Influence of renal function and platelet turnover on the antiplatelet effect of aspirin

Würtz, Morten; Wulff, Lise N.; Grove, Erik Lerkevang; Kristensen, Steen Dalby; Hvas, Anne‐Mette

doi:10.1016/j.thromres.2011.07.019

Cited by 24 publications

(18 citation statements)

References 39 publications

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“…These data can be supported by the results of Larsen et al who recently demonstrated positive correlation between hsCRP and immature platelet count as well as with thrombopoietin level [15]. Even though vWF Ag values were higher by 5 % in diabetics, they did not correlate with %RP which is in accordance to previous data [14]. Our data indicates that altered metabolic profile in T2DM is associated with platelet alterations that can cause poor antiplatelet, particularly clopidogrel, therapy response and subsequent recurrent ischemic events.…”

Section: Discussionsupporting

confidence: 88%

“…We observed negative, weak correlation between %RP and aspirin response, which is not in accordance to previously published data [10,11]. Recent study pointed that usage of different [14] so one may hypothesize that different methodology of antiplatelet therapy response evaluation should be taken into account. Several previously published studies showed significantly higher prevalence of aspirin resistance in upper tertile when patients were stratified according to the proportion of circulating RP [10,11] but we estimated aspirin therapy response in whole group of patients without this type of stratification.…”

Section: Discussioncontrasting

confidence: 71%

“…Mean values of %RP in these studies can't be compared to the mean values of %RP obtained by CELL-DYNN Sapphire. Mean values of %RP in our both groups of patients can't be compared with the results of the studies [9,14,15] where IPF was determined by Sysmex technology and one must observe that these studies did not separate diabetics from non-diabetic patients.…”

Section: Discussionmentioning

confidence: 90%

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Reticulated platelets and antiplatelet therapy response in diabetic patients

Mijović

Kovačević

Žarkov

et al. 2015

J Thromb Thrombolysis

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Increased platelet turnover and high level of reticulated platelets are associated with low response to antiplatelet therapy in diabetes mellitus type 2. This study evaluated association between percentage of reticulated platelets (%RP) and the response to antiplatelet therapy in patients with type 2 diabetes mellitus (T2DM). This prospective, pilot, case-control, clinical trial included 79 subjects stratified in three groups: group I included 30 patients with T2DM, group II included 34 non-diabetic patients and 15 healthy age and sex matched healthy volunteers were enrolled in control group. Platelet response to clopidogrel and aspirin was assessed by Multiplate(®) aggregometry analyzer. Individual response to dual antiplatelet therapy was estimated by the percentage of decrease in overall platelet aggregability (%DPA) obtained after antiplatelet therapy, calculated by presented formulas: %DPAadp = 100 × (1 - ADP/TRAP) and %DPAaspi = 100 × (1 - ASPI/TRAP). %RP was significantly higher in diabetics, than in non-diabetics, (3.17 ± 1.26 vs. 2.39 ± 1.56; p < 0.05). Significantly lower response to clopidogrel (31.55 ± 13.02 vs. 50.24 ± 11.38; p < 0.001) and aspirin (52.33 ± 22.67 vs. 64.31 ± 16.47; p < 0.05) therapy was observed in diabetics. %RP negatively correlated with response to clopidogrel therapy, but positively with metabolic profile indicators in diabetics (p < 0.05, all). Correlation of %RP with metabolic profile indicators and poor response to antiplatelet therapy suggest that altered metabolic profile can affect platelet turnover in T2DM leading to low responsiveness to antiplatelet therapy in these patients.

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Section: Discussionsupporting

confidence: 88%

Section: Discussioncontrasting

confidence: 71%

Section: Discussionmentioning

confidence: 90%

See 1 more Smart Citation

Reticulated platelets and antiplatelet therapy response in diabetic patients

Mijović

Kovačević

Žarkov

et al. 2015

J Thromb Thrombolysis

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“…Our observation is in accordance with Wurtz et al; in fact, they did not find any correlation between AA-induced platelet aggregation measured by the VerifyNow Õ and platelet turnover measured by immature platelet count [26].…”

Section: Discussionsupporting

confidence: 94%

Arachidonic acid-stimulated platelet tests: Identification of patients less sensitive to aspirin treatment

et al. 2015

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Serum thromboxane-B2 (TxB2), together with arachidonic acid (AA)-induced platelet aggregation, are, at the moment, the most used tests to identify patients displaying high on-aspirin treatment platelet reactivity (HAPR). Both tests are specific for aspirin action on cyclooxygenase-1. While the correlation between serum TxB2 assay and clinical outcome is established, data are conflicting with regard to aspirin treatment and a possible association with AA-stimulated platelet markers and clinical outcome. To understand such discrepancy, we performed a retrospective study to compare both assays. We collected data from 132 patients receiving a daily dose of aspirin (100 mg/day) and data from 48 patients receiving aspirin on alternate days. All Patients who received a daily dose of aspirin were studied for AA-induced platelet aggregation together with serum TxB2 levels and AA-induced TxB2 formation was also studied in 71 patients out of entire population. Consistent with recommendations in the literature, we defined HAPR by setting a cut-off point at 3.1 ng/ml for serum levels of thromboxane B2 and 20% for AA-induced platelet aggregation. According to this cut-off point, we divided our overall population into two groups: (1) TxB2 < 3.1 ng/ml and (2) TxB2 > 3.1 ng/ml. We found low agreement between such tests to identify patients displaying HAPR. Our results show that AA-induced platelet aggregation >20% identify a smaller number of HAPR patients in comparison with TxB2. A good correlation between serum TxB2 and arachidonic acid-induced TxB2 production was found (r = 0.76619).

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“…Increased platelet activation and turnover may, however, contribute to platelet dysfunction in these patients. Recently, Würtz et al [57], evaluated the antiplatelet effect of aspirin in patients with moderately reduced renal function and concluded that the reduced effect of aspirin could be explained by the increased RPs.…”

Section: Kidney Dysfunctionmentioning

confidence: 99%