Non-HDL cholesterol is an independent risk factor for aspirin resistance in obese patients with type 2 diabetes

Kim, Jong Dai; Park, Cheol‐Young; Ahn, Kue Jeong; Cho, Jae Hyoung; Choi, Kyung Mook; Kang, Jun Goo; Kim, Jae Hyun; Lee, Ki Young; Lee, Byung Wan; Mok, Ji Oh; Moon, Min Kyong; Park, Joong Yeol; Park, Sung Woo

doi:10.1016/j.atherosclerosis.2014.01.015

Cited by 15 publications

(15 citation statements)

References 32 publications

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“…In our experiment using a pre-treatment with RF-9, we could not verify its antagonistic effect on KP, moreover we demonstrated a synergy with KP-13. Our results can be supported by the data published by Kim et al (2014), reporting that RF-9, the presumed antagonists of NPFF1R, is in fact the agonist of both NPFF1R and the KP receptor (KISS1R). The reason that the RF-9 pre-treatment induced even stronger platelet activation (compared to the case when only KP was used), can be found in that the elevation of the ic.…”

Section: Nondiabetic Ratssupporting

confidence: 89%

“…We may think that the reduced ex vivo aggregability of diabetic platelets to KP-13 is explained by the in vivo activation of diabetic platelets, which is demonstrated by the degranulation of thrombocytes, the glycation of receptors, and the alteration of membrane fluidity (Randriamboavonjy et al 2012). On the other hand, it has already been reported that the glycation of cyclooxygenase enzyme (Angiolillo and Suryadevara 2009) and diabetic dyslipidemia (Watala et al 2005;Kim et al 2014) play a role in the development of aspirin resistance. Simonin et al (2006) reported that RF-9 binding to the NPFF-receptor, type 2 (NPFF2R) KP receptor might have a potentially antagonistic effect on KP-13.…”

Section: Nondiabetic Ratsmentioning

confidence: 99%

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Effects of kisspeptin on diabetic rat platelets

Mezei

Váczi

Török

et al. 2017

Can. J. Physiol. Pharmacol.

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Hyperglycemia, hyperlipidemia, and free radicals result in platelet activation and atherogenesis. Kisspeptin (KP) is able to regulate metabolism, hemostasis, and the development of atherosclerosis. We examined whether platelet aggregation of streptozotocin-induced diabetic rats depends on the inducer type and if KP-13 and RF-9 (a kisspeptin receptor modifier) can influence platelet function. We measured the speed and the maximum of aggregation, along with the area under the curve. Serum glucose and calcium levels and urine formation of diabetic animals increased, while the body mass and platelet count decreased. Collagen was the most effective inducer of platelet aggregation. The aggregability of nondiabetic platelets was elevated in the presence of 5 × 10 mol/L KP-13. This effect was less expressed in diabetic animals. The effectivity of RF-9 was stronger than that of KP-13 in nondiabetic platelets, however it was ineffective in diabetic animals. RF-9 pre-treatment did not change the effects of 5 × 10 mol/L KP-13 in either animal group. The in vivo activation of diabetic platelets, which may be due to elevated serum calcium, induces thrombocytopenia and may lead to reduced in vitro aggregability. We could not demonstrate the antagonistic effect of RF-9 against KP-13 in isolated platelets.

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Section: Nondiabetic Ratssupporting

confidence: 89%

Section: Nondiabetic Ratsmentioning

confidence: 99%

Effects of kisspeptin on diabetic rat platelets

Mezei

Váczi

Török

et al. 2017

Can. J. Physiol. Pharmacol.

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“…[71, 72] Using a VerifyNow® assay threshold of 550 ARUs, Kim and colleagues observed HPR in 9.8% in their cohort of 1,045 Korean patients with type 2 diabetes taking low dose aspirin. [73] Another study using the VerifyNow® assay showed comparable rates of HPR among patients with type 1 and type 2 diabetes (21.7% vs. 16.2%). [74]…”

Section: Aspirin Resistance In Diabetesmentioning

confidence: 99%

State-of-the-Art: Hypo-responsiveness to Oral Antiplatelet Therapy in Patients with Type 2 Diabetes Mellitus

Kumbhani

Marso

McGuire

2015

Curr Cardiovasc Risk Rep

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Diabetes mellitus is a global pandemic, associated with a high burden of cardiovascular disease. There are multiple platelet derangements in patients with diabetes, and antiplatelet drugs remain the first-line agents for secondary prevention as well as for high-risk primary prevention among patients with diabetes. This review provides a summary of oral antiplatelet drug hypo-responsiveness in patients with diabetes, specifically aspirin and Clopidogrel resistance. Topics discussed include antiplatelet testing, definitions used to define hypo-response and resistance, its prevalence, association with clinical outcomes and strategies to mitigate resistance. The role of prasugrel and ticagrelor, as well as investigational agents, is also discussed.

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“…The prevalence of aspirin resistance in our study was 7.5% according to VerifyNow and 18.9% according to PFA-100, and these results are similar to a previous study. According to our previous study of 1056 type 2 diabetes mellitus patients from 11 hospitals, aspirin resistance measured in ARUs using VerifyNow was detected in 102 of 1045 subjects (prevalence 9.8%) and was associated with HDL-cholesterol (6). Another study of patients with type 2 diabetes mellitus reported that the prevalence of aspirin resistance measured by the PFA-100 system was 21.5% (22).…”

Section: Discussionmentioning

confidence: 97%

Effect of aspirin versus cilostazol for inhibition of antiplatelet aggregation in type 2 diabetes mellitus patients (ESCORT-DM Study)

Hong

Lee

Park

2020

Preprint

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Abstract BackgroundThe role of aspirin in primary prevention of cardiovascular disease in patients with diabetes is controversial. In contrast, some studies have suggested beneficial effects of cilostazol on cardiovascular disease in patients with diabetes. Here we prospectively investigated the antiplatelet effects of cilostazol compared with aspirin in patients with diabetes and cardiovascular risk factors.MethodsWe randomly assigned 116 patients with type 2 diabetes and cardiovascular risk factors but no evident cardiovascular disease to receive aspirin at a dose of 100 mg or cilostazol at a dose of 200 mg daily for 14 days. The primary efficacy outcome was antiplatelet effects of aspirin and cilostazol assessed with the VerifyNow system (aspirin response units; ARU) and PFA-100 (closure time; CT). Secondary outcomes were changes of clinical laboratory data.ResultsThe decrease of ARU (-0.4 ± 7.1% vs. -28.9 ± 9.9%, p < 0.001) and the increase of CT (25.7 ± 54.1% vs. 99.6 ± 63.5%, p < 0.001) were significantly greater in aspirin compared cilostazol. The prevalence of aspirin resistance was 7.5% according to VerifyNow (defined by ARU ≥ 550) and 18.9% according to PFA-100 (CT < 192 s). Compared with aspirin, cilostazol treatment was associated with increased HDL cholesterol (7.1 ± 12.7% vs. 4.2 ± 18.0%, p = 0.006) and decreased triglycerides (-9.4 ± 33.7% vs. 4.4 ± 17.57%, p = 0.016). However, there were no significant changes in total and LDL cholesterol, CRP level, and CD40 ligand between cilostazol and aspirin groups.ConclusionsAspirin showed better antiplatelet effects assessed with VerifyNow and PFA-100 compared with cilostazol. However, there were favorable changes in atherogenic dyslipidemia only in the cilostazol treatment group.Trial registrationNCT02933788, dated october 14, 2016

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Non-HDL cholesterol is an independent risk factor for aspirin resistance in obese patients with type 2 diabetes

Cited by 15 publications

References 32 publications

Effects of kisspeptin on diabetic rat platelets

Effects of kisspeptin on diabetic rat platelets

State-of-the-Art: Hypo-responsiveness to Oral Antiplatelet Therapy in Patients with Type 2 Diabetes Mellitus

Effect of aspirin versus cilostazol for inhibition of antiplatelet aggregation in type 2 diabetes mellitus patients (ESCORT-DM Study)

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