Relationship between cytochrome P450 2C19*17 genotype distribution platelet aggregation and bleeding risk in patients with blood stasis syndrome of coronary artery disease treated with clopidogrel

2012 ◽  
Vol 10 (6) ◽  
pp. 647-654 ◽  
Author(s):  
ZL Dai
Keyword(s):  
Coronary Artery Disease ◽  
Cytochrome P450 ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Blood Stasis ◽  
Bleeding Risk ◽  
Blood Stasis Syndrome ◽  
Genotype Distribution ◽  
Cytochrome P450 2C19 ◽  
Artery Disease

scholarly journals Effects of Cytochrome P450 2C19 and Paraoxonase 1 Polymorphisms on Antiplatelet Response to Clopidogrel Therapy in Patients with Coronary Artery Disease

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e110188 ◽  
Author(s):  
Damrus Tresukosol ◽  
Bhoom Suktitipat ◽  
Saowalak Hunnangkul ◽  
Ruttakarn Kamkaew ◽  
Saiphon Poldee ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Cytochrome P450 ◽  
Coronary Artery ◽  
Paraoxonase 1 ◽  
Cytochrome P450 2C19 ◽  
Clopidogrel Therapy ◽  
Artery Disease

Genetic predictors for symptoms recurrenсe in coronary artery disease after percutaneous coronary intervention

2017 ◽  
pp. 81-86
Author(s):  
Г.А. Березовская ◽  
Е.С. Клокова ◽  
Н.Н. Петрищев
Keyword(s):  
Coronary Artery Disease ◽  
Percutaneous Coronary Intervention ◽  
Coronary Artery ◽  
Coronary Intervention ◽  
Folate Metabolism ◽  
Genotype Distribution ◽  
Polymorphic Markers ◽  
Percutaneous Coronary ◽  
Artery Disease

Гены тромбообразования и фолатного обмена играют важную роль в развитии и прогрессии ишемической болезни сердца (ИБС). Однако о возможной роли полиморфных маркеров в рецидиве ИБС после чрескожного коронарного вмешательства (ЧКВ) известно недостаточно. Цель исследования: Оценить роль генетических факторов системы тромбообразования и фолатного обмена (полиморфных маркеров генов F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB ), в возобновление клиники ИБС после ЧКВ. Методика: Исследование проводили с использованием выборки из 90 больных ИБС в возрасте от 40 до 75 лет: 75 пациентов после планового ЧКВ (60 мужчин и 15 женщин) и 15 лиц после экстренного ЧКВ (12 мужчин и 3 женщины). Молекулярно-генетическое исследование было выполнено с помощью комплекта реагентов «Сердечно-сосудистые заболевания СтрипМетод»® (ViennaLab Diagnostics GmbH, Австрия), выявляющие следующие варианты: F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB . Результаты: В результате исследования была показана ассоциация полиморфного маркера G103T ( Val34Leu ) гена F13A1 (фактор свертываемости крови 13, субъединица A1) с развитием рецидивирующего состояния ИБС после ЧКВ. Выявлены статистически значимые различия в распределении частот генотипов полиморфного маркера Val34Leu гена F13A1 . Показано, что частота генотипа Val/Val у пациентов с осложнениями была выше, чем у пациентов без таковых: 0,700 и 0,400 соответственно (c = 7,78; p = 0,020), при этом генотип Val/Val проявил себя как фактор риска развития осложнений: ОШ = 3,50 (95%ДИ 1,37-8,93). При сравнении аллелей выявили, что частота аллеля L у больных с осложнениями была ниже, чем у лиц без таковых: 0,167 и 0,375 соответственно (p = 0,004), и носительство аллеля L уменьшало вероятность развития осложнений: ОШ = 0,33 (95%ДИ 0,15-0,72). Заключение: Носительство варианта 34V гена F13A1 , кодирующего A-субъединицу фактора свёртывания 13, предрасполагает к возобновлению клинических проявлений ИБС после ЧКВ. Genes of thrombosis and folate metabolism play an important role in development and progression of coronary artery disease (CAD). However, a possible role of polymorphic markers in CAD relapse following percutaneous coronary intervention (PCI) is not sufficiently understood. Background. Reports have indicated an association of genetic factors generally related with thrombophilia and recurrence of symptoms for coronary artery disease (CAD) following a percutaneous coronary intervention (PCI) due to restenosis and in-stent thrombosis. However, the relapse can also be caused by progression of atherosclerosis and endothelial dysfunction in unoperated blood vessels. Aim: To assess the role of genetic risk factors involved in thrombosis and folate metabolism (polymorphic markers of F5, F2, F13A1, PAI1, HPA1, MTHFR, and FGB genes) in recurrence of CAD symptoms after PCI. Methods: The study included 90 patients with CAD aged 40-75; 75 of these patients had undergone elective PCI (60 men and 15 women) and 15 patients - emergency PCI (12 men and 3 women). Molecular genetic tests were performed using a CVD StripAssays® reagent kit (ViennaLab Diagnostics GmbH, Austria) to identify the following genetic variations: F5, F2, F13A1, PAI1, HPA1, MTHFR, and FGB . Results: The study results showed a significant association of the G103T ( Val34Leu ) polymorphism in the F13A1 gene with relapses of IHD after PCI. Significant differences were found in genotype distribution frequencies of the Val34Leu polymorphism in the F13A1 gene. The frequency of Val / Val genotype was higher in patients with complications than without complications, 0.700 and 0.400, respectively (c = 7.78, p = 0.020). Furthermore, the Val/Val genotype can be classified as a risk factor for complications (OR = 3.50; 95% CI, 1.37-8.93). The L allele frequency was lower in patients with complications than in those without complications (0.167 and 0.375, respectively, p = 0.004), and carriage of the L allele reduced the likelihood of complications (OR = 0.33; 95% CI 0.15-0.72). Conclusion: Carriage of the 34V variant in the F13A1 gene that encodes the coagulation factor XIII A subunit predisposes to a relapse of CAD symptoms after PCI.

Thrombopoietin and platelet aggregation in patients with stable coronary artery disease

Platelets ◽  
2017 ◽  
Vol 28 (8) ◽  
pp. 822-824
Author(s):  
Sanne Bøjet Larsen ◽  
Erik Lerkevang Grove ◽  
Søs Neergaard-Petersen ◽  
Morten Würtz ◽  
Anne-Mette Hvas ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Artery Disease

CYP3A4 *1B Gene Polymorphism in Coronary Artery Disease Patients with Obesity Undergoing Statin Treatment

2021 ◽  
Vol 18 ◽  
Author(s):  
Elifcan Gezer ◽  
Mehtap Cevik ◽  
Cansu Selcan Akdeniz ◽  
Ismail Polat Canbolat ◽  
Selen Yurdakul ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Statin Therapy ◽  
Plasma Lipid ◽  
Blood Cholesterol ◽  
Study Group ◽  
Genotype Distribution ◽  
Obese Patients ◽  
Artery Disease

Objective: Coronary artery disease (CAD) is the one of the leading cause of morbidity and mortality worldwide and statins are frequently prescribed in the treatment of CAD to help lower blood cholesterol levels. Since the main enzyme involved in the metabolism of statins is CYP3A4, we aimed to investigate the effect of CYP3A4 * 1B genotypes on plasma lipid profile in Turkish cardiovascular disease subject with and without obesity taking statin. Materials and Methods: The study group consisted of 85 cardiovascular disease patients who were prescribed statins and had routine biochemical analysis data. Polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) assay were performed for genotyping of CYP3A4 *1B (rs2740574) polymorphism. Results: Genotype distribution of CYP3A4 *1B polymorphism was found for homozygous wild (AA) and homozygous polymorphic (GG) genotypes as 94.1% and 5.9% respectively. We did not detect patients with heterozygous genotype in our study group. We found that the mean LDL-c, TG and TC levels were higher in patients with CYP3A4 *1B GG compared to AA genotype. The frequency of CYP3A4 *1B GG genotype frequency (9.5%) was detected higher in the obese patients compared to the non-obese patients (7.7%) (χ2=0.037, p=0.85). Conclusions: Our results demonstrate that CYP3A4 *1B homozygous polymorphic genotype distribution tend to be higher in obese patients compared to non- obese patients with cardiovascular disease which may point *1B allele to have a slight effect on serum lipids during statin therapy. Additional studies with higher samples are needed for evaluating the role of CYP3A4 *1B on lipids in patients under statin therapy.

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