The baseline data from GLORIA-AF phase 2 demonstrate that in newly diagnosed nonvalvular atrial fibrillation patients, NOAC have been highly adopted into practice, becoming more frequently prescribed than VKA in Europe and North America. Worldwide, however, a large proportion of patients remain undertreated, particularly in Asia and North America. (Global Registry on Long-Term Oral Antithrombotic Treatment in Patients With Atrial Fibrillation [GLORIA-AF]; NCT01468701).

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Aim: This study evaluated the impact of hyperuricemia (HUR) on outcome in patients with different types of impaired renal function (IRF) and acute myocardial infarction (AMI) treated invasively. Methods: Out of 3,593 consecutive AMI patients treated invasively, 1,015 IRF patients were selected. The IRF group consisted of patients with baseline kidney dysfunction (BKD group) and/or patients with contrast-induced nephropathy (CIN group). HUR was defined as a serum uric acid concentration (SUAC) >420 µmol/l (>7 mg/dl). Independent predictors of death and major adverse cardiovascular events (MACE) were selected by the multivariate Cox-regression model. Results: Remote mortality rates were higher in HUR patients: IRF (32.7 vs. 18.6%), BKD (41.3 vs. 25.9%), CIN (35.4 vs. 16.7%); all p < 0.001. HUR was an independent predictor of death in BKD (hazard ratio (HR) 1.38, p < 0.05). Each 100-µmol/l increase in SUAC was associated with a significant increase of HR for mortality: 1.087 in IRF patients, 1.108 in BKD patients, 1.128 in CIN patients; all p < 0.05. Remote major adverse cardiovascular event rates were higher in HUR patients: IRF (55.4 vs. 48.9%), CIN (56.8 vs. 48%); both p < 0.05. Conclusions: In AMI patients treated invasively, an increase in SUAC is an independent predictor of death within all types of renal dysfunction; HUR defined as SUAC >420 µmol/l (>7 mg/dl) is a predictor only in BKD patients.

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BackgroundDiabetes (DM) deteriorates the prognosis in patients with coronary heart disease. However, the prognostic value of different glucose abnormalities (GA) other than DM in subjects with acute myocardial infarction (AMI) treated invasively remains unclear.AimsTo assess the incidence and impact of GA on clinical outcomes in AMI patients treated with percutaneous coronary intervention (PCI).MethodsA single-center, prospective registry encompassed 2733 consecutive AMI subjects treated with PCI. In all in-hospital survivors (n = 2527, 92.5%) without the history of DM diagnosed before or during index hospitalization standard oral glucose tolerance test (OGTT) was performed during stable condition before hospital discharge and interpreted according to WHO criteria. The mean follow-up period was 37.5 months.ResultsThe incidence of GA was as follows: impaired fasting glycaemia - IFG (n = 376, 15%); impaired glucose tolerance - IGT (n = 560, 22%); DM (n = 425, 17%); new onset DM (n = 384, 15%); and normal glucose tolerance – NGT (n = 782, 31%). During the long-term follow-up, death rate events for previously known DM, new onset DM and IGT were significantly more frequent than those for IFG and NGT (12.3; 9.6 and 9.4 vs. 5.6 and 6.4%, respectively, P < 0.05). The strongest and common independent predictors of death in GA patients were glomerular filtration rate < 60 ml/min/1,73 m^2 (HR 2.0 and 2.8) and left ventricle ejection fraction < 35% (HR 2.5 and 1.8, all P < 0.05) respectively.ConclusionsGlucose abnormalities are very common in AMI patients. DM, new onset DM and IGT increase remote mortality. Impaired glucose tolerance bears similar long-term prognosis as diabetes.

Objective-A rare mutation in low-density lipoprotein receptor-related protein 6 gene (LRP6) was identified as the primary molecular defect underlying monogenic form of coronary artery disease. We hypothesized that common variants in LRP6 could predispose subjects to elevated LDL-cholesterol (LDL-C). Methods and Results-Twelve common (minor allele frequency Ն0.1) single nucleotide polymorphisms in LRP6 were genotyped in 703 individuals from 213 Polish pedigrees (Silesian Cardiovascular Study families). The family-based analysis revealed that the minor allele of rs10845493 clustered with elevated LDL-C in offspring more frequently than expected by chance (Pϭ0.0053). The quantitative analysis restricted to subjects free of lipid-lowering treatment confirmed the association between rs10845493 and age-, sex-, and BMI-adjusted circulating levels of LDL-C in families as well as 2 additional populations Ϫ 218 unrelated subjects from Silesian Cardiovascular Study replication panel and 1138 individuals from Young Men Cardiovascular Association cohort (Pϭ0. 0268, Pϭ0.0476, and Pϭ0.0472, respectively). In the inverse variance weighted meta-analysis of the 3 populations each extra minor allele copy of rs10845493 was associated with 0.14 mmol/L increase in age-, sex-, and BMI-adjusted LDL-C (SEϭ0.05, Pϭ0.0038). Key Words: gene Ⅲ genetics Ⅲ LDL-cholesterol Ⅲ lipids Ⅲ association L ow-density lipoprotein cholesterol (LDL-C) is the most powerful independent predictor of death from cardiovascular disease. 1 The association between circulating concentrations of LDL-C and death from coronary artery disease (CAD) is continuous across a wide spectrum of cardiovascular risk. 2 Similarly, there is a linear relationship between LDL-C lowering and the attenuation in risk of death from cardiovascular disease-each 1%-reduction in LDL-C plasma levels correlates with a 1%-decrease in CAD mortality. 3 LDL-C shows Ͼ50% heritability 4 and correlates with familial predisposition to CAD even in young apparently healthy subjects. [5][6] The recent genome-wide association scans (GWAs) and the subsequent replication studies have identified several common polymorphic variants with very significant impact on LDL-C levels. 7-8 However, the collective contribution of the variants identified through GWAs to the overall interindividual variation in LDL-C is modest and does not fully explain its entire heritability. 8 Clearly, additional strategies are needed to identify the remaining genetic contributors to human hyperlipidemia. One of the potential approaches to uncover these loci is a systematic analysis of common alleles in genes responsible for rare monogenic syndromes of human cardiovascular disorders. Using this conceptual strategy in relation to genes underlying monogenic forms of hypertension and hypotension, we have recently revealed that common alleles within the locus responsible for type 2 Bartter syndrome (KCNJ1) are associated with blood pressure in the general population. 9 Lowdensity lipoprotein receptor-related protein 6 gene (LRP6)-re...

Increase of HbA1c in patients with newly detected glucose abnormalities was associated with significantly reduced survival after AMI treated invasively. Moreover, increase of HbA1c in patients with IGT and newDM was one of the strongest independent risk factors of death in these populations.