outcome in combination with early revascularisation, but seems to affect clopidogrel responsiveness. The more potent thienopyridine prasugrel has not yet been sufficiently evaluated during therapeutic hypothermia. We investigated 23 consecutive AMI patients (61 ± 11 years) following out-of-hospital resuscitation undergoing revascularisation and therapeutic hypothermia. Prasugrel efficacy was assessed by the platelet-reactivity-index (PRI) before and 2, 4, 6, 12, 24, 48, and 72 hours(h) following a loading dose of 60 mg via a gastric tube. Mean PRI (±SD) was 70 ± 12 % prior to loading and 60 ± 16 % (2 h, ns), 52 ± 21 % (4 h, p< 0.01), 42 ± 26 % (6 h, p< 0.01), 37 ± 21 % (12 h, p< 0.01), 27 ± 23 % (24 h, p< 0.01), 18 ± 14 % (48 h, p< 0.01), and 13 ± 10 % (72 h, p< 0.01) after loading. Sufficient platelet inhibition occurred later compared to stable AMI patients (6 h vs 2 h); however, high on-treatment platelet reactivity significantly decreased over time and was non-existent after 72 h (PRI> 50 %: 2 h: 72 %, 4 h: 52 %, 6 h: 43 %, 12 h: 29 %, 24 h: 17 %, 48 h: 5 %, 72 h: 0 %). There was no relation between 30-day mortality rate (26 %) and PRI values. Prasugrel significantly reduced platelet reactivity even during vasopressor use, analgosedation and therapeutic hypothermia. Despite a significant delay compared to stable AMI patients, sufficient platelet inhibition was reached in 83 % of patients within 24 h. Therefore, prasugrel administration via gastric tube might be a useful therapeutic strategy in these patients at high risk, providing potent and effective P2Y12 inhibition.

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