Background: Coronary stent infections in general and stent abscesses (SAs) in particular are rare but often deadly complications. Most SAs manifest with fever and chest pain within 30 days after intervention and require antibiotics and stent removal. Case Report: A 45-year-old man with second ST elevated myocardial infarction and cardiogenic shock was admitted to a hospital that had no cardiac catheterization laboratory. The patient underwent fibrinolytic therapy with alteplase but died 1 h later. His medical history revealed posterior myocardial infarction 7 years before, which had been successfully treated with a bare metal stent of the right coronary artery. The post-discharge observation had been unremarkable with no evidence of ischaemia or infection but gross non-compliance. Autopsy revealed complete closure of the left main coronary artery and a surprise additional finding, namely SA; the stented portion of the artery was enveloped by an abscess, and purulent material completely occluded the stent, which was floating in pus. Impressions: Since coronary angioplasty is so common, the incidence of late silent SA is probably higher than expected, especially considering that there is often a lack of clinical manifestations. Clinicians should be cognizant of this complication. More attention may be required to assess the condition of existing stents during repeated interventions. Gross non-compliance and/or early withdrawal from dual anti-platelet therapy may be directly responsible for the development of silent delayed SA.
To study the distribution of alleles and genotypes of polymorphic markers of genes CYP2C9 and VKORC1 of Russian patients who live in Moscow, and in order to assess the influence of genetic factors on warfarin therapy 400 patients have been genotyped. The dosage of warfarin which is required for achievement of INR target values has been different among owners of different geno- types of polymorphic markers of genes CYP2C9 . Meanwhile the highest average dose has been required for genotype *1/*1 and the lowest – for owners of alleles *2 and *3 . For polymorphism G(- 1639)A of the gene VKORC1 the dosage of warfarin which is required for achievement of the INR target values, has been different among owners of different genotypes. The highest average dose has been required for genotype GG, and the lowest – for genotype AA. The results will allow to work out more accurate algorithm of choosing of the initial dose of warfarin depending on the genotypes of polymorphic markers of genes CYP2C9 and VKORC1.
Цель. Выявление ассоциации наследственных особенностей факторов вос-паления с риском неблагоприятного исхода у больных мерцательной арит-мией (МА). Материал и методы. Наблюдали 258 больных (68,5±0,67 лет) с неклапан-ной МА, фиксируя развитие ишемического инсульта, инфаркта миокарда, венозных и артериальных тромбоэмболий. Срок наблюдения составил 455±11,71 дней. Результаты. Факторами, независимо ассоциированными с развитием ишемического инсульта у больных, не получающих антикоагулянты (n=101), явилось носительство аллеля С полиморфного маркера rs2228145(А/С) гена рецептора ИЛ-6 (ОШ 13,25 ДИ 1,57-112,18, р=0,018), возраст ≥75 лет (ОШ 1,1, ДИ 1,008-1,2, р=0,032) и ФВ ЛЖ (ОШ 0,97 ДИ 0,94-0,99 р=0,027), с развитием "тромботической конечной точки" -СД (ОШ 4,3 ДИ 1,46-12,45 р=0,008), ФВ ЛЖ (ОШ 0,96 ДИ 0,94-0,98, р<0,0001) и носительство аллеля С полиморфного маркера rs2228145(А/С) гена рецептора ИЛ-6 (ОШ 4,03 ДИ 1,07-15,26, р=0,04). Не выявлено ассоциации с неблагоприятными исходами полиморфизма генов ИЛ-6 (G(-174)C и G(-572)C), ИЛ-10 (C(-819) T), ФНО (G(-238)A, G(-308)A и ФНОα rs180630). У получающих адекватную антикоагулянтную терапию (n=157) достоверной ассоциации полимор-физма гена рецептора ИЛ-6 с развитием неблагоприятных исходов также не выявлено. Заключение. Таким образом, носительство аллеля С полиморфного маркера rs2228145(А/С) гена рецептора ИЛ-6 может быть независимым маркером риска неблагоприятного исхода у больных с "неклапанной" МА, потенциально, позволяющим отбирать для лечения больных, не имеющих достаточного уровня риска по общепринятым шкалам. Aim. To reveal the association of hereditary specifics of inflammatory factors with the adverse risk in atrial fibrillation (AF). Material and methods. Totally 258 patients studied (68,5±0,67 y. o.) with nonvalvular AF, recording the events as ischemic stroke, myocardial infarction, venous and arterial thromboembolism. Mean follow-up was 455±11,71 days. Results. Factors that are independently associated with ischemic stroke development in patients not receiving anticoagulants (n=101), were the allele C of polymorphic marker rs2228145(А/С) of gene IL-6 receptor (OR 13,25 CI 1,18, р=0,018), age ≥75 y. o. (OR 1,1, CI 1,008-1,2, р=0,032) and EF LV (OR 0,97 CI 0,99 р=0,027), with a "thrombotic endpoint" development -DM (OR 4,3 CI 1,45 р=0,008), EF LV (OR 0,96 CI 0,98, р<0,0001) and carriage of allele C of polymorphic marker rs2228145(А/С) of receptor to IL-6 gene (OR 4,03 CI 1,(7)(8)(9)(10)(11)(12)(13)(14)(15)26, р=0,04). There was no association with adverse outcomes in genes IL-6 polymorphisms as (G(-174)C and G(-572)C), ИЛ-10 (C(-819)T), ФНО (G(-238)A, G(-308)A and ФНОα rs180630). In those receiving adequate anticoagulant therapy (n=157) there was no significant association of IL-6 receptor gene polymorphism with adverse outcomes. Conclusion.Therefore, the carriage of allele C of polymorphic marker rs2228145(А/С) of the IL-6 receptor gene might be an independent risk marker for adverse outcome in non-valvular AF, potentially, being a selection tool for thos...
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