Obesity and antiplatelet effects of acetylsalicylic acid and clopidogrel in patients with stable angina pectoris after percutaneous coronary intervention

Haberka, Maciej; Mizia-Stec, Katarzyna; Lasota, Bartosz; Kyrcz-Krzemien, S.; Gąsior, Zbigniew

doi:10.20452/pamw.3039

Cited by 6 publications

(4 citation statements)

References 13 publications

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“…On the contrary, Verdoia et al [25] held that MPV elevation did not influence the risk of HTPR with clopidogrel. The same argument was made in the correlation between body mass index (BMI) and HTPR, [26,27] so it is necessary to explore a predictive model of HTPR.…”

Section: Introductionmentioning

confidence: 99%

Clinical outcomes and predictive model of platelet reactivity to clopidogrel after acute ischemic vascular events

Chen

Zhang

et al. 2019

Chinese Medical Journal

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Background: High on-treatment platelet reactivity (HTPR) has been suggested as a risk factor for patients with ischemic vascular disease. We explored a predictive model of platelet reactivity to clopidogrel and the relationship with clinical outcomes. Methods: A total of 441 patients were included. Platelet reactivity was measured by light transmittance aggregometry after receiving dual antiplatelet therapy. HTPR was defined by the consensus cutoff of maximal platelet aggregation >46% by light transmittance aggregometry. CYP2C19 loss-of-function polymorphisms were identified by DNA microarray analysis. The data were compared by binary logistic regression to find the risk factors. The primary endpoint was major adverse clinical events (MACEs), and patients were followed for a median time of 29 months. Survival curves were constructed with Kaplan-Meier estimates and compared by log-rank tests between the patients with HTPR and non-HTPR. Results: The rate of HTPR was 17.2%. Logistic regression identified the following predictors of HTPR: age, therapy regimen, body mass index, diabetes history, CYP2C19 ∗ 2, or CYP2C19 ∗ 3 variant. The area under the curve of receiver operating characteristic for the HTPR predictive model was 0.793 (95% confidence interval: 0.738–0.848). Kaplan-Meier analysis showed that patients with HTPR had a higher incidence of MACE than those with non-HTPR (21.1% vs . 9.9%; χ 2 = 7.572, P = 0.010). Conclusions: Our results suggest that advanced age, higher body mass index, treatment with regular dual antiplatelet therapy, diabetes, and CYP2C19 ∗ 2 or CYP2C19 ∗ 3 carriers are significantly associated with HTPR to clopidogrel. The predictive model of HTPR has useful discrimination and good calibration and may predict long-term MACE.

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Section: Introductionmentioning

confidence: 99%

Clinical outcomes and predictive model of platelet reactivity to clopidogrel after acute ischemic vascular events

Chen

Zhang

et al. 2019

Chinese Medical Journal

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“…Our study did not confirm this "obesity paradox". There is a study that has found that despite the initial period of low platelet response to loading dose of clopidogrel, after 30 days of clopidogrel administration, platelet response was similar between obese and normal-weight patients (35).…”

Section: Discussionmentioning

confidence: 99%

Association of serum levels of lipoprotein A-I and lipoprotein A-I/A-II with high on-treatment platelet reactivity in patients with ST-segment elevation myocardial infarction (STEMI).

Siniarski

Grzybczak²,

Rostoff³

et al. 2018

Anatol J Cardiol

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ObjectiveHigh-density lipoproteins (HDLs) are a very heterogeneous group of particles. Little is known about the impact of their subfractions including lipoprotein A-I (LpA-I) and lipoprotein A-I/A-II (LpA-I/A-II) on platelet function and high on-treatment platelet reactivity (HPR), particularly in the acute phase of ST-segment elevation myocardial infarction (STEMI). The aim of the study was to evaluate the relationship between serum levels of LpA-I and LpA-I/A-II and HPR in STEMI patients.MethodsFifty-two consecutive STEMI patients (26.9% women, mean age 60.6±9.1 years) were enrolled into this study. Clinical and demographic data were collected and HDL subfractions were measured by rocket immunoelectrophoresis. Platelet reactivity was assessed using light transmission aggregometry and quantitative flow cytometry.ResultsWe found a positive correlation between platelet aggregation after both ADP-5 and ADP-20 stimulation and serum level of LpA-I. Compared with subjects with satisfactory platelet response to clopidogrel, patients with HPR had 32.44% higher serum level of LpA-I (p=0.021). On the other hand, patients with HPR assessed by ADP-5 stimulation had 22.13% lower serum level of LpA-I/A-II (p=0.040). Regression analysis showed that LpA-I [odds ratio (OR) 1.03; 95% confidence interval (CI) 1-1.07; p=0.049] and current smoking (OR 0.18; 95% CI 0.04-0.81; p=0.025) were independent predictors of HPR. With receiver operating characteristic (ROC) curve analysis, we designated the cut-off point at serum level of 57.52 mg/dL for LpA-I for predicting HPR (AUC=0.71, p=0.010).ConclusionThis study showed that higher serum level of LpA-I measured in the acute phase of STEMI is an independent risk factor for HPR. Our study is the first to demonstrate an important and distinct activity of LpA-I and LpA-I/A-II that can prove pleiotropic and different functions of HDL subfractions in acute STEMI.

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“…One of the main risk factors for cardiac angina is a atherosclerosis of coronary arteries [2][3][4][5][6] . Other risk factors for cardiac angina include hypertension, diabetes mellitus, obesity, smoking; stress, hypodynamia, infectious diseases, allergic lesions and genetic mutations [7][8][9][10][11][12] .…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial mutations associated with cardiac angina

Рыжкова¹,

Sinyov²,

Sazonova³

et al. 2019

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Aim: Cardiac angina is a disease in which discomfort or retrosternal pain may occur. Atherosclerosis of coronary arteries is one of the main risk factors for cardiac angina. The aim of the investigation was to analyze the association of 11 mitochondrial genome mutations with cardiac angina. In our preliminary studies an association of these mutations with atherosclerosis, a risk factor for cardiac angina, was found. Methods: We used samples of white blood cells collected from 192 patients with cardiac angina and 201 conventionally healthy study participants. DNA from blood leukocyte samples was isolated using a phenol-chloroform method. DNA amplicons containing the investigated regions of 11 mitochondrial genome mutations (m.

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Obesity and antiplatelet effects of acetylsalicylic acid and clopidogrel in patients with stable angina pectoris after percutaneous coronary intervention

Cited by 6 publications

References 13 publications

Clinical outcomes and predictive model of platelet reactivity to clopidogrel after acute ischemic vascular events

Clinical outcomes and predictive model of platelet reactivity to clopidogrel after acute ischemic vascular events

Association of serum levels of lipoprotein A-I and lipoprotein A-I/A-II with high on-treatment platelet reactivity in patients with ST-segment elevation myocardial infarction (STEMI).

Mitochondrial mutations associated with cardiac angina

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