Is light transmittance aggregometry still a useful tool to assess pharmacodynamic effects of antiplatelet therapy?

Platelets ◽  
2014 ◽  
Vol 26 (6) ◽  
pp. 608-609 ◽  
Author(s):  
Paul A. Gurbel ◽  
Martin G. Gesheff ◽  
Christopher J. Franzese ◽  
Kevin P. Bliden ◽  
Udaya S. Tantry
Keyword(s):  
Antiplatelet Therapy ◽  
Light Transmittance ◽  
Pharmacodynamic Effects ◽  
Light Transmittance Aggregometry

The impact of renal function on platelet reactivity and clinical outcome in patients undergoing percutaneous coronary intervention with stenting

2014 ◽  
Vol 112 (12) ◽  
pp. 1174-1181 ◽  
Author(s):  
Nicoline Breet ◽  
Corine de Jong ◽  
Willem Jan Bos ◽  
Jochem van Werkum ◽  
Heleen Bouman ◽  
...  
Keyword(s):  
Renal Function ◽  
Antiplatelet Therapy ◽  
Platelet Function ◽  
Platelet Reactivity ◽  
Light Transmittance ◽  
Clinical Trial Registration ◽  
Platelet Function Test ◽  
Increased Risk ◽  
Function Test ◽  
The Impact

SummaryPatients with chronic kidney disease (CKD) have an increased risk of cardiovascular disease. Previous studies have suggested that patients with CKD have less therapeutic benefit of antiplatelet therapy. However, the relation between renal function and platelet reactivity is still under debate. On-treatment platelet reactivity was determined in parallel by ADP- and AA-induced light transmittance aggregometry (LTA) and the VerifyNow® System (P2Y12 and Aspirin) in 988 patients on dual antiplatelet therapy, undergoing elective coronary stenting. Patients were divided into two groups according to the presence or absence of moderate/severe CKD (GFR<60 ml/min/1.73 m2). Furthermore, the incidence of all-cause death, non-fatal acute myocardial infarction, stent thrombosis and stroke at one-year was evaluated. Patients with CKD (n=180) had significantly higher platelet reactivity, regardless of the platelet function test used. Patients with CKD more frequently had high on-clopidogrel platelet reactivity (HCPR) and high on-aspirin platelet reactivity (HAPR) regardless of the platelet function test used. After adjustment for potential confounders, this was no longer significant. The event-rate was the highest in patients with both high on-treatment platelet reactivity (HPR) and CKD compared to those with neither high on-treatment platelet reactivity nor CKD. In conclusion, the magnitude of platelet reactivity as well as the incidence of HPR was higher in patients with CKD. However, since the incidence of HPR was similar after adjustment, a higher rate of co-morbidities in patients with CKD might be the major cause for this observation rather than CKD itself. CKD-patients with HCPR were at the highest risk of long-term cardiovascular events.Clinical Trial Registration: www.clinicaltrials.gov: NCT00352014.

scholarly journals Polimorfisme COX-1 terhadap Agregasi Platelet pada Pasien Penyakit Jantung Koroner

2021 ◽  
Vol 6 (1) ◽  
pp. 31-35
Author(s):  
Charliandri Saputra Wahab ◽  
J. Nugroho Eko Putranto ◽  
Ike Dhiah Rochmawati
Keyword(s):  
Polymerase Chain Reaction ◽  
Light Transmittance ◽  
Wild Type ◽  
Chain Reaction ◽  
Cyclooxygenase 1 ◽  
Light Transmittance Aggregometry ◽  
Polymerase Chain ◽  
Cox 1

Polimorfisme genetik COX-1 (Cyclooxygenase 1) menjadi salah satu faktor penyebab variasi respon terhadap agregasi platelet. Variasi tersebut dapat menimbulkan Coronary Arthery Disease (CAD) pada pasien penyakit jantung koroner (PJK). Penelitian ini dilakukan di RSUD Sidoarjo di Jawa Timur selama 1 bulan yaitu terhitung mulai bulan November hingga Desember 2017 dengan melibatkan 30 pasien. Metode penelitian yang digunakan yaitu Polymerase Chain Reaction (PCR) agar pemeriksaan polimorfisme COX-1 dan metode Light Transmittance  Aggregometry (LTA) untuk pengukuran agregasi platelet. Dari 30 pasien yang terlibat dengan penelitian ini didapatkan jenis polimorfisme COX-1 homozygout (wild type) sebanyak 4 pasien dengan nilai bp pada kisaran rentang 233-243dan Heterozygot sebanyak 26 pasien dengan kisaran rentang 244-294. Analisis yang dilakukan agar mengetahui hubungan antara polimorfisme COX-1 terhadap agregasi platelet pada pasien PJK yaitu analisis inferensial, dimana diperoleh nilai p=0,423. Dari hasil uji analisis yang diperoleh, maka dapat diambil kesimpulan bahwa tidak hubungan antara polimorfisme COX-1 terhadap agrgasi platelet.

Abstract 17314: Impact of Mild Therapeutic Hypothermia on Platelet Inhibition in Acute Coronary Syndrome

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jan Kaufmann ◽  
Helena Stockmann ◽  
Philipp Stawowy ◽  
Kristof Graf ◽  
Eckart Fleck ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Antiplatelet Therapy ◽  
Therapeutic Hypothermia ◽  
Platelet Function ◽  
Mild Hypothermia ◽  
Plasma Concentrations ◽  
Mild Therapeutic Hypothermia ◽  
Light Transmittance ◽  
Coronary Syndrome ◽  
Platelet Aggregometry

Background: Mild therapeutic hypothermia (MTH) improves outcome for patients with acute coronary syndrome (ACS) after cardiac arrest (CA). Previous data point to an interaction between hypothermia and drug metabolism, thus potentially impacting on platelet function under antiplatelet therapy. Purpose: The aim of the study is to determine clopidogrel metabolism and platelet function in clopidogrel naïve ACS patients treated with mild hypothermia (33°C, n=12) compared with ACS patients (troponin positive) with normal body temperature (n=14). Methods: Platelet function was measured by light transmittance aggregometry (LTA), multiple electrode platelet aggregometry (MEA) and VASP phosphorylation analysis before, 2h, 4h and 24h after administration of a 600 mg clopidogrel loading dose. Furthermore, plasma concentrations of clopidogrel, the active thiol metabolite and the inactive carboxyl metabolite were determined. All patients were screened for CYP2C19*2 polymorphism and scheduled for PCI. Mild hypothermia was carried out according to current guidelines for 24 hours at a target temperature of 33°C. Results: Plasma concentration of clopidogrel and metabolites were lower in the MTH group after 2h and 4h, respectively (all p<0.005). All platelet function tests showed an attenuated response to clopidogrel with respect to baseline platelet activity in the MTH group. This was significant for VASP analysis and LTA (p<0.05). Moreover, there was no difference in genotype and platelet function determined ex vivo with 33°C and 37°C, respectively. Conclusion: Inhibition of platelet function is decreased under MTH, presumably due to a diminished clopidogrel absorption and metabolization. Thus, these patients might have a higher risk for cardiovascular events despite antiplatelet therapy.

The Assessment of High Post-Clopidogrel Platelet Reactivity Using the Vasodilator-Stimulated Phosphoprotein Phosphorylation Index – Comparison with Light Transmittance Aggregometry.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1093-1093
Author(s):  
In-Suk Kim ◽  
Young-Hoon Jeong ◽  
Arum Kim ◽  
Gyeong-Won Lee
Keyword(s):  
Roc Curve ◽  
Platelet Reactivity ◽  
Flow Cytometric Analysis ◽  
Curve Analysis ◽  
Light Transmittance ◽  
Reactivity Index ◽  
Roc Curve Analysis ◽  
Flow Cytometric ◽  
Light Transmittance Aggregometry ◽  
P Index

Abstract Abstract 1093 Background Flow cytometric analysis of platelet reactivity index of vasodilator-stimulated phosphoprotein-phosphorylation (VASP-P) is a suitable test to evaluate the “high post-treatment platelet reactivity (HPPR)”. A reliable cut-off of VASP-P index is needed to identify the HPPR. However, an ideal cut-off identifying HPPR using the VASP-P index remains undetermined. We aimed to show the comparison between light transmittance aggregometry (LTA) and flow cytometric analysis of VASP-P index and assess the cut-offs of identifying HPPR using VASP-P index. Methods We enrolled consecutively patients undergoing percutaneous coronary intervention (PCI) in real clinical practice (n = 516). They all received clopidogrel and aspirin, performed LTA (5 and 20 μmol/l ADP-induced, and 1.6 nmol/l arachidonic acid (AA)-induced PR) and flow cytometric analysis of VASP-P index simultaneously and compared the different platelet measures. Based on previously suggested cut-offs, 5 μmol/l ADP-induced maximal platelet reactivity (PRmax) > 42.9%, 5 μmol/l ADP-induced PRmax > 50%, 20 μmol/l ADP-induced PRmax > 62%, 20 μmol/l ADP-induced PRmax > 64.5%, and 1.6 mmol/l AA-induced PRmax > 20%, the cut-offs of identifying HPPR using flow cytometric analysis of VASP-P were determined by receiver-operating characteristics (ROC) curve analysis. Results Excellent correlations were observed between LTA with ADP-induced PRmax and flow cytometric analysis of VASP-P according to the ROC curve analyses. The ROC curve analyses demonstrated that 5 μmol/l ADP-induced PRmax > 42.9% could distinguish between patients with and without VASP-P index > 54.9% (area under curve [AUC] 0.926, 95% confidence interval (CI) 0.903–0.949, sensitivity 82.8%, and specificity 88.5%, p < 0.001) and 5 μmol/l ADP-induced PRmax > 50% could distinguish between patients with and without VASP-P index > 57.4% (AUC 0.937, 95% CI 0.914–0.961, sensitivity 91.5%, and specificity 85.2%, p < 0.001). ROC curve analysis demonstrated 20 μmol/l ADP-induced PRmax > 62% could distinguish between patients with and without VASP-P index > 55.2% (AUC 0.948, 95% CI 0.927–0.969, sensitivity 95.7%, and specificity 87.3%, p < 0.001) and 20 μmol/l ADP-induced PRmax > 64.5% could distinguish between patients with and without VASP-P index > 55.9% (AUC 0.925, 95% CI 0.900–0.951, sensitivity 88.3%, and specificity 83.0%, p < 0.001), respectively. However, fair correlation was observed between AA-induced PRmax and VASP-P index and 1.6 nmol/l AA-induced PRmax > 20% could distinguish between patients with and without VASP-P index > 52.4% (AUC 0.761, 95% CI 0.719–0.802, sensitivity 68.5%, and specificity 72.7%, p < 0.001). We defined the ideal threshold of VASP-P index > 56%. The VASP-P index > 56% showed a substantial agreement with 5 μmol/l and 20 μmol/l ADP-induced PRmax (Table 1). However, VASP-P index > 56% showed a moderate agreement with 1.6 nmol/l AA)-induced PRmax > 20% (Table 1). Conclusion There are significant correlations between the suggested cut-offs of HPPR. Because VASP-P index > 56 is well matched with 5 μmol/l ADP-induced PRmax > 42.9%, 5 μmol/l ADP-induced PRmax > 50%, 20 μmol/l ADP-induced PRmax > 62%, and 20 μmol/l ADP-induced PRmax > 64.5%., it might suggest that VASP-P index > 56 has a practical implication for stratification of high-risk ischemic events. Disclosures: No relevant conflicts of interest to declare.

Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin

Pharmacology ◽  
2017 ◽  
Vol 100 (3-4) ◽  
pp. 127-130 ◽  
Author(s):  
Annemarie Mohring ◽  
Kerstin Piayda ◽  
Lisa Dannenberg ◽  
Saif Zako ◽  
Theresa Schneider ◽  
...  
Keyword(s):  
Gold Standard ◽  
Cardiovascular Events ◽  
Platelet Reactivity ◽  
Area Under The Curve ◽  
Platelet Inhibition ◽  
Light Transmittance ◽  
Characteristic Analysis ◽  
Specific Test ◽  
Current Gold Standard ◽  
Light Transmittance Aggregometry

Platelet inhibition by aspirin is indispensable in the secondary prevention of cardiovascular events. Nevertheless, impaired aspirin antiplatelet effects (high on-treatment platelet reactivity [HTPR]) are frequent. This is associated with an enhanced risk of cardiovascular events. The current gold standard to evaluate platelet hyper-reactivity despite aspirin intake is the light-transmittance aggregometry (LTA). However, pharmacologically, the most specific test is the measurement of arachidonic acid (AA)-induced thromboxane (TX) B2 formation. Currently, the optimal cut-off to define HTPR to aspirin by inhibition of TX formation is not known. Therefore, in this pilot study, we aimed to calculate a TX formation cut-off value to detect HTPR defined by the current gold standard LTA. We measured platelet function in 2,507 samples. AA-induced TX formation by ELISA and AA-induced LTA were used to measure aspirin antiplatelet effects. TX formation correlated nonlinearly with the maximum of aggregation in the AA-induced LTA (Spearman's rho R = 0.7396; 95% CI 0.7208-0.7573, p < 0.0001). Receiver operating characteristic analysis and Youden's J statistics revealed 209.8 ng/mL as the optimal cut-off value to detect HTPR to aspirin with the TX ELISA (area under the curve: 0.92, p < 0.0001, sensitivity of 82.7%, specificity of 90.3%). In summary, TX formation ELISA is reliable in detecting HTPR to aspirin. The calculated cut-off level needs to be tested in trials with clinical end points.

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