Study of Injection Molding Process to Improve Geometrical Quality of Thick-Walled Polycarbonate Optical Lenses by Reducing Sink Marks.

This study investigates the challenges and potential of conventional injection molding for producing thick-walled optical components. The research primarily focuses on optimizing process parameters and mold design to enhance product quality. The methods include software simulations and experimental validation using polycarbonate test samples (optical lenses). Significant parameters such as melt temperature, mold temperature, injection pressure, and packing pressure were varied to assess their impact on geometric accuracy and visual properties. The results show that lower melt temperatures and higher mold temperatures significantly reduce the occurrence of dimensional defects. Additionally, the design of the gate system was found to be crucial in minimizing defects and ensuring uniform material flow. Effective packing pressure was essential in reducing volumetric shrinkage and sink marks. Furthermore, we monitored the deviation between the predicted and actual defects relative to the thickness of the sample wall. After optimization, the occurrence of obvious defects was eliminated across all sample thicknesses (lenses), and the impact of the critical defect, the sink mark on the planar side of the lens, was minimized. These findings demonstrate the substantial potential of conventional injection molding to produce high-quality thick-walled parts when these parameters are precisely controlled. This study provides valuable insights for the efficient design and manufacturing of optical components, addressing the growing demand for high-performance thick-walled plastic products.

The Impact of Surface Roughness on Conformal Cooling Channels for Injection Molding.

Injection molding technology is widely utilized across various industries for its ability to fabricate complex-shaped components with exceptional dimensional accuracy. However, challenges related to injection quality often arise, necessitating innovative approaches for improvement. This study investigates the influence of surface roughness on the efficiency of conformal cooling channels produced using additive manufacturing technologies, specifically Direct Metal Laser Sintering (DMLS) and Atomic Diffusion Additive Manufacturing (ADAM). Through a combination of experimental measurements, including surface roughness analysis, scanning electron microscopy, and cooling system flow analysis, this study elucidates the impact of surface roughness on coolant flow dynamics and pressure distribution within the cooling channels. The results reveal significant differences in surface roughness between DMLS and ADAM technologies, with corresponding effects on coolant flow behavior. Following that fact, this study shows that when cooling channels' surface roughness is lowered up to 90%, the reduction in coolant media pressure is lowered by 0.033 MPa. Regression models are developed to quantitatively describe the relationship between surface roughness and key parameters, such as coolant pressure, Reynolds number, and flow velocity. Practical implications for the optimization of injection molding cooling systems are discussed, highlighting the importance of informed decision making in technology selection and post-processing techniques. Overall, this research contributes to a deeper understanding of the role of surface roughness in injection molding processes and provides valuable insights for enhancing cooling system efficiency and product quality.

WNT10A variants: following the pattern of inheritance in tooth agenesis and self-reported family history of cancer.

OBJECTIVES: The aim of this study was the analysis of WNT10A variants in seven families of probands with various forms of tooth agenesis and self-reported family history of cancer. MATERIALS AND METHODS: We enrolled 60 young subjects (aged 13 to 17) from the Czech Republic with various forms of tooth agenesis. Dental phenotypes were assessed using Planmeca ProMax 3D (Planmeca Oy, Finland) with Planmeca Romexis software (version 2.9.2) together with oral examinations. After screening PAX9, MSX1, EDA, EDAR, AXIN2 and WNT10A genes on the Illumina MiSeq platform (Illumina, USA), we further analyzed the evolutionarily highly conserved WNT10A gene by capillary sequencing in the seven families. RESULTS: All the detected variants were heterozygous or compound heterozygous with various levels of phenotypic expression. The most severe phenotype (oligodontia) was found in a proband who was compound heterozygous for the previously identified WNT10A variant p.Phe228Ile and a newly discovered c.748G > A variant (p.Gly250Arg) of WNT10A. The newly identified variant causes substitution of hydrophobic glycine for hydrophilic arginine. CONCLUSIONS: We suggest that the amino acid changes in otherwise highly conserved sequences significantly affect the dental phenotype. No relationship between the presence of WNT10A variants and a risk of cancer has been found. CLINICAL RELEVANCE: Screening of PAX9, MSX1, EDA, EDAR, AXIN2 and WNT10A genes in hope to elucidate the pattern of inheritance in families.

Influence of Cross-Linking Agent Concentration/Beta Radiation Surface Modification on the Micro-Mechanical Properties of Polyamide 6.

This study focuses on the problematic of polyamide 6 containing various concentrations of cross-linking agent that was exposed to electron radiation. It is important to improve the material properties of polymers as much as possible. This endeavor can be realized by numerous methods, one of which is radiation exposure. This study investigates the effect of electron beam radiation in doses ranging from 66 to 132 kGy on the micro-mechanical properties of polymers, specifically polyamide 6 filled with 1, 3 and 5 wt.% of cross-linking agent triallyl isocyanurate (TAIC). The changes in the material brought by the radiation exposure were quantified by measurements of indentation hardness and modulus, which were the main measured micro-mechanical properties. Furthermore, thermo-mechanical analysis (TMA) was chosen to confirm the results of the material cross-linking, while the effect of degradation was investigated by Fourier-transform infrared spectroscopy (FTIR). In pursuit of complete evaluation, the topography of the test subject's surface was explored by atomic force microscopy (AFM). The optimal concentration/radiation ratio was found in polyamide 6 enriched by 5 wt.% concentration of TAIC, which was irradiated by 132 kGy. Material treated in such a way had its indentation hardness by 33% and indentation modulus improved by 26% in comparison with the untreated material. These results were subsequently confirmed by the TMA and FTIR methods.

Polyamide Surface Layer Nano-Indentation and Thermal Properties Modified by Irradiation.

This study describes the effect of electron radiation on the nano-mechanical properties of surface layers of selected polyamide (PA) types. Electron radiation initiates the cross-linking of macromolecules in the polyamide structure, leading to the creation of a 3D network which fundamentally changes the properties of the tested polymers. Selected types of polyamide (PA 6, PA 66 and PA 9T) were exposed to various intensities of electron radiation (33 kGy, 66 kGy, 99 kGy, 132 kGy, 165 kGy and 198 kGy). The cross-linked polyamides' surface properties were measured by means of the modern nano-indentation technique (Depth Sensing Indentation; DSI), which operates on the principle of the immediate detection of indenter penetration depth in dependence on the applied load. The evaluation was preformed using the Oliver-Pharr method. The effect of electron radiation on the tested polyamides manifested itself in the creation of a 3D network, which led to an increase of surface layer properties, such as indentation hardness, elastic modulus, creep and temperature resistance, by up to 93%. The increase of temperature and mechanical properties substantially broadens the field of application of these materials in technical practice, especially when higher temperature resistance is required. The positive changes to the nano-mechanical properties as well as mechanical and temperature capabilities instigated by the cross-linking process were confirmed by the gel volume test. These measurements lay the foundation for a detailed study of this topic, as well as for a more effective means of modifying chosen properties of technical polyamide products by radiation.

The low expression of circulating microRNA-19a represents an additional mortality risk in stable patients with vascular disease.

BACKGROUND: Secondary prevention of atherosclerotic vascular diseases represents a cascade of procedures to reduce the risk of future fatal and non-fatal cardiovascular events. We sought to determine whether the expression of selected microRNAs influenced mortality of stable chronic cardiovascular patients. METHODS: The plasma concentrations of five selected microRNAs (miR-1, miR-19, miR-126, miR-133 and miR-223) were quantified in 826 patients (mean age 65.2 years) with stable vascular disease (6-36 months after acute coronary syndrome, coronary revascularization or first-ever ischemic stroke). All-cause and cardiovascular mortality rates were followed during our prospective study. RESULTS: Low expression (bottom quartile) of all five miRNAs was associated with a significant increase in five-year all-cause death, even when adjusted for conventional risk factors, treatment, raised troponin I and brain natriuretic protein levels [hazard risk ratios (HRRs) were as follows: miR-1, 1.65 (95% CI: 1.16-2.35); miR-19a, 2.27 (95% CI: 1.59-3.23); miR-126, 1.64 (95% CI: 1.15-2.33); miR-133a, 1.46 (95% CI: 1.01-2.12) and miR-223, 2.05 (95% CI: 1.45-2.91)]. Nearly similar results were found if using five-year cardiovascular mortality as the outcome. However, if entering all five miRNAs (along with other covariates) into a single regression model, only low miR-19a remained a significant mortality predictor; and only in patients with coronary artery disease [3.00 (95% CI: 1.77-5.08)], but not in post-stroke patients [1.63 (95% CI: 0.94-2.86)]. CONCLUSIONS: In stable chronic coronary artery disease patients, low miR-19a expression was associated with a substantial increase in mortality risk independently of other conventional cardiovascular risk factors.

Next generation sequencing reveals a novel nonsense mutation in MSX1 gene related to oligodontia.

Tooth agenesis is one of the most common craniofacial disorders in humans. More than 350 genes have been associated with teeth development. In this study, we enrolled 60 child patients (age 13 to 17) with various types of tooth agenesis. Whole gene sequences of PAX9, MSX1, AXIN2, EDA, EDAR and WNT10a genes were sequenced by next generation sequencing on the Illumina MiSeq platform. We found previously undescribed heterozygous nonsense mutation g.8177G>T (c.610G>T) in MSX1 gene in one child. Mutation was verified by Sanger sequencing. Sequencing analysis was performed in other family members of the affected child. All family members carrying g.8177G>T mutation suffered from oligodontia (missing more than 6 teeth excluding third molars). Mutation g.8177G>T leads to a stop codon (p.E204X) and premature termination of Msx1 protein translation. Based on previous in vitro experiments on mutation disrupting function of Msx1 homeodomain, we assume that the heterozygous g.8177G>T nonsense mutation affects the amount and function of Msx1 protein and leads to tooth agenesis.

Prospective study of metabolic syndrome as a mortality marker in chronic coronary heart disease patients.

BACKGROUND: We aimed to clarify the impact of metabolic syndrome (MetS) as assessed by different definitions on the cardiovascular mortality in patients with coronary heart disease (CHD). METHODS: A total of 1692 patients, 6-24months after myocardial infarction and/or coronary revascularization at baseline, were followed in a prospective cohort study. MetS was identified using four different definitions: standard National Cholesterol Education Program definition (NCEP-ATPIII) based on the presence of ≥3 of the following factors: increased waist circumference, raised blood pressure, hypetriglyceridemia, low high-density lipoprotein cholesterol, and increased fasting glycemia; modified NCEP-ATPIII definition (similar, but omitting antihypertensive treatment as an alternative criterion); presence of "atherogenic dyslipidemia"; or "hypertriglyceridemic waist". The primary outcome was a fatal cardiovascular event at 5years. RESULTS: During 5-year follow-up, 117 patients (6.9%) died from a cardiovascular cause. Patients with MetS by modified NCEP-ATPIII (n=1066, 63.0% of the whole sample) had significantly higher 5-year cardiovascular mortality [adjusted hazard risk ratio (HRR) 2.01 [95%CI:1.26-3.22]; p=0.003] than subjects without MetS. However, when testing single MetS component factors, the majority of attributable mortality risk was driven by increased fasting glycemia (≥5.6mmol/L) [HRR 2.69 (95%CI:1.29-5.62), p=0.009] and the significance of MetS disappeared. None of the other MetS definitions, i.e., standard NCEP-ATPIII (n=1210; 71.5%), "hypertriglyceridemic waist" (n=455; 26.9%) or "atherogenic dyslipidemia" (n=223; 13.2%) were associated with any significant mortality risk. CONCLUSIONS: The co-incidence of MetS has a limited mortality impact in CHD patients, while an increase in fasting glycemia seems to be more a specific marker of mortality risk.

The abnormal status of uncarboxylated matrix Gla protein species represents an additional mortality risk in heart failure patients with vascular disease.

BACKGROUND: Matrix Gla protein (MGP) is a natural inhibitor of tissue calcification. In a previous study, we observed the positive association between abnormal concentrations of uncarboxylated MGP species and increased mortality risk in stable vascular patients. We explore whether co-incidence of abnormal status of uncarboxylated MPG and heart failure (HF) affects the mortality risk. METHODS: We examined 799 patients (mean age 65.1 years) with stable vascular disease and followed them in a prospective study. Both, desphospho-uncarboxylated and total uncarboxylated MGP (dp-ucMGP or t-ucMGP) were quantified by pre-commercial ELISA assays. RESULTS: Elevated (>100 ng/L) circulating brain natriuretic peptide (BNP) and abnormal status of plasma uncarboxylated MGP species (i.e.: dp-ucMGP ≥ 977 pmol/L or t-ucMGP ≤ 2825 nmol/L) were all identified as robust predictors of all-cause 5-year mortality. However, their co-incidence represented a substantial additional risk. We observed the highest mortality risk in patients with elevated BNP plus high dp-ucMGP compared to those with normal BNP plus low dp-ucMGP; fully adjusted HRR's were 4.86 (3.15-7.49). Likewise, the risk was increased when compared with patients with elevated BNP plus low dp-ucMGP; HRR 2.57 (1.60-4.10). Similar result we observed when co-incidence of elevated BNP and low t-ucMGP was analyzed [corresponding HRR's were 4.16 (2.62-6.61) and 1.96 (1.24-3.12)]. CONCLUSIONS: The concomitant abnormality of uncarboxylated MGP and mild elevation of BNP leads in chronic patients with vascular disease to about two-fold increase of the relative mortality risk. We hypothesize that abnormal homeostasis of MGP is involved in the pathophysiology of HF.

Novel PAX9 gene polymorphisms and mutations and susceptibility to tooth agenesis in the Czech population.

OBJECTIVES: Tooth agenesis is one of the most common developmental anomalies in humans. Genetic and environmental factors may be of etiological importance in this condition. Among genes involved in tooth morphogenesis, mutations in PAX9, MSX1, AXIN2, WNT10a, and EDA genes have been associated with tooth agenesis. The aim of our study was to investigate the relationship between the PAX9 gene variants and tooth agenesis in the Czech population. METHODS: The selected regions of the PAX9 gene were analysed by direct sequencing and compared with the reference sequence from the GenBank online database (NCBI). RESULTS: We found several novel variants in the PAX9 gene, e.g. insertion g.5100_5101insC (rs11373281) with simultaneous substitution g.5272C>G (rs4904155) in exon 1, and mutation g.10934C>T (Gly203Gly, rs61754301) in exon 3. In subjects with full dentition we observed polymorphisms g.10276A>G (rs12882923) and g.10289A>G (rs12883049) in IVS2 (intervening sequence 2) previously related to tooth agenesis in Polish study. CONCLUSIONS: In our study we excluded a direct effect of rs12882923 and rs12883049 polymorphisms on the dental agenesis in the Czech population. All described PAX9 genetic variants were present both in patients with tooth agenesis and controls. We expect that tooth agenesis in our cohort of patients is caused by mutations in regions different from PAX9 exons analyzed in our study.

Quality of life predictors in chronic stable post-stroke patients and prognostic value of SF-36 score as a mortality surrogate.

Perceived quality of life (QoL) and psychological well-being represents an important target of secondary prevention practice in post-stroke patients. We aimed to identify the major covariates of impaired QoL in stable post-stroke patients and whether impaired QoL itself represents independent mortality predictor.The study consisted of a cross-sectional and a prospective part. Three hundred forty-one patients [mean age 69.0 (SD 9.1)] were interviewed at least 6 months after discharge from hospital for their first-ever ischemic stroke. QoL was objectivized using 36-Item Short-Form Health Survey (SF-36) scoring. Standard health-related questionnaires, including Hospital Anxiety and Depression Scale (HADS), risk factors, and biochemical markers, were assessed. To estimate the 5-year all-cause and cardiovascular mortality, we ascertained the vital status and declared cause of death.Anxiety, depression (HADS score ≥11), brain natriuretic peptide levels ≥100 ng/mL, residual motor impairment at interview, Rankin Scale ≥4 at discharge from hospitalization, and raised blood pressure were identified as main determinants of impaired QoL in the cross-sectional part. The 5-year all-cause and cardiovascular mortality rates were 25.8 and 19.9 %, respectively. After adjustment for potential covariates, patients with an SF-36 score ≤40 at baseline had more than a twofold higher risk of all-cause and cardiovascular mortality (with HRRs 2.01 (95 % CI 1.21-3.32), p < 0.007 and 2.32 (95 % CI 1.32-4.09), p < 0.003, respectively) during the 5 years of follow-up.In conclusion, anxiety, depression, and raised brain natriuretic peptide levels were the most important covariates of impaired QoL in post-stroke patients. Moreover, a decreased SF-36 score (≤40) represents an independent surrogate of increased additive mortality risk.

Blood pressure control and risk profile in poststroke survivors: a comparison with the general population.

OBJECTIVE: Recurrent strokes are associated with higher mortality, greater disability, and increased healthcare costs compared with first-ever stroke. Lifestyle measures and drug treatment in secondary prevention decrease the risk of recurrence while improving the quality of life of patients. The objective of this study was to determine the prevalence of hypertension and other cardiovascular risk factors in stroke survivors and population controls. METHODS AND RESULTS: A total of 424 poststroke survivors (aged 66.0 ±â€Š10.4 years) were examined 6-36 months after their first ischemic stroke. Controls of similar age and from the same geographic region were selected from the database of the Czech post-Multinational MONItoring of trends and determinants in CArdiovascular disease Study. Hypertension was found to be the most prevalent risk factor affecting 91.5% of stroke survivors and 71.8% of controls. Use of antihypertensive drugs was reported in 79.5% of stroke survivors and 56.7% of controls. However, blood pressure lower than 140/90 mmHg was achieved in only 49.5% of hypertensive stroke survivors. More than 60% of stroke survivors used statins but low-density lipoprotein-cholesterol lower than 2.5 mmol/l was achieved in only 47.4 and 37% of male and female poststroke survivors, respectively. About a third of poststroke patients continue to smoke, and obesity is a major problem, particularly in women (prevalence 47%), who also have a high prevalence of diabetes. CONCLUSION: We found a high prevalence and poor control of major cardiovascular risk factors in patients surviving their first-ever ischemic stroke, thus showing poor implementation of guidelines for secondary prevention in clinical practice.

The obesity paradox and survivors of ischemic stroke.

BACKGROUND: Although obesity is a risk factor for stroke and achieving normal weight is advocated to decrease stroke risk, the risk associated with obesity and weight loss after stroke has not been well established. The aim of this study was to assess the association of obesity at the time of stroke admission and weight loss after stroke with total mortality. METHODS: We analyzed 736 consecutive patients (mean age, 66 ± 11 years; 58% men) hospitalized for their first ischemic stroke. Body weight at hospital admission and at the outpatient visit during follow-up was used in the analysis. RESULTS: After multivariate adjustment, obesity at admission was associated with lower mortality risk as compared with normal weight (hazard ratio [HR], .50, P = .03). At the outpatient visit, with a median follow-up time of 16 months, 21% of patients had lost more than 3 kg of weight. Stroke severity, heart failure, transient ischemic attack, and depression after stroke were independently associated with significant weight loss. Weight loss of more than 3 kg was associated with increased mortality risk (HR, 5.87; P = .001) independently of other factors. Similar results were seen when weight loss was defined as losing more than 3% of baseline weight (HR, 4.97; P = .004). Weight gain of more than 5% of the baseline weight tended to be associated with better survival when compared with no weight change (log-rank test, P = .07). CONCLUSIONS: Normal weight at hospital admission and weight loss after ischemic stroke are independently associated with increased mortality. Overweight and obesity at baseline do not decrease the risk associated with weight loss.

A screen of a large Czech cohort of oligodontia patients implicates a novel mutation in the PAX9 gene.

Tooth agenesis is one of the most common developmental anomalies in humans. To date, many mutations involving paired box 9 (PAX9), msh homeobox 1 (MSX1), and axin 2 (AXIN2) genes have been identified. The aim of the present study was to perform screening for mutations and/or polymorphisms using the capillary sequencing method in the critical regions of PAX9 and MSX1 genes in a group of 270 individuals with tooth agenesis and in 30 healthy subjects of Czech origin. This screening revealed a previously unknown heterozygous g.9527G>T mutation in the PAX9 gene in monozygotic twins with oligodontia and three additional affected family members. The same variant was not found in healthy relatives. This mutation is located in intron 2, in the region recognized as the splice site between exon 2 and intron 2. We hypothesize that the error in pre-mRNA splicing may lead to lower expression of PAX9 protein and could have contributed to the development of tooth agenesis in the affected subjects.

The titanium PV I endosteal implant from beta-titanium alloy Ti 38Nb 6Ta.

AIM: The aim of this study was to use the beta-titanium alloy Ti38Nb6Ta for production of a new construction line of implants, perform testing on animals and preclinical tests. MATERIALS AND METHODS: Within this study, a new PV I implant with five construction variants was developed. The implant includes three types of threads - microthreads and flat threads of two types with a different depth. Further, the PV I implant was tested on minipigs. Subsequently, preclinical tests of 150 implants were performed and assessed. The age interval of patients was from 18 to 74 years. RESULTS: Beta titanium alloy exhibited higher strength than titanium alloys. Anti-corrosion resistance was also higher. The implant from beta-alloy was inserted in the tibias of minipigs. Sections showed good osseointegration of the PV I implant. During the preclinical tests, 150 implants were inserted with the success rate of 99.33% after the two year assessment. The assessment also included handicapped patients who are not usually assessed in classical studies. Finally, the implantation protocol and documentation of a new implantation system PV I was designed. At the same time the industrial sample of this implant was formed and accepted. CONCLUSION: A new anti-rotation PV I implant with microthreads and conical anchorage of the abutment into the fixture was formed. The beta-titanium alloy Ti38Nb6Ta used for the implant was biocompatible and had higher mechanical and physical properties than the existing titanium alloys. The PV I implant was recommended for clinical application.

The association between uncarboxylated matrix Gla protein and lipoprotein-associated phospholipase A2.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is independently associated with cardiovascular risk, probably via inflammatory activity in sclerotic plaque. We speculated whether Lp-PLA2 has a role in the aetiology of vascular calcifications, estimated from circulating uncarboxylated matrix Gla protein (MGP) species and whether we could find a potential interaction of Lp-PLA2 and MGP in terms of mortality. MATERIALS AND METHODS: We examined 798 patients (mean age 65.1 years) with stable vascular disease and followed them in a prospective study. Both, desphospho-uncarboxylated and total MGP (dp-ucMGP or t-ucMGP) were quantified by pre-commercial ELISA assays, developed by VitaK (Maastricht, The Netherland) RESULTS: Lp-PLA2 activity was independently positively associated with desphospho-uncarboxylated MGP (dp-ucMGP) [ß coeff = 0.098, p=0.006]. 1SD of Lp-PLA2 activity was associated with 37% increased risk (p=0.001) of elevated dp-ucMGP (≥977 pmol/L, top quartile). In the Cox proportional hazard model adjusted for conventional risk factors, the patients in the highest quartile of dp-ucMGP or lowest quintile of total-uncarboxylated ucMGP (<2660 nmol/L) had higher risk of all-cause mortality [HRR 2.79 (95% CI 1.97-3.94) and HRR 1.69 (95% CI 1.18-2.42), respectively]. We observed no effect of high Lp-PLA2 activity (≥195 nmol/min/mL) on total mortality. CONCLUSIONS: We assume that Lp-PLA2 is involved in vascular calcification and that dp-ucMGP is a more appropriate biomarker of residual risk than Lp-PLA2 itself.

Low blood pressure during the acute period of ischemic stroke is associated with decreased survival.

OBJECTIVES: There is no agreement on optimal blood pressure (BP) level during the acute phase of stroke, because studies on the relation between BP and stroke outcome have shown contradicting results. The aim of this study was to compare the relationship of admission, maximal, discharge BP and its components during hospitalization for the first-ever acute ischemic stroke with total mortality after stroke. METHODS: In 532 consecutive patients (mean age 66 ±â€Š10 years, 59% of men) hospitalized for their first-ever ischemic stroke, the association between BP and total mortality during a median follow-up of 66 weeks (interquartile range 33-119 weeks) was analyzed. RESULTS: In multivariate analysis, both admission mean BP (MBP) and discharge SBP quartiles were independent predictors of mortality and outperformed other parameters of BP. After multivariate adjustments, patients with admission MBP below 100 mmHg had a higher risk of death than those with MBP between 100-110 and 110-121 mmHg, whereas the risk of mortality did not differ from the group with admission MBP above 122 mmHg. Similarly, patients with discharge SBP below 120 mmHg had an increased risk of death as compared to groups with SBP between 120-130 and 130-141 mmHg, whereas the risk of death was similar to that with discharge SBP above 141 mmHg. CONCLUSION: Among patients hospitalized for their first-ever ischemic stroke, the risk of all-cause death is significantly increased in those with admission MBP below 100 mmHg and discharge SBP below 120 mmHg, even after adjustments for other confounders.

The predictive potential of asymptomatic mild elevation of cardiac troponin I on mortality risk of stable patients with vascular disease.

OBJECTIVES: Due to improved analytical performance of the newest generation of troponin assays, several patients have mild elevations of this parameter. Nevertheless, they do not show any signs of acute coronary syndrome. We speculated whether non-acute cardiac troponin I (cTnI) concentrations may improve prediction of residual mortality risk in clinically stable outpatients with chronic vascular disease. DESIGN AND METHODS: We followed 830 patients (mean age 65.2years) after myocardial infarction, coronary revascularization or first ischemic stroke (pooled Czech samples of EUROASPIRE III and EUROASPIRE-stroke surveys, interviewed in 2006/2007) in a prospective cohort study. In addition to standard protocol, troponin I and brain natriuretic peptide (BNP) was estimated from frozen samples. Vital status and declared cause of death from death certificates was registered to ascertain a 5-year all-cause and cardiovascular mortality. RESULTS: During a median follow up of 2050days (5.6years) 168 patients died. In the multivariate Cox proportional hazard model, cTnI≥0.03ng/mL independently predicted an all-cause 5-year mortality with HRR 1.76 (95% CI: 1.09-2.83). In the Cox model, the better predictor of mortality was BNP >150ng/L [HRR 3.47 (95% CI: 2.23-5.41)]. However, the combination of BNP with cTnI did not substantially improve its sensitivity or predictive power. CONCLUSION: We cannot confirm the utility of asymptomatic mild cTnI elevation as a tool to detect residual risk of stable patients with vascular disease. On the other hand, BNP seems to be more appropriate for this purpose.

The DRD2/ANKK1 Taq1A polymorphism is associated with smoking cessation failure in patients with coronary heart disease.

AIM: We speculated whether DRD2 or CHRN subunit polymorphisms might be associated with the risk of smoking cessation failure in subjects after coronary heart disease (CHD) manifestation. METHODS: A total of 964 patients with CHD, mean age 64.3 years (standard deviation [SD] 9.0), examined in the EUROASPIRE III and IV surveys were genotyped for rs1800497 (DRD2/ANKK1 Taq1A), rs578776 (CHRNA5-A3-B4), rs16969968 (CHRNA5) and rs1051730 (CHRNA3) SNPs. RESULTS: The presence of DRD2/ANKK1 Taq1A minor T allele was independently associated with increased relative risk of smoking persistence (odds ratio: 1.79; 95% CI: 1.13-4.35). We observed no association between CHRN SNPs and smoking habit. CONCLUSION: DRD2/ANKK1 Taq1A polymorphism is associated with a decreased likelihood of smoking cessation in patients after CHD manifestation.

Unexpected inverse relationship between impaired glucose metabolism and lipoprotein-associated phospholipase A2 activity in patients with stable vascular disease.

BACKGROUND: Elevated lipoprotein-associated phospholipase A2 activity (aLp-PLA2) is associated with increased risk of cardiovascular events. In patients with stable atherovascular disease, we aimed to investigate whether impaired glucose metabolism might be associated with higher risk of elevated aLp-PLA2. METHODS: We conducted a cross-sectional study in 825 stable patients after acute coronary syndrome, coronary revascularization or after first ischemic stroke (Czech part of EUROASPIRE III surveys). We measured aLp-PLA2 using diaDexus commercial kit. RESULTS: In multiple step-wise regression analysis, the aLp-PLA2 was significantly positively associated with male gender, current smoking, LDL cholesterol and metabolic syndrome and negatively with statin treatment, body mass index and LDL/apoB ratio. After adjustment for these confounders, we observed an inverse relationship between aLp-PLA2 and fasting glycemia [ß coefficient -2.18 (p<0.0001)] or glycated hemoglobin A1c (HbA1c) [ß coefficient -5.89 (p<0.0001)]. Moreover, we found a positive association between aLp-PLA2 and pancreatic ß cell function [ß coefficient +0.10 (p<0.0001)], but not with an insulin sensitivity. CONCLUSION: In present study, we cannot confirm any additive risk of impaired glucose metabolism in terms of increased activity of Lp-PLA2. On the contrary, presence of inadequately controlled diabetes mellitus was independently associated with lower risk of elevated aLp-PLA2 .