scholarly journals Simultaneous administration of high-dose atorvastatin and clopidogrel does not interfere with platelet inhibition during percutaneous coronary intervention

2016 ◽  
pp. 45 ◽  
Author(s):  
Rolf Kreutz ◽  
Jeffrey Breall ◽  
Anjan Sinha ◽  
Elisabeth von der Lohe ◽  
Richard Kovacs ◽  
...  
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Coronary Intervention ◽  
Platelet Inhibition ◽  
High Dose ◽  
Simultaneous Administration ◽  
Percutaneous Coronary

High-Dose Clopidogrel Loading in Percutaneous Coronary Intervention

2005 ◽  
Vol 39 (5) ◽  
pp. 918-922 ◽  
Author(s):  
Kristen L Longstreth ◽  
James R Wertz
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Coronary Intervention ◽  
Drug Manufacturer ◽  
Platelet Inhibition ◽  
High Dose ◽  
Loading Dose ◽  
Percutaneous Coronary ◽  
Safety Studies ◽  
Risk Patients ◽  
Time Required

OBJECTIVE: To review the use of a 600-mg clopidogrel loading dose in patients undergoing percutaneous coronary intervention (PCI). DATA SOURCES: Human clinical trials and platelet studies available through PubMed (1966–March 2005), bibliographies of pertinent articles, and citations supplied by the drug manufacturer were accessed. DATA SYNTHESIS: The administration of a 600-mg loading dose of clopidogrel can decrease the time required for maximum platelet inhibition to 2 hours compared with ⩾6 hours achieved with 300 mg. This higher loading dose has been investigated in multiple platelet studies and one observational report. Several randomized controlled trials have used a 600-mg loading dose; however, these studies were not designed to evaluate the efficacy and safety of this loading regimen. To date, only one randomized trial has compared the 600-mg loading dose with a 300-mg loading dose. CONCLUSIONS: When compared with a conventional loading regimen of 300 mg in lower-risk patients, pretreatment with clopidogrel 600 mg was shown to be more effective in reducing periprocedural events and demonstrated similar safety. Studies are needed to clarify the use of a 600-mg loading dose in higher-risk patients, with concomitant glycoprotein IIb/IIIa receptor antagonism, or when administration is delayed until immediately before or after PCI.

scholarly journals Use of Thromboelastography Platelet Mapping for Assessment of Individual Platelet Response Secondary to Oral Antiplatelet Therapy after Percutaneous Coronary Intervention: An Attempt to Start Personalized Antiplatelet Therapy in India

2021 ◽  
Author(s):  
Suvro Sankha Datta ◽  
Dibyendu De ◽  
Nadeem Afroz Muslim
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Antiplatelet Therapy ◽  
Platelet Reactivity ◽  
Coronary Intervention ◽  
Platelet Inhibition ◽  
P Value ◽  
Platelet Response ◽  
Percutaneous Coronary ◽  
The Individual ◽  
Platelet Functions

AbstractHigh on-treatment platelet reactivity (HPR) with P2Y12 receptor antagonists in patients treated with dual antiplatelet therapy (DAPT) is strongly associated with adverse ischemic events after percutaneous coronary intervention (PCI). This prospective study was conducted to assess individual platelet response and HPR to antiplatelet medications in post-PCI cases by thromboelastography platelet mapping (TEG-PM). Total 82 patients who were on aspirin and on either clopidogrel, prasugrel, or ticagrelor were evaluated. The percentage of platelet inhibition to arachidonic acid (AA) and adenosine disdiphosphate (ADP) was calculated by [100-{(MA ADP/AA–MA Fibrin) / (MA Thrombin–MA Fibrin) × 100}], taking 50% response as cut-off for HPR. HPR to clopidogrel and prasugrel was 14.29 and 12.5%, respectively. No HPR was detected to aspirin and ticagrelor. The mean percentage of platelet inhibition was significantly higher in patients with ticagrelor 82.99, 95% confidence interval (CI) of [77.3, 88.7] as compared with clopidogrel 72.21, 95% CI of [65.3, 79.1] and prasugrel 64.2, 95% CI of [52.5, 75.9] (p-value of 0.041 and 0.003, respectively). Aspirin along with ticagrelor is associated with a higher mean percentage of platelet inhibition, and lower HPR as compared with the usage of aspirin combined with clopidogrel or prasugrel. Additionally, it might also be concluded that TEG-PM could be used effectively to measure the individual platelet functions which would make oral antiplatelet therapy more personalized for cardiac patients.

Anticoagulation profile of high-dose vs. standard-dose enoxaparin for percutaneous coronary intervention

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Z Liu ◽  
Q Chen ◽  
J Li ◽  
X Zhu ◽  
L Xu ◽  
...  
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Single Dose ◽  
Dose Group ◽  
Standard Dose ◽  
Coronary Intervention ◽  
High Dose ◽  
Funding Source ◽  
Minor Bleeding ◽  
Therapeutic Anticoagulation ◽  
Percutaneous Coronary

Abstract Background Although enoxaparin 0.5 mg/kg is a recommended anticoagulation regimen for percutaneous coronary intervention (PCI), a randomized study demonstrated that more patients receiving enoxaparin 0.75 mg/kg compared to those receiving 0.5 mg/kg achieved therapeutic anticoagulation without increase of major bleeding. However, no detailed data regarding the anticoagulation profile of enoxaparin 0.75 mg/kg was reported in the study. Purpose This study prospectively assessed the anticoagulation profile of enoxaparin 0.75 mg/kg vs. 0.5 mg/kg in troponin-negative patients undergoing elective trans-radial coronary angiography (CAG). Methods Eligible patients were randomly assigned to the Planned Single-dose group (0.75 mg/kg) or the Planned Staged-dose group (0.5±0.25 mg/kg). In the Planned Single-dose group, all patients received enoxaparin 0.75 mg/kg before CAG irrespective of their indication for subsequent PCI. In the Planned Staged-dose group, enoxaparin 0.5 mg/kg was administered to all patients before CAG and additional 0.25 mg/kg was given only to those undergoing subsequent PCI immediately before PCI. Patients without indication for subsequent PCI in each group were defined as High-dose (0.75 mg/kg) and Standard-dose (0.5 mg/kg) groups, respectively. Anti-Xa levels were assessed at 0 min (immediately before), 10 min, and 90 min after enoxaparin administration. Therapeutic anticoagulation was defined as anti-Xa level of 0.5–1.8 IU/ml. Bleeding was according to the thrombolysis in myocardial infarction (TIMI) criteria. Results In 170 randomized patients, 48 of 85 patients in the Planned Single-dose group and 47 of 85 patients in the Planned Staged-dose group were included in the High-dose and Standard-dose groups, respectively. The baseline characteristics were well balanced between the two groups. The anti-Xa levels were higher in the High-dose vs. Standard-dose group both at 10 min (1.354±0.228 IU/ml vs. 0.976±0.213 IU/ml, p<0.001) and 90 min (0.827±0.195 IU/ml vs. 0.583±0.169 IU/ml, p<0.001) (Figure 1). The percentages of patients with therapeutic anticoagulation were similar at 10 min (100% [46/46] vs. 100% [46/46], p=1.000) but higher at 90 min (100% [41/41] vs. 75% [33/44], p=0.001) in the High-dose vs. Standard-dose group. No TIMI major or minor bleeding occurred within 24 h of randomization in both groups. Conclusions Enoxaparin 0.75 mg/kg compared to 0.5 mg/kg provided higher anticoagulation which was adequate for up to 90 min of administration. Enoxaparin 0.75 mg/kg would be a superior anticoagulation regimen for PCI, especially when the procedure duration is long. Figure 1. High-dose vs. Standard-dose Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): 2016 Peking Union Medical College Hospital (PUMCH) Science Fund for Junior Faculty

Abstract 4917: Clopidogrel Resistance and Coronary Artery Plaque Burden in Patients Undergoing Percutaneous Coronary Intervention

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Amala Chirumamilla ◽  
Akiko Maehara ◽  
Gary S Mintz ◽  
Roxana Mehran ◽  
Adriano Caixeta ◽  
...  
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Coronary Intervention ◽  
Platelet Inhibition ◽  
Smoking History ◽  
Plaque Burden ◽  
Process Data ◽  
Clopidogrel Resistance ◽  
Reference Segment ◽  
Percutaneous Coronary ◽  
Verify Now

Background: Clopidogrel anti-inflammatory effect and plaque burden are important factors for atherothrombotic process. Data are lacking on relationship of plaque burden and clopidogrel resistance in patients undergoing percutaneous coronary intervention (PCI) Methods: We identified 138 patients who had intravascular ultrasound during PCI between Jan 2007 to June 2007. Using the Verify Now Point-of-care assay, P2Y12 platelet reaction units (PRU) and percent inhibition of platelet activation (IPA) were measured 16 –24 hours after the loading dose of clopidogrel (600mg for patients not on clopidogrel daily, and 300mg for patients on clopidogrel 75mg daily) but before the next day of clopidogrel dose. CR was defined as PRU >200 or as IPA<10% or <20%. Results: Mean age of patients was 66±11 years and 74% were males. PRU>200 was found in 53 patients (38.4%) and PRU ≤200 in 85 patients (61.6%). Presence of myocardial infarction, hyperlipidemia, renal disease, smoking history, stable or unstable angina at admission were similar between the PRU groups and between IPA groups. Hypertension, diabetes, older age and reference site plaque burden were higher in clopidogrel resistance (Table ). With use of alternative definitions, reference segment plaque burden was also higher in clopidogrel resistance patients: 0.50±0.12 vs 0.41±0.13 in <10% vs ≥10% platelet inhibition (p=0.05), and 0.49±0.12 vs 0.41±0.13 in <20% vs ≥20% platelet inhibition (p=0.03) Conclusion: Clopidogrel resistance patients have more high risk baseline characteristics and higher plaque burden at the reference vessel segment, implying diffuse intracoronary atherosclerosis compared to clopidogrel sensitive patients who underwent PCI

Clopidogrel pretreatment in primary percutaneous coronary intervention: Prevalence of high on-treatment platelet reactivity and impact on preprocedural patency of the infarct-related artery

2013 ◽  
Vol 110 (07) ◽  
pp. 110-117 ◽  
Author(s):  
Javier Berdejo ◽  
Gerard Roura ◽  
Josep Gómez-Lara ◽  
Rafael Romaguera ◽  
Luis Teruel ◽  
...  
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Primary Percutaneous Coronary Intervention ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Poor Response ◽  
Antiplatelet Agents ◽  
Coronary Intervention ◽  
Platelet Inhibition ◽  
Percutaneous Coronary ◽  
Infarct Related Artery

SummaryTo date, there is limited data on levels of platelet inhibition achieved in patients with ST-elevation myocardial infarction (STEMI) who are loaded with clopidogrel and aspirin (ASA) prior to undergoing primary percutaneous coronary intervention (P-PCI). The aim of this investigation was to evaluate the percentage of STEMI patients with high on-treatment platelet reactivity (HPR) to clopidogrel at the time of initiating P-PCI and its association with the initial patency of the infarct-related artery (IRA). This prospective pharmacodynamic study included 50 STEMI patients, previously naïve to oral antiplatelet agents, who received 500-mg ASA and 600-mg clopidogrel loading doses prior to P-PCI. Platelet function assessment was performed at the beginning of the procedure using various assays, including VerifyNow™ system (primary endpoint), light transmission aggregometry and multiple electrode aggregometry. The percentage of patients with suboptimal response to clopidogrel and ASA assessed with the VerifyNow™ system was 88.0% and 28.6%, respectively. Similar results were obtained with the other assays used. A higher percentage of patients with initial patency of the IRA was observed among those patients without HPR compared with those with HPR to clopidogrel (66.7% vs 15.9%; p=0.013), while no differences were observed regarding postprocedural angiographic or electrocardiographic outcomes. In conclusion, this study shows that a high percentage of STEMI patients have inadequate levels of clopidogrel-induced and, to a lesser extent, aspirin-mediated platelet inhibition when starting a P-PCI procedure, and suggests that a poor response to clopidogrel might be associated with impaired initial TIMI flow in the IRA.

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