Despite aggressive antiplatelet therapy in the setting of percutaneous coronary intervention, the incidence of stent thrombosis remains approximately 0.5% to 0.8%. We report on a 53-year-old male patient with recurrent coronary stent thrombosis treated by coronary re-interventions and anticoagulation. Initial diagnostic selective coronary angiography revealed 90% proximal circumflex coronary artery stenosis in a patient with 3rd degree of stabile angina by Canadian Cardiology Society classification. After premedication with a loading dose of 600 mg clopidogrel, 300 mg aspirin and intravenous enoxaparine 1 mg/kg, a bare-metal stent was implanted. The initial postprocedural course was normal. On the third day after the intervention, the patient was subjected to reintervention because of the stent thrombosis, and on the fifth day after reintervention – to the third percutaneous coronary angioplasty, also because of the stent thrombosis. Clopidogrel resistence was suspected and treatment with warfarin was initiated, after which there were no new cardiac events. Three months later, anticoagulation was discontinued, and as an antiplatelet agent aspirin 100 mg daily remained in therapy. Up to now (one-year), follow-up of the patient has been uneventful. In the case of suspected clopidogrel resistance, alternative therapeutic options have to be considered, like introducing per os anticoagulation (e.g. warfarin), introducing ticlopidin instead of clopidogrel, or, in the near future, possibly introducing prasugrel, a similar agent currently in transition from investigation into clinical use.

In this study we investigated the association of the interleukin-1 receptor antagonist gene variable number tandem repeat (IL1RN VNTR) polymorphism and of the inhibitor of kappa B-like protein (IKBL) gene polymorphism with myocardial infarction (MI) in a group of patients with type 2 diabetes. The IL1RN VNTR and the IKBL+ 738T > C gene polymorphisms were tested in 374 Caucasians: 151 cases with MI and 223 subjects with no history of coronary artery disease. The IL1RN VNTR polymorphism was not a risk factor for MI in Caucasians with type 2 diabetes (genotype 22 vs. the rest: odds ratio (OR) 1.6; 95% confidence interval (CI) = 0.8-3.5; p = 0.2). We also failed to demonstrate that IKBL+ 738T > C gene polymorphism was associated with MI in patients with type 2 diabetes (OR = 0.9; 95% CI = 0.3-2.6; p = 0.9). We provide evidence that the IL1RN VNTR and the IKBL + 738T > C gene polymorphisms are not risk factors for MI in Caucasians with type 2 diabetes.

Genetic epidemiology studies of hereditary hemochromatosis (HHC) have shown a high prevalence of the C282Y mutation in individuals of the North Western European origin, whereas lower prevalence of HFE gene mutations was detected in the populations from southern European countries. However, no HFE mutation prevalence data have been provided for the population of Bosnia-Herzegovina so far. Therefore, the aim of this study was to determine the frequency of the C282Y and H63D HFE gene mutations in the population of Bosnia-Herzegovina. Among 200 analysed subjects 8 (4%) were C282Y heterozygotes; no C282Y homozygotes were found. The frequency of the H63D allele was 11.5%. There were 33 (16.5%) heterozygotes and 6 (3%) homozygotes for the H63D mutation. One (0.5%) compound heterozygote C282Y/H63D was identified. The observed C282Y and H63D allele frequency was 2.25% (95% confidence interval: 1.2-4.2) and 11.5% (95% confidence interval: 8.7-14.9), respectively. The prevalence of the C282Y and H63D mutations was estimated in Bosnia-Herzegovina, which fit well in the European northwest-to-southeast gradient of the C282Y mutation distribution. In addition, these results have an important implication for clinical evaluation of HHC in Bosnia-Herzegovina.

Angiotensin II is the major effector molecule of renin-angiotensin system; its production can be conveniently interrupted by angiotensin-converting enzyme (ACE). Typical plasma levels of ACE accompany the I/D polymorphism; however, a controversy exists as to whether the DD genotype of the ACE polymorphism affects the risk for the development of coronary artery disease (CAD) and to what extent the ACE polymorphism is associated with CAD in different populations. We compared the I/D polymorphism in 212 CAD patients younger than 50 years with 165 healthy control individuals. They were all from the Tuzla region in Bosnia and Herzegovina. Patients with CAD had a higher prevalence of the DD genotype (36.3%) than controls (25.6%). The odds ratio for the ACE DD genotype in CAD patients was 1.7 (95% confidence interval 1.0-2.7; p < 0.05). We may conclude that the D/D genotype of the ACE gene polymorphism is associated with an increased risk for CAD in the Bosnian population.