Academic literature on the topic 'High on-aspirin platelet reactivity'
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Journal articles on the topic "High on-aspirin platelet reactivity"
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Alemanno, Laura, Isabella Massimi, Vanessa Klaus, Maria Guarino, Teresa Maltese, Luigi Frati, Dominick Angiolillo, and Fabio Pulcinelli. "Impact of Multidrug Resistance Protein-4 Inhibitors on Modulating Platelet Function and High on-Aspirin Treatment Platelet Reactivity." Thrombosis and Haemostasis 118, no. 03 (February 15, 2018): 490–501. http://dx.doi.org/10.1055/s-0038-1629920.
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AbstractPlatelet multidrug resistance protein 4 (MRP4) plays a modulating role on platelet activation. Platelet function and thrombus formation are impaired in MRP4 knockout mice models, and, among aspirin-treated patients, high on-aspirin residual platelet reactivity (HARPR) positively correlates with MRP4 levels. To better understand the effects of MRP4 on platelet function, the aim of this investigation was to assess the impact of cilostazol-induced inhibition of MRP4-mediated transport and assess aspirin-induced antiplatelet effects and rates of HARPR in human subjects.Cilostazol-dependent inhibition of MRP4-mediated transport was assessed with the release of the fluorescent adduct bimane-glutathione and aspirin entrapment. Effect of Cilostazol on cAMP inhibition was evaluated by vasodilator-stimulated phosphoprotein (VASP). Platelet function was studied by collagen and TRAP-6-induced platelet aggregation and secretion.Cilostazol reduced the release of bimane-glutathione and enhanced aspirin entrapment demonstrating an inhibitory effect on MRP4 in platelets. VASP phosphorylation was absent until 10 seconds after addition of cilostazol, and becomes evident after 30 seconds. An inhibitory effect on platelet aggregation and secretion was found in activated platelets, with threshold concentration of agonists, 10 seconds after addition of cilostazol, supporting a role of MRP4 on platelet function that is cAMP independent. Cilostazol effects were also shown in aspirin-treated platelets. A reduction of platelet aggregation and secretion were observed in aspirin-treated patients with HARPR.This study supports the role of MRP4 on modulating platelet function which occurs through cAMP-independent mechanisms. Moreover, inhibition of MRP4 induced by cilostazol enhances aspirin-induced antiplatelet effects and reduces HARPR.
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Wang, Yilong, Yi Lin, Xia Meng, Weiqi Chen, Guohua Chen, Zhimin Wang, Jialing Wu, et al. "Effect of ticagrelor with clopidogrel on high on-treatment platelet reactivity in acute stroke or transient ischemic attack (PRINCE) trial: Rationale and design." International Journal of Stroke 12, no. 3 (February 23, 2017): 321–25. http://dx.doi.org/10.1177/1747493017694390.
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Rationale and aim Little is known about the safety and efficacy of the combination of ticagrelor and aspirin in acute ischemic stroke. This study aimed to evaluate whether the combination of ticagrelor and aspirin was superior to that of clopidogrel and aspirin in reducing the 90-day high on-treatment platelet reactivity for acute minor stroke or transient ischemic attack, especially for carriers of cytochrome P450 2C19 loss-of-function allele. Sample size and design This study was designed as a prospective, multicenter, randomized, open-label, active-controlled, and blind-endpoint, phase II b trial. The required sample size was 952 patients. It was registered with ClinicalTrials.gov (NCT02506140). Study outcomes The primary outcome was the proportion of patients with high on-treatment platelet reactivity at 90 days. High on-treatment platelet reactivity is defined as the P2Y12 reaction unit >208 measured using the VerifyNow P2Y12 assay. Conclusion The Platelet Reactivity in Acute Non-disabling Cerebrovascular Events study explored whether ticagrelor combined with aspirin could reduce further the proportion of patients with high on-treatment platelet reactivity at 90 days after acute minor stroke or transient ischemic attack compared with clopidogrel and aspirin.
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Massimi, Isabella, Lavinia Lotti, Flavia Temperilli, Massimo Mancone, Gennaro Sardella, Simone Calcagno, Ombretta Turriziani, Luigi Frati, and Fabio M. Pulcinelli. "Enhanced platelet MRP4 expression and correlation with platelet function in patients under chronic aspirin treatment." Thrombosis and Haemostasis 116, no. 12 (November 2016): 1100–1110. http://dx.doi.org/10.1160/th16-04-0316.
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SummaryPlatelet multidrug resistance protein4 (MRP4)-overexpression has a role in reducing aspirin action. Aspirin in vivo treatment enhances platelet MRP4 expression and MRP4 mediated transport inhibition reduces platelet function and delays thrombus formation. The aim of our work was to verify whether MRP4 expression is enhanced in platelets obtained from patients under chronic aspirin treatment and whether it correlates with residual platelet reactivity. We evaluated changes on mRNA and protein-MRP4 expression and platelet aggregation in four populations: healthy volunteers (HV), aspirin-free control population (CTR), patients who started the treatment less than one month ago (ASA<1 month patients) and aspirinated patients who started the treatment more than two months ago (ASA>2 months patients). In platelets obtained from ASA>2 months patients, it was found a statistically significant MRP4 enhancement of both mRNA and protein expression compared to HV, CTR and ASA<1 month patients. Platelets obtained from ASA>2 months patients that present high levels of platelet MRP4, have higher serum TxB2 levels and collagen-induced platelet aggregation compared to patient with low levels of MRP4 in platelets. In addition collagen induced platelet aggregation is higher in in vitro aspirinated platelets obtained from patients with high levels of MRP4 patients compared to those obtained from patients with low MRP4 levels. We can assert that, in patients under chronic aspirin treatment, platelets that present high MRP4 levels have an increase of residual platelet reactivity, which is due in part to incomplete COX-1 inhibition, and in part to COX-1–independent mechanism.
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Barale, Cristina, Franco Cavalot, Chiara Frascaroli, Katia Bonomo, Alessandro Morotti, Angelo Guerrasio, and Isabella Russo. "Association between High On-Aspirin Platelet Reactivity and Reduced Superoxide Dismutase Activity in Patients Affected by Type 2 Diabetes Mellitus or Primary Hypercholesterolemia." International Journal of Molecular Sciences 21, no. 14 (July 15, 2020): 4983. http://dx.doi.org/10.3390/ijms21144983.
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Platelet hyperactivation is involved in the established prothrombotic condition of metabolic diseases such as Type 2 Diabetes Mellitus (T2DM) and familial hypercholesterolemia (HC), justifying the therapy with aspirin, a suppressor of thromboxane synthesis through the irreversible inhibition of cyclooxygenase-1 (COX-1), to prevent cardiovascular diseases. However, some patients on aspirin show a higher than expected platelet reactivity due, at least in part, to a pro-oxidant milieu. The aim of this study was to investigate platelet reactivity in T2DM (n = 103) or HC (n = 61) patients (aspirin, 100 mg/day) and its correlation with biomarkers of redox function including the superoxide anion scavenger superoxide dismutase (SOD) and the in vivo marker of oxidative stress urinary 8-iso-prostaglandin F2α. As results, in T2DM and HC subjects the prevalence of high on-aspirin platelet reactivity was comparable when both non-COX-1-dependent and COX-1-dependent assays were performed, and platelet reactivity is associated with a lower SOD activity that in a stepwise linear regression appears as the only predictor of platelet reactivity. To conclude, in T2DM and HC, similarly, the impairment of redox equilibrium associated with a decrease of SOD activity could contribute to a suboptimal response to aspirin.
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Saris, Anno, Monique van Oostrom, Jaapjan Snoep, Frits Rosendaal, Jaap Zwaginga, Jeroen Eikenboom, Pieter van der Meer, Johanna van der Bom, and Tobias Bonten. "Effect of aspirin intake at bedtime versus on awakening on circadian rhythm of platelet reactivity." Thrombosis and Haemostasis 112, no. 12 (2014): 1209–18. http://dx.doi.org/10.1160/th14-05-0453.
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SummaryThe risk of acute cardiovascular events is highest during morning hours, and platelet activity peaks during morning hours. The effect of timing of aspirin intake on circadian rhythm and morning peak of platelet reactivity is not known. It was our objective to evaluate the effect of timing of aspirin intake on circadian rhythm and morning peak of platelet reactivity. A randomised open-label cross-over trial in healthy subjects (n=14) was conducted. Participants used acetylsalicylic acid (80 mg) on awakening or at bedtime for two periods of two weeks, separated by a four-week wash-out period. At the end of both periods blood was drawn every 3 hours to measure COX-1-dependent (VerifyNow- Aspirin; Serum Thromboxane B2 [STxB2]) and COX-1-independent (flow cytometry surface CD62p expression; microaggregation) platelet activity. VerifyNow platelet reactivity over the whole day was similar with intake on awakening and at bedtime (mean difference: –9 [95 % confidence interval (CI) –21 to 4]). However, the morning increase in COX-1-dependent platelet activity was reduced by intake of aspirin at bedtime compared with on awakening (mean difference VerifyNow: –23 Aspirin Reaction Units [CI –50 to 4]; STxB2: –1.7 ng/ml [CI –2.7 to –0.8]). COX-1-independent assays were not affected by aspirin intake or its timing. Low-dose aspirin taken at bedtime compared with intake on awakening reduces COX-1-dependent platelet reactivity during morning hours in healthy subjects. Future clinical trials are required to investigate whether simply switching to aspirin intake at bedtime reduces the risk of cardiovascular events during the high risk morning hours.
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Mohring, Annemarie, Kerstin Piayda, Lisa Dannenberg, Saif Zako, Theresa Schneider, Kirsten Bartkowski, Bodo Levkau, et al. "Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin." Pharmacology 100, no. 3-4 (2017): 127–30. http://dx.doi.org/10.1159/000477303.
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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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Armstrong, Paul C., Thomas Hoefer, Rebecca B. Knowles, Arthur T. Tucker, Melissa A. Hayman, Plinio M. Ferreira, Melissa V. Chan, and Timothy D. Warner. "Newly Formed Reticulated Platelets Undermine Pharmacokinetically Short-Lived Antiplatelet Therapies." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 5 (May 2017): 949–56. http://dx.doi.org/10.1161/atvbaha.116.308763.
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Objective— Aspirin together with thienopyridine P2Y 12 inhibitors, commonly clopidogrel, is a cornerstone of antiplatelet therapy. However, many patients receiving this therapy display high on-treatment platelet reactivity, which is a major therapeutic hurdle to the prevention of recurrent thrombotic events. The emergence of uninhibited platelets after thrombopoiesis has been proposed as a contributing factor to high on-treatment platelet reactivity. Here, we investigate the influences of platelet turnover on platelet aggregation in the face of different dual-antiplatelet therapy strategies. Approach and Results— Traditional light transmission aggregometry, cytometry, advanced flow cytometric imaging, and confocal microscopy were used to follow the interactions of populations of platelets from healthy volunteers and patients with stable cardiovascular disease. Newly formed, reticulated platelets overproportionately contributed to, and clustered at, the core of forming aggregates. This phenomenon was particularly observed in samples from patients treated with aspirin plus a thienopyridine, but was absent in samples taken from patients treated with aspirin plus ticagrelor. Conclusions— Reticulated platelets are more reactive than older platelets and act as seeds for the formation of platelet aggregates even in the presence of antiplatelet therapy. This is coherent with the emergence of an uninhibited subpopulation of reticulated platelets during treatment with aspirin plus thienopyridine, explained by the short pharmacokinetic half-lives of these drugs. This phenomenon is absent during treatment with ticagrelor, because of its longer half-life and ability to act as a circulating inhibitor. These data highlight the important influences of pharmacokinetics on antiplatelet drug efficacies, especially in diseases associated with increased platelet turnover.
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Pettersen, A. A., H. Arnesen, and I. Seljeflot. "A brief review on high on-aspirin residual platelet reactivity." Vascular Pharmacology 67-69 (April 2015): 6–9. http://dx.doi.org/10.1016/j.vph.2015.03.018.
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Berger, Martin, Alexander Dressel, Marcus E. Kleber, Winfried März, Peter Hellstern, Nikolaus Marx, and Katharina Schütt. "Platelet Reactivity and Cardiovascular Mortality Risk in the LURIC Study." Journal of Clinical Medicine 12, no. 5 (February 28, 2023): 1913. http://dx.doi.org/10.3390/jcm12051913.
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Background: The clinical and prognostic implications of platelet reactivity (PR) testing in a P2Y12-inhibitor naïve population are poorly understood. Objectives: This explorative study aims to assess the role of PR and explore factors that may modify elevated mortality risk in patients with altered PR. Methods: Platelet ADP-induced CD62P and CD63 expression were measured by flow-cytometry in 1520 patients who were referred for coronary angiography in the Ludwigshafen Risk and Cardiovascular Health Study (LURIC). Results: High- and Low-platelet reactivity to ADP were strong predictors of cardiovascular and all-cause mortality and risk equivalent to the presence of coronary artery disease. (High platelet reactivity 1.4 [95% CI 1.1–1.9]; Low platelet reactivity: 1.4 [95% CI 1.0–2.0]). Relative weight analysis indicated glucose control (HbA1c), renal function ([eGFR]), inflammation (high-sensitive C-reactive protein [hsCRP]) and antiplatelet therapy by Aspirin as consistent mortality risk modifiers in patients with Low- and High-platelet reactivity. Pre-specified stratification of patients by risk modifiers HbA1c (<7.0%), eGFR (>60 mL/min/1.73 m2) and CRP (<3 mg/L) was associated with a lower mortality risk, however irrespective of platelet reactivity. Aspirin treatment was associated with reduced mortality in patients with high platelet reactivity only (p for interaction: 0.02 for CV-death [<0.01 for all-cause mortality]. Conclusions: Cardiovascular mortality risk in patients with High- and Low platelet reactivity is equivalent to the presence of coronary artery disease. Targeted glucose control, improved kidney function and lower inflammation are associated with reduced mortality risk, however independent of platelet reactivity. In contrast, only in patients with High-platelet reactivity was Aspirin treatment associated with lower mortality.
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Larsen, Sanne, Erik Grove, Steen Kristensen, and Anne-Mette Hvas. "Reduced antiplatelet effect of aspirin is associated with low-grade inflammation in patients with coronary artery disease." Thrombosis and Haemostasis 109, no. 05 (2013): 920–29. http://dx.doi.org/10.1160/th12-09-0666.
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SummaryInflammation has been proposed to modify platelet function. This may lead to increased platelet reactivity and reduced antiplatelet drug efficacy in patients with coronary artery disease (CAD). However, this hypothesis has not been investigated in stable CAD patients receiving aspirin as mono antiplatelet therapy. It was the objective of this study to investigate the association between platelet reactivity, the inflammatory markers high-sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6), and platelet activation. We performed a cross-sectional study on 524 stable high-risk CAD patients. Among these, 91% had a history of myocardial infarction, 23% had type 2 diabetes, and 13% had both. All patients received 75 mg aspirin daily as mono antiplatelet therapy. Platelet reactivity was assessed by multiple electrode aggregometry (Multiplate®, MEA) and VerifyNow®. Inflammation was evaluated by hs-CRP and IL-6. Platelet activation was assessed by soluble P-selectin (sP-selectin), and cyclooxygenase-1 inhibition was evaluated by measurement of serum thromboxane B2. Hs-CRP levels were significantly higher in upper platelet reactivity tertile patients than in lower platelet reactivity tertile patients (p≤0.02). Similar results were obtained with IL-6, though not statististically significant (p≥0.15). Platelet activation evaluated by sP-selectin was significantly higher in patients with MEA reactivity levels in the upper tertile than in the lower tertile (p=0.0001). Optimal compliance was confirmed by low serum thromboxane B2 levels in all patients. In conclusion, increased levels of hs-CRP were associated with augmented platelet reactivity in stable high-risk CAD patients receiving aspirin as mono antiplatelet therapy. These findings may suggest that chronic low-grade inflammation reduce the antiplatelet effect of aspirin.
Dissertations / Theses on the topic "High on-aspirin platelet reactivity"
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Yamane, Keiichiro. "Impact of Platelet Reactivity on Long-term Clinical Outcomes and Bleeding Events in Japanese Patients Receiving Antiplatelet Therapy with Aspirin." Kyoto University, 2013. http://hdl.handle.net/2433/174767.
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Grifoni, Elisa. "Funzione piastrinica e rischio di eventi avversi in pazienti con arteriopatia periferica sottoposti a rivascolarizzazione percutanea (Platelet function and risk of adverse events in peripheral artery disease patients undergoing percutaneous revascularization)." Doctoral thesis, 2018. http://hdl.handle.net/2158/1125789.
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Background and Aim: Lots of studies demonstrated that a different entity of on-treatment platelet function inhibition is associated with different clinical outcomes in patients with acute coronary syndromes. In particular, high on-treatment platelet reactivity (HPR) has been associated with an increased risk of ischemic complications (especially stent thrombosis), and there is a growing body of evidence that, on the contrary, low on-treatment platelet reactivity (LPR) could be associated with bleeding risk. Few data are available in the literature on the association between a different entity of platelet inhibition on-antiplatelet treatment and clinical outcomes in patients with peripheral artery disease (PAD).
Aim of this study was to evaluate, in patients with PAD undergoing percutaneous revascularization, the degree of on-treatment platelet reactivity, and its association with ischemic and hemorrhagic adverse events at follow-up.
Methods: In this observational, prospective, single center study, consecutive patients with PAD undergoing percutaneous transluminal angioplasty (PTA) with or without stenting, were enrolled. All patients were treated with dual antiplatelet therapy with aspirin and a P2Y12 inhibitor. Platelet function was assessed by Light Transmission Aggregometry (LTA) using arachidonic acid (AA) and adenosine diphosphate (ADP) as agonists of platelet aggregation, on blood samples obtained within 24 hours from PTA. HPR was defined by LTA ≥20% if induced by AA, and LTA ≥70% if induced by ADP. Follow-up was performed in order to record the occurrence of ischemic and bleeding events.
Results: The study enrolled 177 patients [118 males, median age 75 (IQR 68-81) years]. HPR by AA was found in 52% of patients, and showed a non significant association with older age and a higher prevalence of renal failure, whereas HPR by ADP was found in 32% of patients, and was significantly associated with older age. During follow-up [median duration 23 (IQR 13-27) months] 23 deaths (13%) were recorded; 27 patients (17.5%) underwent target limb revascularization, 2 (1.3%) amputation, and 6 (3.9%) myocardial revascularization. Twenty-four patients (15.6%) experienced a minor bleeding complication. At multivariate analysis HPR by AA and HPR by ADP were independent predictors of death [HR 3.75 (1.20-11.66), P=0.023 and HR 4.78 (1.57-14.52), P=0.006, respectively]. Moreover, patients with dual HPR both by AA and by ADP showed a significantly higher risk of death than those without (P<0.001). The median value of LTA by ADP was significantly lower in patients with bleeding complications than in those without [26.5 (22-39.2)% vs 62 (44.5-74)%, P<0.001). At ROC curve analysis the cut-off of platelet aggregation induced by ADP with the best sensitivity and specificity for increased risk of bleeding was 41%. LTA by ADP lower than 41% was independently associated with bleeding [HR 14.59 (2.55-24.01), P=0.001] at multivariate analysis.
Conclusions: In PAD patients undergoing PTA, HPR by ADP and AA were predictors of death, whereas LPR by ADP was predictor of bleeding complications. These results suggest the potential utility of assessing platelet function, even in the setting of PAD, in order to ensure the patient the best tailored antiplatelet therapy.
Books on the topic "High on-aspirin platelet reactivity"
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Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0076.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
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Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_001.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
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Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_002.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
Book chapters on the topic "High on-aspirin platelet reactivity"
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Hernandiz, Amparo, Jose Luis Díez, Antonio Moscardo, Ana Latorre, Maria Dolores Domenech, Maria Teresa Santos, and Juana Valles. "Platelet Reactivity in Patients with Coronary Stenting Treated with Dual Antiplatelet Therapy and after Withdrawal of Clopidogrel: Impact of Bioactive Titanium Stent versus Everolimus-coated Stent." In Frontiers in Cardiovascular Drug Discovery: Volume 4, 65–82. BENTHAM SCIENCE PUBLISHERS, 2019. http://dx.doi.org/10.2174/9781681083995119040005.
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Objective:To study platelet reactivity at different times while on dual antiplatelet therapy (DAPT) with aspirin (ASA) and clopidogrel in patients treated with bioactive stents (TITAN2®) or everolimus-coated stents (XIENCE V®) and one month afterclopidogrel cessation. Background: Coronary intervention damages the endothelium and causes platelet response leading to thrombotic occlusion, which is prevented with DAPT. Methods:We studied 20 patients with bioactive stent and stable ischemia (BAS-SI group); 31 patients with bioactive stent and acute coronary syndrome (BAS-ACS group) and 31 patients with stable ischemia and everolimus-coated stent (EVE group). DAPT was administered (ASA 100 mg/day and clopidogrel 75 mg/day) for one year in BAS-ACS and EVE groups and for 1 month in BAS-SI group. Platelet aggregation induced by different agonists and platelet recruitment were analyzed at different times of DAPT and 1 month after clopidogrel cessation. Results: After one month of DAPT, platelet aggregation showed no difference between groups; at 12 months of DAPT, the response to collagen and ADP increased in EVE group. Platelet recruitment at 1 month was higher in the BAS-ACS than the other groups; after 12 months, recruitment increased in the EVE group with respect to BASACS. Platelet aggregation and recruitment in diabetics were significantly higher in all situations than in non-diabetic patients. Clopidogrel withdrawal increased ADPinduced aggregation and collagen-induced aggregation and recruitment. Conclusion: Platelet reactivity in patients with DAPT varies with time, depending on the subset of patients, the type of the stent implanted and the time after implantation.
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Guttmann, Oliver P., Ronald Binder, Oliver Gämperli, and Andreas Baumbach. "Antithrombotics for Acute and Chronic Coronary Syndromes." In Manual of Cardiovascular Medicine, 117–24. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198850311.003.0014.
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Thrombus formation involves activation of aggregating platelets as well as the formation of fibrin after activation of the coagulation cascade. Fibrin eventually binds to glycoprotein IIB/IIIA receptors on platelets thereby forming a very solid occlusive clot. There are several molecules interfering with platelet activation: (1) aspirin, which blocks the formation of thromboxane A2; (2) clopidogrel, prasugrel, and ticagrelor which block P2Y12 receptors and their activation by ADP; (3) glycoprotein inhibitors that interfere with glycoprotein IIB/IIIA on platelets, the final common pathway of platelet activation, and finally (4) thrombin inhibitors blocking PAR-1 receptors on platelets. Commonly, after an acute coronary syndrome (ACS) or after percutaneous coronary interventions (PCI) or even bypass surgery, dual antiplatelet therapy (DAPT) is recommended consisting of aspirin plus a P2Y12 inhibitor. The duration of treatment after the acute event is commonly 12 months for those with ACS and 6 months for those with a high bleeding risk. In patients with high ischaemic risk, prolonged DAPT treatment can be considered, but often such patients also have a high bleeding risk. Intravenous platelet inhibitors, such as Reopro, tirofiban, and others, are used mainly during PCI, particularly in patients with ACS. Inhibitors of coagulation cascade, such as factor Xa or factor II inhibitors or vitamin K antagonists are mainly used in patients with ACS and concomitant atrial fibrillation. In these patients, mainly aspirin or in some the P2Y12 inhibitor is skipped for some weeks or months.
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Balik, Martin. "Perioperative cardiac care of the high-risk non-cardiac patient." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 990–1008. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0075.
Full textAbstract:
Non-cardiac surgery conveys a cardiac risk related to the status of the patient's cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
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Aruch, Daniel, and Ronald Hoffman. "Thrombocytosis and essential thrombocythaemia." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5239–47. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0518.
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The term thrombocytosis refers to a platelet count elevated above 450 × 109/litre, which can be (1) primary—including essential thrombocythaemia, chronic myeloid leukaemia, polycythaemia vera, and myelodysplastic syndromes; or (2) secondary—including iron deficiency, infection, blood loss, and malignancy. Essential thrombocythaemia: aetiology—the JAK2 V617F missense mutation typical of polycythaemia vera is found in about 50% of cases. In addition, 10% of patients have a mutation in the thrombopoietin receptor gene, MPL, and 30% have a mutation in calreticulin (CALR). Approximately 10% of patients have none of these mutations and are referred to as ‘triple negative’ essential thrombocythaemia. Diagnosis requires all of the following four major criteria: (1) platelet count greater than 450 × 109/litre; (2) bone marrow biopsy showing proliferation mainly of the megakaryocyte lineage with increased numbers of enlarged, mature megakaryocytes with hyperlobulated nuclei without a significant increase or left shift in neutrophil granulopoiesis or erythropoiesis and very rarely minor (grade 1) increase in reticulin fibres; (3) failure to meet the criteria for other myeloproliferative neoplasms; and (4) presence of JAK2, CALR, or MPL mutations. Alternatively, diagnosis can be met when the first three major criteria are present and the one minor criterion, namely the presence of another clonal marker or absence of evidence for reactive thrombocytosis. Treatment requires risk stratification based on the age of the patient and any prior history of thrombosis, with treatment being reserved for those at a high risk of developing complications and not introduced simply on the basis of platelet counts alone unless there is extreme thrombocytosis (>1500 × 109/litre). Therapies include low-dose aspirin and cytoreduction.
Conference papers on the topic "High on-aspirin platelet reactivity"
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Chong, B. H., F. Ismail, J. Cade, A. S. Gallus, S. Gordon, and C. N. Chesterman. "HEPARIN-INDUCED THROMBOCYTOPENIA: IN VITRO STUDIES WITH LOW MOLECULAR WEIGHT HEPARINOID, ORG 10172." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643926.
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Heparin-induced thrombocytopenia (HIT), an adverse effect of heparin therapy, may be associated with serious thrombosis resulting in severe disability or death. An IgG heparin-dependent antibody may be demonstrated in HIT by platelet aggregation studies with patient serum/plasma and standard (s) heparin. A recent study showed high cross-reactivity of the antibody with low molecular weight (LMW) heparins as most of the 22 patient sera tested gave a positive reaction with various LMW heparins including CY222, CY216, PK10169 and Kabi 2165 (Messmore HL et al, Blood 64(5), 1984 suppl). However, cross-reactivity rate with Org 10172, a LMW heparinoid which has strong anti-Xa but negligible antithrombin activity, is unknown. We tested the plasma of 17 patients with HIT for cross-reactivity with Org 10172. Although all 17 patient plasmas reacted positively with s.heparin (0.2 1.0 IU/ml), only 3 patient plasmas gave a positive but weaker reaction with Org 10172 (0.2-1.0 IU/ml).Further studies were performed to investigate the effect of adding Org 10172 (0.2 to 2.0 anti-Xa U/ml) to a reaction mixture of normal platelet-rich plasma, patient plasma and s.heparin (0.2 IU/ml). With 7 patient plasmas which showed no cross-reactivity with Org 10172, the antibody-induced platelet aggregation was inhibited when the concentration of Org 10172 exceeded 0.5 to 1.0 anti-Xa U/ml. When the study was repeated with other s.heparin concentrations (0.05, 0.1, 0.4 IU/ml), this inhibitory effect was again present provided the ratio of Org 10172 concentration (anti-Xa U/ml) to heparin concentration (IU/ml) exceeds 2.5 to 5. However, this inhibitory effect was not observed with the 3 patient plasmas which showed cross-reactivity with the heparinoid whqp. the same concentrations of Org 10172 were added. This inhibitory effect appeared to be specific for platelet aggregation induced by the heparin-dependent antibody as Org 10172 (<10 anti-Xa U/ml) did not affect platelet aggregation induced by collagen (2 ug/ml) and ADP (2.5 uM). These findings together with our experience of 3 cases of HIT successfully treated with Org 10172 suggest that this LMW heparinoid may be a useful drug for the treatment of HIT.
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Badimon, L., J. J. Badimon, and V. Fuster. "ACUTE THROMBOSIS IN STENOTIC AREAS: IMPORTANCE OF THE VASCULAR MATRIX EXPOSED TO BLOOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642842.
Full textAbstract:
The platelet response to angioplasty or spontaneous plaque rupture leads to acute thrombotic occlusion under certain conditions. We analyzed the role of local shear rate (flow and vessel cross-section related), the nature of the exposed matrix and the effect of thrombin inhibition in platelet acute response to injury. Collagen type I (exposed in plaque rupture) and de-endothelialized pig aorta (mild injury) were exposed to pig blood in a tubular perfusion chamber with well characterized flow conditions, placed within an extracorporeal circuit in swine (N=20). Platelet deposition was measured by labeling autologous platelets with Indium and optical morphometry of epoxy embedded specimens. Selected specimens were analyzed by electron microscopy. Unanticoagulated blood and blood from animals treated with 300u/Kg of heparin were perfused over the substrate for 3 and 10 min at local shear rates typical of unobstructed arteries (212s™1 - 424s™1) and of stenotic vessel (824s™1 - 1690s™1). Platelet deposition (Platelets × 106/cm2 ± SE) for 3 min perfusions were:Platelet deposition is dependent on the reactivity of the vascular matrix exposed to blood and on the local shear rate. The greatest rate of thrombus growth is observed with collagen and high shear rate conditions which may precipitate acute thrombotic occlusion in stenotic regions, mainly when the coagulation pathway is not inhibited (255×l06 platelets/ cm2 in 3 minutes. The relative contribution of rheology and the isolated components of the atherosclerotic plaque matrix exposed to blood in the onset of acute coronary syndromes will be differentiated with this experimental model.
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David, J. L., V. Legrand, and H. E. Kulbertus. "RELEVANCE OF FREE PLATELET COUNT RATIO (PCR) TO CIRCULATING PLATELET AGGREGATES (CPA) AND TO THE RELEASE OF B-THROMBOGLOBULIN(β-tg) INDUCED BY EXERCICE IN PATIENTS WITH CORONARY HEART DISEASE (CHD). EFFECTS OF TICLOPIDINE (T) TREATMENT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643026.
Full textAbstract:
CPA are considered as a possible cause of blood flow impairment and as a risk factor of sudden death in patients with CHD. The relevance of a low PCR to the presence of CPA is still debated. Indeed in a critical and well designed evaluation of this index, Sanibaldi et al.(1986) have shown that PCR obtained by counting free platelets in diluted whole blood was not lowered in patients with “thrombotic tendency”. They suggested that low CPA reported in other clinical studies may result from an artifact of blood sampling or from ex-vivo procedures.In order to reevalute the meaning of a low PCR, selected patients with CHD have been submitted to an exercice resulting in platelet stimulation. Free platelets were counted, whole blood and plasma β-tg were simultaneously determined by RIA after careful blood sampling performed before the exercice, at its end and 30 min later. Patients were previously treated by Placebo (P)or by T 500 mg per day given in a cross-over double blind manner.It was shown that : 1) after P treatment, PCR was lowered and β-tg was increased, both significantly, at the end of exercice; 30 min later, PCR was normalized whereas β-tg remained high presumably because β-tg is not cleared from plasma within 30 min. 2) T treatment significantly inhibited both platelet responses.In conclusion, when platelets are submitted to systemic and sustained stimuli occurring during exercice stress, lowered PCR reflects the presence of circulating platelet aggregates which can be dispersed ex-vivo by EDTA. In these conditions, the meaning of this index is strongly confirmed by the simultaneous release of βtg. T treatment significantly reduces platelet reactivity to exer cice stress and may reduce the effects of platelet aggregation and release on compromised microcirculation.
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Kos, M., F. X. Hainz, I. Assmann, M. Kundi, I. Pabinger, S. Panzer, Ch Korninger, Ch Kunz, and K. Lechner. "RISK FACTORS FOR AIDS AND ARC IN MULTITRANSHJSED HAEMOPHILIACS: ASSOCIATION OF A WEAK GAG P 18 IN WESTERN BLOT (WB) AND IMMUNE THROMBOCYTOPENIA?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644680.
Full textAbstract:
Lymphocyte subsets, platelet counts, immune globulin levels and antibody to HIV (Elisa, WB) were determined in 87 multitransfused asymptomatic haemophiliacs in 1982/83. Between 1982 and 1987 6 patients developed AIDS and 5 ARC (3 immune thrombocytopenia and 2 lymphadenopathy). AIDS or ARC developed in seropositive patients only (11/49). Patients who subsequently developed AIDS or ARC showed significantly lower numbers of T helper lymphocytes (378/mm3 versus 605/mm3; p 0.01), lower platelet counts (157x109 versus 194x109; p 0.05) and higher levels of IgG (2528 mg/dl versus 1992 mg/dl; p 0.01). AIDS or ARC occured in 4 of 7 patients(57.1%) with a low HIV antibody level ( 2000), but only in 7 of 42 (16.6%) with a high level of antibody to HIV ( 2000). A weak gag p 24 in WB was found in 4 of 11 patients (36.3%) who subsequently acquired AIDS or ARC , while none of the patients whq remained asymptomatic displayed this reactivity pattern in WB. 9 patients showed a weak gag p 18 in WB. 8 of them (88.8%) have platelet counts below 120x109 /1, 3 developed imiruine thrombocytopenia with platelet counts of less than 50xl09. Oily 6 of 40 patients (15%) without this reactivity pattern in WB have platelet counts lower than 120x109 and none below 50xl09.We conclude that a weak gag p 24 in WB has a strong positive predictive power for the development of AIDS or ARC in seropositive haemophiliacs. A weak gag p 18 in WB could possibly be associated with the occurence of immune thrombocytopenia in these patients.
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FAUVEL-LAFEVE, F., and Y. J. LEGRAND. "IMMUNOCHEMICAL IDENTIFICATION OF A THROMBOSPONDIN -LIKE ANTIGEN IN ARTERIAL THROMBOGENIC MICROFIBRILS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643823.
Full textAbstract:
The biochemical structure of arterial microfibrils (MFS) is unknown. Presently, the most probable hypothesis is that elastin associated MFS contain several antigenic determinants with MW varying between 31 and 200 KD.From our previous studies we know that MFS extracted by 6 M GuCl contain a major glycoprotein with a 128 KD MV (GP128). GP 128 is essential for the reactivity of MFS towards blood platelets but due tc the high insolubility of the extracted material it was not possible to isolate and study this GP 128. We have used immunoblotting to determine if MFS contain determinants recognized by antibodies against connective tissue glycoproteins such as fibronectin, type VI collagen or anti-platelet thrombospondin (TSP). 'The results showed that MFS do not contain fibronectin or type VI collagen but that anti-TSP IgG reacted with GP 128. Furthermore, the Fab fragments from anti-TSP IgG inhibited platelet aggregation induced by MFS but not by collagen or ADP . In a second step,to raise antibodies against GP 128, we prepared blots from entire MFS, the nitrocellulose band corresponding to GP 128 was cut, dissolved in DMSO, and wrs injected to rabbits. Such obtained antibodies recognized only GP 128 in arterial MFS and also TSP in a platelet lysate confirming that GP 128 and TSP have a common antigenic structure. IgG from anti-GP 128 inhibit platelet aggregation induced by MFS but not by collagen or ADP. Previously reported observations showed that tissue TSP and endothelial cells derived GP 128 have a similar affinity for chromatography supports and have the same effect on platelet-MFS interactions. All these results led us to propose that TSP, GP 128, and MFS recognize a common determinant on platelet membrane. This assumption would be strenghened if GP 128 indeed is derived from tissue TSP.
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Schrör, K., P. Löbel, and E. Steinhagen-Thiessen. "SYNVINOLIN (SYN) IN TYPE Ha HYPERLIPOPROTEINAEMIA : NORMALIZED PLATELET HYPERREACTIVITY ASSOCIATED WITH AN IMPROVED RESPONSIVENESS AGAINST PGI2 AND ENHANCED PGI2 RECEPTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643460.
Full textAbstract:
Patients with familial hyperlipoproteinaemia (HLP) are at high risk for the premature development of atherosclerosis. This study was designed to investigate the effect of long-term treatment (8 months) with the HMG-CoA-reductase inhibitor SYN (20-40 mg/day) on platelet reactivity and PGIo receptors in 12 HLP patients (B) as compared with 11 untreated HLP patients (A) and 11 healthy subjects (C). Treatment with SYN reduced the plasma cholesterol to 234 ± 12 mg/dl as compared to 307 ± 21 (A) and 195 ± 14 mg/dl (C), respectively. Collagen (0.6 pg/ml) induced platelet thromboxane (TXB2) formation was 50±6 ng/ml in group A and significantly reduced to 32 ± 3 (B) which was not different from the 28±3 ng/ml in group C. Similar results were obtained by measuring pTatelet ATP secretion and aggregation. SYN treatment significantly improved the reduced number of PGI2 receptors (determined according to Schillinger & Prior, 1980) and normalized the iloprost (ILO, 30 nM) induced cAMP stimulation in platelet-rich plasma while the kg remained unchanged:These data demonstrate that SYN-treatment of HLP patients at doses that reduce plasma cholesterol by about 25% results in sig-ficant improvement of platelet function. This includes both normalization of platelet hyperreactivity against proaggregatory agents as well as platelet hyporeactivity aganist PGI2. The last effect might involve an increase of the (reduced) number of PGI2 receptors in HLP type IIa.
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Cordova, C., F. Violi, D. Praticò, A. Ghiselli, C. Alessandri, and F. Balsano. "CYCLOOXYGENASE INDIPENDENT PLATELET AGGREGATION:RELATION WITH ASPI RIN CONCENTRATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644828.
Full textAbstract:
Low doses of aspirin (20 mg/day) were previously reported to be uneffective in preventing platelet aggregation (PA) induced by pairs of aggregating agents such as PAF and adrenalin.This was in part attributed to the inability of such treatment to inhibit lipo oxygenase-dependent PA.The latter can be observed in vitro in"aspl rinated"platelets stimulated with high quantities of aggregating -agents.The aim of this study was to evaluate if the lipooxygenase-dependent PA was influenced by aspirin in a dose-dependent fashion. PA was studied in platelet rich plasma (PRP)(Born's method) by using threshold doses of aggregating agents (TDA) such as PAF(4-75 nM),epinephrine(0.6-2 μM) and collagen(2-4 μg/ml).PA performed in PRP pretrated with 100μM aspirin was fully prevented;in the same samples thromboxane (Tx) A2 evaluated by its metabolite Tx B2 was almost absent.Increasing amount of PAF(20 fold TDA),epinephrine(20 fold TDA) and collagen (36 fold TDA) do aggregate"aspirinated"pla telets;similarly"aspirinated"platelets aggregate when stimulated-with a pair of aggregating agents (TDA of PAF+epinephrine).This phenomenon was not detected if platelets were incubated with higher amounts of aspirin (250-500 μM).The study suggests that aspirin could influence lipooxygenase-dependent PA.This hypothesis is sup ported by a research showing the aspirin inhibits dose-dependently platelet HETE formation.A further study is now in progress to eva luate the influence of high doses of aspirin on cyclooxygenase-i"n dependent PA in vivo.
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Backhouse, C. M., A. C. Meek, K. R. Poskitt, and C. N. McCollum. "PULMONARY MICROEMBOLISATION IN SURGICAL SHOCK: THE EFFECT OF CYCLO-OXYGENASE INHIBITION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643458.
Full textAbstract:
Thromboxane release from platelet microemboli during major arterial surgery may mediate depression of cardio-pulmonary function. The effect of cyclo-oxygenase inhibition by aspirin has been studied in a porcine model of aortic surgery.Following autologous platelet labelling with 111-lndium, 24 pigs (20-25kg) were randomised to low dose (LD) aspirin (0.5mg/kg), high dose (HD) aspirin (10mg/kg) or placebo.Arterial and Swann Ganz catheters were inserted prior to surgery consisting of midline laparotomy, small bowel extériorisation, 1.5 hours of aortic clamping and 1 hour shock before resuscitation. On induction, during shock and at 3 days, platelet and leucocyte counts, lung platelet uptake (LPU), venous aggregates by screen filtration (SFP), mean arterial pressure (BP), cardiac output (CO), pulmonary shunt (PS) and alveolar-arterial pO2 difference (A-adO2) were measured.During shock following aortic declamping aspirin preserved blood pressure by increasing vascular resistance rather than CO. Venous aggregates by SFP tended to be lower on aspirin with significantly reduced LPU, subsequent pulmonary shunting and A-adO2. The improvement in PS but not A-adO2 remained significant at 3 days (p<0.05).Cyclo-oxygenase inhibition improved pulmonary function during surgical shock either by inhibiting platelet microemboli or by a direct effect on pulmonary arteriovenous shunts.
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Cunha-Ribeiro, L. M., S. Cunha, T. Brandão, F. S. Goncalves, A. Almeida-Dias, and J. M. Pina-Cabral. "CHANGES IN PLATELET HALF-LIFE, SENSITIVITY TO PROSTANOIDS AND AGGREGATION INDUCED IN THE DOG BY BODY HYPOTHERMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644543.
Full textAbstract:
During body cooling, there is a progressive thrombocytopenia, which is reversible after rewarming and is not prevented by previous treatement with aspirin, ticlopidine or prostacyclin.In this work, in order to evaluate if hypothermia induces alterations of platelet function we studied, in the dog, the platelet aggregation (PA) and the inhibitory action of PGE1 and of a stable prostacyclin analog, l loprost, before hypothermia(37°C.) and after rewarming(37°C.).Platelet half-life was also studied in another group of dogs before induction of hypothermia and after rewarming and recuperation of the animals. PA has been evaluated by platelet counting in whole blood.P1atelet half-life was estimated by serial determinations of MDA following administration of aspirin.PA induced by ADP (30μM) decreased 40% after rewarming(n=8). Platelet sensitivity to PGE1 (35 nM -1.4 μM f.c.) and Iloprost (7nM-172nM f.c.) was also decreased after rewarming: inhibition index 2.08±1.082 versus 1.19±0.362 (n=8; p<0.01) and 2.48<1.250 versus 1.10±0.227 (n=8; p<0.005) respectively.Platelet half-life increased after hypothermia from 3.99±0.730 days to 4.48±0.846 days(n=8 p<0.05).In the control group(n=6) platelet half-life determined twice with one week interval, did not change significantly.We conclude that body hypothermia decreases platelet reactivity to ADP; renders platelets less sensitive to the inibitory effect of prostanoids and increases platelet half-1 ife.These results are probably due to alterations in platelet membrane induced by cooling and rewarming the animals.
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Lloyd, J. V., S. E. Rodgers, D. M. Siebert, F. Bochner, G. H. McIntosh, and M. James. "PRESYSTEMIC DEACETYLATION OF LOW DOSES OF ENTERIC COATED ASPIRIN IN A PIG MODEL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643856.
Full textAbstract:
The antithrombotic effect of aspirin might be enhanced if platelet cyclooxygenase could be inhibited in the portal ciculation while sparing cyclooxygenase in the systemic vascular endothelium. This might be achieved by modifying the dose and formulation to maximise presystemic aspirin clearance by the liver. To test this hypothesis low dose enteric coated aspirin (Astrix, 50mg single dose, lOOmg single dose and lOOmg daily for 1 week) was orally administered to pigs with permanent indwelling arterial and portal vein catheters. Plasma aspirin concentrations were measured by high performance liquid chromatography in blood obtained simultaneously from the artery and portal vein for 6 hours after dosage. Platelet aggregation and thromboxane generation were measured in 4 pigs before and after the lOOmg chronic dosage regimen. Aortic prostacyclin production was measured in aspirin treated (lOOmg daily for 1 week) and untreated pigs after sacrifice. After the 50mg single dose the arterial:portal areas under the plasma concentration versus time curve (AUC) ratio was 0.63±0.09 (n=6). In 3 pigs which received all 3 dosage regimens the arterial:portal AUC ratios were 0.48±0.05 after 50mg single dose, 0.52±0.02 after lOOmg single dose and 0.47+0.03 after lOOmg daily for 1 week. Platelet aggregation in response to sodium arachidonate (1.65mM) was completely abolished after chronic aspirin administration. Thromboxane production (pg/106 platelets) by this stimulus decreased from 536±117 before aspirin to 57±14 after aspirin (n=4; p=0.017). Aortic prostacyclin synthesis (ng/disc after 10 min incubation) was 1.66±0.28 (n=4) in untreated pigs and 0.97±0.25 (n=4) in treated pigs (p=0.06).With this slow release aspirin formulation there was substantial but incomplete clearance of aspirin by the liver. This may not be sufficient to spare cyclooxygenase in the systemic vessels from the effect of aspirin.