scholarly journals Stent thrombosis in a patient with high on-treatment platelet reactivity despite ticagrelor treatment

2014 ◽  
Vol 4 (1) ◽  
pp. 85-87 ◽  
Author(s):  
Anees Musallam ◽  
Eli I Lev ◽  
Ariel Roguin
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Stent Thrombosis ◽  
Platelet Reactivity ◽  
Platelet Inhibition ◽  
Loading Dose

We describe, to the best of our knowledge, the first incidence of stent thrombosis in a patient treated with ticagrelor, who exhibited high on-treatment platelet reactivity (HTPR) according to platelet reactivity testing. He was on clopidrogel and tested for platelet reactivity using the VerifyNow P2Y12 assay. The test showed a PRU of 249 and only 12% platelet inhibition. The patient was then switched to ticagrelor, with a loading dose of 180 mg given. The patient had stent thrombosis three weeks later with an acute myocardial infarction (MI). The patient had good platelet inhibition when started on Ticagrelor treatment (PRU=33), but had HTPR when the stent thrombosis occurred three weeks later (PRU=339).

Platelet reactivity in patients with subacute stent thrombosis compared with non–stent-related acute myocardial infarction

2007 ◽  
Vol 153 (1) ◽  
pp. 41.e1-41.e6 ◽  
Author(s):  
Eli I. Lev ◽  
Carlos L. Alviar ◽  
Mehmet E. Arikan ◽  
Bijal P. Dave ◽  
Juan F. Granada ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Stent Thrombosis ◽  
Platelet Reactivity

Platelet Inhibition by Adjunctive Cilostazol Versus High Maintenance-Dose Clopidogrel In Patients with Acute Myocardial Infarction According to Cytochrome P450 2C19 Genotype

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3322-3322
Author(s):  
In-Suk Kim ◽  
Young-Hoon Jeong ◽  
Arum Kim ◽  
Gyeong-Won Lee
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
Maintenance Dose ◽  
Conflicts Of Interest ◽  
Platelet Reactivity ◽  
Platelet Inhibition ◽  
Cyp2c19 Genotype ◽  
Loss Of Function

Abstract Abstract 3322 Objectives The aim of this study was to assess the degree of platelet inhibition by adjunctive cilostazol in patients with acute myocardial infarction (AMI) according to CYP2C19 genotype. Background Although adjunctive cilostazol intensifies platelet inhibition in AMI patients, it is not established whether this regimen can overcome the loss-of-function effect of CYP2C19 variants. Methods We randomly assigned 126 AMI patients with available CYP2C19 genotyping to receive adjunctive cilostazol (triple group; n = 64) or high maintenance-dose (MD) clopidogrel of 150-mg/day (high-MD group; n = 62). Using conventional aggregometry and VerifyNow, platelet reactivity was measured at pre-discharge and 30-day follow-up. Primary endpoint was change in maximal platelet aggregation (Aggmax). High post-treatment platelet reactivity (HPPR) was defined as 5 μmol/l ADP-induced Aggmax > 50%. Results In non-carriers, the two groups did not differ with respect to changes in platelet measures, and could achieve fewer rates of HPPR at 30-day follow-up (< 5%). In carriers, changes in 5 and 20 μmol/l ADP-induced Aggmax were significantly higher in the triple (n = 39) versus high-MD group (n = 38) (21.8 ± 13.9% vs. 9.0 ± 13.3%, p < 0.001, and 24.2 ± 17.2% vs. 7.7 ± 15.5%, p < 0.001, respectively). Likewise, changes in late platelet aggregation and P2Y12 reaction unit were consistently greater in the triple vs. high-MD group. Fewer patients in the triple group met the criteria of HPPR at 30-day follow-up compared with the high-MD group (2.6% vs. 21.1%, p = 0.014). Conclusions Among AMI patients with CYP2C19 variants, adjunctive cilostazol enhances platelet inhibition and reduces the rate of HPPR, as compared with high-MD clopidogrel. (Adjunctive Cilostazol Versus High-MD ClopidogrEL in Patients With Acute Myocardial Infarction According to CYP2C19 genotype [ACCEL-AMI-CYP2C19]; NCT00915733). Disclosures: No relevant conflicts of interest to declare.

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.

How Long Does It Take for Clopidogrel and Ticagrelor to Inhibit Platelets in Patients Undergoing Primary Percutaneous Coronary Intervention? A Detailed Pharmacodynamic Analysis: Time Course of Platelet Reactivity in STEMI (TOPS)

2017 ◽  
Vol 43 (04) ◽  
pp. 439-446 ◽  
Author(s):  
Thomas Bergmeijer ◽  
Thea Godschalk ◽  
Paul Janssen ◽  
Kim Berge ◽  
Nicoline Breet ◽  
...  
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Antiplatelet Therapy ◽  
Stent Thrombosis ◽  
Primary Percutaneous Coronary Intervention ◽  
Platelet Reactivity ◽  
Coronary Intervention ◽  
Platelet Inhibition ◽  
Light Transmittance ◽  
Loading Dose ◽  
Percutaneous Coronary

AbstractAntiplatelet therapy plays a pivotal role in patients with an ST-segment elevation myocardial infarction (STEMI) to prevent further atherothrombotic events, such as stent thrombosis. Although the risk of stent thrombosis is highest in the first hours after primary percutaneous coronary intervention (pPCI), little is known about when an adequate level of platelet inhibition is achieved following a clopidogrel or ticagrelor loading dose in STEMI patients. Patients presenting with STEMI in whom pPCI was performed and who were loaded with 600 mg clopidogrel or 180 mg ticagrelor were eligible for enrolment in this nonrandomized, open label, single-center study. Platelet reactivity was measured before PCI, 6 and 24 hours after loading dose and after 2, 7, and 14 days, using the VerifyNow P2Y12 assay as well as 20 µmol/L adenosine diphosphate stimulated light transmittance aggregometry (LTA). We analyzed the time until a VerifyNow result of < 236 P2Y12 reaction units or LTA maximum platelet aggregation of < 64.5% was reached. A total of 28 patients were participated in this study. Platelet reactivity dropped below the high platelet reactivity cutoff level after 11.4 (VerifyNow) and 5.7 (LTA) hours in patients who were loaded with clopidogrel, and after 2.4 (VerifyNow) and 3.9 (LTA) hours in patients who were loaded with ticagrelor. Despite the administration of a clopidogrel or ticagrelor loading dose, it still takes multiple hours (2–11) to reach adequate platelet inhibition in STEMI patients. This might indicate the need for additional antiplatelet therapy in the first hours after loading in patients undergoing pPCI with stenting.

Clopidogrel resistance in diabetic patient with acute myocardial infarction due to stent thrombosis

2014 ◽  
Vol 32 (5) ◽  
pp. 461-465 ◽  
Author(s):  
Matej Samoš ◽  
Radoslava Šimonová ◽  
Frantisek Kovář ◽  
Lukas Duraj ◽  
Jana Fedorová ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Diabetic Patient ◽  
Stent Thrombosis ◽  
Clopidogrel Resistance

scholarly journals Early Stent Thrombosis in Patients Undergoing Primary Coronary Stenting for Acute Myocardial Infarction: Incidence, a Simple Risk Score, and Prognosis

2009 ◽  
Vol 16 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Mehmet Ergelen ◽  
Huseyin Uyarel ◽  
Damirbek Osmonov ◽  
Erkan Ayhan ◽  
Emre Akkaya ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Stent Thrombosis ◽  
Risk Score ◽  
Cardiovascular Mortality ◽  
Large Population ◽  
Coronary Stenting ◽  
Therapy Discontinuation ◽  
Clopidogrel Therapy

Background: One of the major concerns remaining in the treatment with stenting of patients with acute myocardial infarction (AMI) is the occurrence of stent thrombosis (ST). The aim of the current study is to investigate the incidence, predictors, and long-term outcomes of early ST after primary coronary stenting for AMI in a large population. Methods: We reviewed 1960 consecutive patients (mean age 56 ± 11.6 years, 1658 males) treated with primary coronary stenting for AMI between 2003 and 2008. All clinical, angiographic, and follow-up data were retrospectively collected. Early ST was defined as thrombosis that occurred in the first 30 days after primary coronary stenting. Results: Early ST was observed in 89 (4.5%) patients. Five variables, selected from the multivariate analysis, were weighted proportionally to their respective odds ratio (OR) for early ST (premature clopidogrel therapy discontinuation [10 points], stent diameter ≤3 mm [5 points], current smoker [4 points], diabetes mellitus [DM; 3 points], and age >65 years [2 points]). Three strata of risks were defined (low risk, score 0-4; intermediate risk, score 5-12; and high risk, score 13-24) and had a strong association with early ST and long-term cardiovascular mortality. Long-term cardiovascular mortality was 5-fold more in patients with early ST than that without ST (24.1% vs 4.7%, respectively, P < .001). Conclusions: Early ST after primary coronary stenting in AMI is strongly related with increased long-term cardiovascular mortality. Premature clopidogrel therapy discontinuation is the most powerful predictor of early ST.

scholarly journals Early, Subacute Coronary Stent Thrombosis: A Complication of COVID-19 Infection

2021 ◽  
pp. 1-4
Author(s):  
Sadeq Tabatabai ◽  
Nooshin Bazargani ◽  
Kamaleldin Al-Tahmody ◽  
Jasem Mohammed Alhashmi
Keyword(s):  
Myocardial Infarction ◽  
Health Care ◽  
Acute Myocardial Infarction ◽  
Stent Thrombosis ◽  
Coronary Angioplasty ◽  
Anterior Wall ◽  
Coronary Stent ◽  
Antithrombotic Agents ◽  
Health Care Burden ◽  
Primary Coronary Angioplasty

Soon after it was discovered in Wuhan, China, in December 2019, coronavirus disease 2019 (COVID-19) blow-out very fast and became a pandemic. The usual presentation is respiratory tract infection, but cardiovascular system involvement is sometimes fatal and also a serious personal and health care burden. We report a case of a 57-year-old man who was admitted with anterior wall acute myocardial infarction secondary to early coronary stent thrombosis and associated with COVID-19 infection. He was managed with primary coronary angioplasty and discharged home. Procoagulant and hypercoagulability status associated with severe acute respiratory syndrome coronavirus 2 infection is the most likely culprit. Choosing aggressive antithrombotic agents after coronary angioplasty to prevent stent thrombosis during the COVID-19 pandemic may be the answer but could be challenging.

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