Coronary Artery Disease Subjects Research Articles

Impact of Chronic Kidney Disease on Carotid Atherosclerosis According to Blood Pressure Category

We aimed to clarify the association of chronic kidney disease (CKD) with carotid atherosclerosis and the impact of CKD on carotid atherosclerosis according to blood pressure categories in an urban general population. We studied 3466 Japanese individuals (35-93 years old) in the Suita Study. Carotid atherosclerosis was expressed as the maximum carotid intima-media thickness and the presence of stenosis (>25%). The estimated glomerular filtration rate was calculated using the equations recommended by the Japanese Society of Nephrology. CKD was defined as estimated glomerular filtration rate <60 mL/min per 1.73 m2. Blood pressure categories were defined by the European Society of Hypertension and European Society of Cardiology 2007 criteria. The multivariable-adjusted maximum carotid intima-media thickness and odds ratio for stenosis in subjects with estimated glomerular filtration rate<50 mL/min per 1.73 m2 were greater than those in subjects with estimated glomerular filtration rate≥90 mL/min per 1.73 m(2). When subjects were stratified according to blood pressure categories, the multivariable-adjusted maximum carotid intima-media thickness was significantly greater in CKD subjects than in non-CKD subjects only in subjects with hypertension. Similarly, the impact of CKD on stenosis was evident only in subjects with hypertension (multivariable-adjusted odds ratios for stenosis [95% confidence interval] were 2.21 [1.53-3.19] in non-CKD/hypertension and 3.16 [2.05-4.88] in CKD/hypertension compared with non-CKD/optimal blood pressure). In a general population, the association of CKD with carotid atherosclerosis was modest, but CKD was independently associated with carotid atherosclerosis in subjects with hypertension.

A novel polymorphism (901G &gt; a) of C5L2 gene is associated with coronary artery disease in Chinese Han and Uyghur population

BackgroundC5L2, a G protein-coupled receptor (GPCR), has been demonstrated to be a ligand for acylation-stimulating protein (ASP). The aim of the present study is to evaluate the association of a novel variation (901A > G) of C5L2 gene with coronary artery disease (CAD).MethodsWe identified a novel single nucleotide polymorphism (SNP), (901G > A), in exon 2 using a polymerase chain reaction direct-sequencing method. This nucleotide change causes the amino-acid order from Arginine to glutaminate at codon 300. We analyzed the relationship between this SNP and CAD in two independent case–control studies: one was in a Han population (492 CAD patients and 577 control subjects) and the other was in a Uygur population (319 CAD patients and 554 control subjects).ResultsThe frequency of AG genotype in CAD subjects was less than that in the control subjects not only in Han (1.8% vs 8.6%, P < 0.001, OR = 0.143, 95% CI: 0.068 ~ 0.302) but also in Uygur population (0.9% vs 5.2%, P = 0.001, OR = 0.246, 95% CI: 0.072 ~ 0.837). After adjustment for known CAD risk factors such as hypertension, diabetes, smoking, age and gender, the difference remained significant.ConclusionThe 901G > A polymorphism of C5L2 may be a genetic maker of CAD in the Han and Uygur population in western China.

Linear and nonlinear analysis of normal and CAD-affected heart rate signals

Coronary artery disease (CAD) is one of the dangerous cardiac disease, often may lead to sudden cardiac death. It is difficult to diagnose CAD by manual inspection of electrocardiogram (ECG) signals. To automate this detection task, in this study, we extracted the heart rate (HR) from the ECG signals and used them as base signal for further analysis. We then analyzed the HR signals of both normal and CAD subjects using (i) time domain, (ii) frequency domain and (iii) nonlinear techniques. The following are the nonlinear methods that were used in this work: Poincare plots, Recurrence Quantification Analysis (RQA) parameters, Shannon entropy, Approximate Entropy (ApEn), Sample Entropy (SampEn), Higher Order Spectra (HOS) methods, Detrended Fluctuation Analysis (DFA), Empirical Mode Decomposition (EMD), Cumulants, and Correlation Dimension. As a result of the analysis, we present unique recurrence, Poincare and HOS plots for normal and CAD subjects. We have also observed significant variations in the range of these features with respect to normal and CAD classes, and have presented the same in this paper. We found that the RQA parameters were higher for CAD subjects indicating more rhythm. Since the activity of CAD subjects is less, similar signal patterns repeat more frequently compared to the normal subjects. The entropy based parameters, ApEn and SampEn, are lower for CAD subjects indicating lower entropy (less activity due to impairment) for CAD. Almost all HOS parameters showed higher values for the CAD group, indicating the presence of higher frequency content in the CAD signals. Thus, our study provides a deep insight into how such nonlinear features could be exploited to effectively and reliably detect the presence of CAD.

Diagnostic value of exercise-induced changes in circulating high sensitive troponin T in stable chest pain patients

AbstractObjective: We investigated the diagnostic value of exercise-induced increase in cardiac Troponin T (cTnT) in stable chest pain subjects.Methods: CTnT was measured before and 20 h after an exercise test in 157 subjects suspected of coronary artery disease (CAD).Results: CAD subjects (n = 41) had higher baseline cTnT levels compared to non-CAD subjects (n = 116), 6.39 ng/l and 3.00 ng/l, respectively, p < 0.0001, and were more likely to increase in cTnT (70.7% versus 27.6%, p < 0.0001). Net Reclassification Index for the combined variable was 19%, p = 0.02.Conclusions: Exercise-induced increase in cTnT was found to be associated with CAD and cTnT measurements improved the diagnostic evaluation.

An MTHFR Variant, Plasma Homocysteine Levels and Late-Onset Coronary Artery Disease in Subjects from Southern Iran

There have been many controversial debates on the role of Hyperhomocysteinaemia (HHcy) as an independent risk factor for Coronary Artery Disease (CAD) during recent years. Furthermore, an alanine/valine (Ala/Val) gene polymorphism at 222nd amino acid of 5,10-methylenetetrahydrofolate reductase (MTHFR) has been considered as a factor that could render this enzyme thermolabile and less active which in turn may yield a subsequent increase in plasma total homocysteine (tHcy) levels. To assess whether this polymorphism is associated with increased risk of CAD and plasma levels of tHcy in a population from southern Iran, a total of 457 patients with angiographically documented multi-vessel CAD were compared with a control group comprised of 371 subjects with <30% stenosis in all major vessels. Nevertheless our results failed to admit a significant difference between CAD individuals and control subjects for Ala/Val polymorphism and plasma Hcy concentrations. However, plasma Hcy concentrations were significantly higher in individuals with Val/Val genotype than subjects with Ala/Ala genotype, but it didn't show a significant association with CAD in our population. Moreover, as the multiple linear regression analysis indicated, smoking habit, folate levels and the MTHFR Val/Val genotype were the only major predictors of tHcy concentrations in the current investigation.

Association between interleukin 6 and interleukin 16 gene polymorphisms and coronary heart disease risk in a Chinese population

To investigate the role of interleukin 6 (IL6) and IL16 single nucleotide polymorphisms (SNPs) in coronary artery disease (CAD) risk in a Chinese population. Patients with CAD and healthy control subjects were recruited. IL6 (rs1800795 and rs1800796) and IL16 (rs8034928, rs3848180, rs4577037, rs1131445, rs4778889 and rs11556218) genotyping was performed on the MassARRAY® platform (Sequenom®, San Diego, CA, USA). Frequencies of rs8034928 variant C allele and rs11556218 variant T allele were higher in patients with CAD (n = 326) than controls (n = 341). The rs8034928 C/C genotype (odds ratio [OR] 2.03; 95% confidence intervals [CI] 1.16, 3.62) and C allele (OR 1.97; 95%CI 1.15, 3.45) were associated with increased risk of CAD compared with wild type. Similarly, the rs11556218 T/T genotype (OR 2.44; 95%CI 1.15, 5.44) and T allele (OR 2.37; 95%CI 1.13, 5.24) were associated with increased CAD risk compared with wild type. The SNPs rs8034928 and rs11556218 are associated with CAD risk in the Chinese population, and may be useful predictive markers for CAD susceptibility.

Age-related impact of depressive symptoms on functional capacity measured with 6-minute walking test in coronary artery disease

Patients affected by coronary artery disease (CAD) have a high prevalence of depressive disorders. It has been suggested that depressive symptoms significantly reduce exercise stress test performance in CAD patients, whereas their influence on functional capacity tests, such as the 6-minute walking test (6WT), has been less investigated. The aim of this study was to evaluate the correlation between depressive symptoms and 6WT in patients with CAD and the role of age on this relationship. We enrolled 148 CAD patients. Global functional capacity was measured with 6WT and the presence of depressive symptoms with the 30-item Geriatric Depression Scale (GDS). GDS score was analysed as a continuous variable or categorized as depression absent (score <10), probable (10-14), or present (≤15). A significant inverse correlation was observed between GDS score and distance walked at 6WT. Patients positive for depressive symptoms (probable or present) had a significantly worse performance compared to those with GDS score <10. In multivariable analysis adjusted for indexes of cardiovascular disease severity and comorbidity, the presence of depressive symptoms proved to be an independent predictor of distance walked at 6WT; the predictivity of depressive symptoms on 6WT was age dependent. Depressive symptoms negatively affect 6WT performance among older CAD subjects. Non-cardiovascular parameters, such as psycho-affective disorders, must be taken into account for the interpretation of 6WT performance in old age.

Plasma Tissue Factor Pathway Inhibitor Levels in Angiographically Defined Coronary Artery Disease Among Saudis

This study was aimed to determine plasma levels of total (TFPI-T) and free (TFPI-F) tissue factor pathway inhibitor, plasminogen activator inhibitor-1 (PAI-1), and tissue plasminogen activator (t-PA) in a cohort of Saudi patients with chronic stable angiographically defined coronary artery disease (CAD) and to determine its correlation with its severity. This cross sectional study was conducted in the department of physiology and department of cardiology, College of Medicine, and King Khalid University Hospital and King Saud University, Riyadh. Sixty known cases of CAD who had undergone angiography (35 males and 25 females) were selected. A control group included 39 (20 males and 19 females) healthy subjects. Fasting venous blood samples were analyzed for total (TFPI-T) and free (TFPI-F) tissue factor pathway inhibitor, plasminogen activator inhibitor-1 (PAI-1), and tissue plasminogen activator (t-PA). Gensini scores and vessel scores were determined for assessing CAD severity. There were non-significant differences between age, body mass index (BMI) and Blood pressure between the controls and CAD subjects. A comparison of hemostatic markers between control and CAD patients showed significantly higher levels of Fibrinogen, PAI-1, TFPI-T and TFPI-F in CAD patients compared to control subjects. But there was no difference in plasma t-PA levels. TFPI-T had a significant positive correlation with severity of disease determined by Gensini Scores (r=0.344; p=0.006) and vessel scores (r=0.338; p=0.015). Plasma levels of total tissue factor pathway inhibitor are significantly related with the presence and severity of CAD. Elevated levels of TFPI-T may be considered as useful diagnostic and prognostic markers in patients with CAD.

Calcium–phosphorus product concentration is a risk factor of coronary artery disease in metabolic syndrome

BackgroundHigh serum phosphorus and the calcium–phosphorus product concentration has been associated with increased mortality and cardiovascular events in patients with chronic kidney disease. ObjectiveThis study was designed to determine the relationship between calcium–phosphorus product concentration and the presence of coronary artery calcification in subjects with metabolic syndrome (MetS). MethodsWe reviewed the medical records of 2056 general subjects with a mean age of 55.1 ± 9.9 years and a glomerular filtration rate of 88.9 ± 16.2 mL/min/1.73 m2. The enrolled subjects consisted of 384 (18.7%) subjects with MetS and 1672 (81.3%) subjects without MetS. The severity of coronary artery calcification was assessed by the coronary artery calcification score (CACS) using multi-detector computed tomography (MDCT). ResultsThe CACS correlated with calcium–phosphorus product concentration in subjects with MetS (r = 0.184, P < 0.01). The odds ratio of calcium–phosphorus product concentration having CACS >50 was 1.053 in subjects with MetS (P < 0.05). After adjustment for age, sex, diabetes, and dyslipidemia, calcium–phosphorus product concentrations had a positive correlation with CACS in subjects with MetS. In single regression analysis, calcium–phosphorus product concentration as independent variable was the significant predictor of CACS in subjects with MetS. Using a multivariate analysis, calcium–phosphorus product concentration remained a significant factor associated with CACS in subjects with MetS. ConclusionsCalcium–phosphorus product concentration was weakly associated with CACS and an independent factor predicting for CACS by MDCT in subjects with MetS. These results suggest that calcium–phosphorus product concentration might be considered as a risk factor of coronary artery disease in subjects with MetS.

Plasma fetuin‐A is associated with endothelial dysfunction and subclinical atherosclerosis in subjects with nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD), a hepatic manifestation of metabolic syndrome (MetS) is closely associated with an increased risk of cardiovascular disease. Fetuin-A is associated with MetS and NAFLD. We investigated the relationship of circulating fetuin-A level with markers of endothelial dysfunction and presence of carotid atherosclerosis in subjects with NAFLD. The consecutive 115 patients with NAFLD and age-matched 74 healthy subjects were enrolled. Plasma levels of fetuin-A and markers of endothelial dysfunction [asymmetric dimethyl arginine (ADMA) and adiponectin] were measured by ELISA method. Insulin sensitivity was determined by homeostasis model assessment of insulin resistance (HOMA-IR) index. Carotid artery intima-media thickness (cIMT) was assessed by high-resolution ultrasonography. Fetuin-A and ADMA were higher and, adiponectin was lower in NAFLD group than the control group (P=0·004, P<0·001 and P<0·001, respectively). In addition, NAFLD group had greater cIMT measurements than the controls (P<0·001). However, no difference was found for fetuin-A, ADMA, adiponectin and cIMT between two groups when the findings were adjusted according to the glucose, lipids and HOMA-IR index. In correlation analysis, fetuin-A was found to be positively correlated with triglyceride (r=0·23, P=0·001), HOMA-IR (r=0·29, P<0·001), ADMA (r=0·24, P=0·001), cIMT (r=0·3, P=0·003) and, negatively correlated with HDL-C (r=-0·17, P=0·02) and adiponectin (r=-0·19, P=0·01) levels. Multiple linear regression analysis showed that fetuin-A was independently associated with ADMA and cIMT levels. This study demonstrated for the first time that circulating fetuin-A in NAFLD is independently associated with endothelial dysfunction and subclinical atherosclerosis.

Hemostatic markers and their relationship with severity of coronary artery disease in Saudi adults

Objectives This study was aimed to determine total (TFPI-T) & free (TFPI-F) tissue factor pathway inhibitor, plasminogen activator inhibitor-1 (PAI-1), and tissue plasminogen activator (t-PA) in a cohort of Saudi patients with chronic stable angiographically defined coronary artery disease (CAD) and to see its correlation with its severity and diffuseness determined by Gensini and vessel scoring. Methods This cross sectional study was conducted in the department of physiology and department of cardiology, College of Medicine & King Khalid University Hospital, King Saud University, Riyadh. Sixty known cases of CAD who had undergone angiography (35 males & 25 females) were selected. Fasting Venous blood samples were analyzed for total (TFPI-T) & free (TFPI-F) tissue factor pathway inhibitor, plasminogen activator inhibitor-1 (PAI-1), and tissue plasminogen activator (t-PA). Gensini scoring system and vessel scoring was determined to determine the CAD severity. Results There were non-significant differences between age, body mass index (BMI) and blood pressure between control and CAD subjects. Comparison of haemostatic markers between control and CAD patients showed significantly higher levels of fibrinogen, PAI-1, TFPI-T and TFPI-F in CAD patients compared to control subjects. But there was no difference in plasma t-PA levels. TFPI-T had a significant positive correlation with severity of disease determined by Gensini Scores ( r = 0.344, P = 0.006) and vessel scores ( r = 0.338, P = 0.015). Conclusions TFPI-T has a significant positive relationship with Gensini scores and vessel score of CAD severity. This suggests that TFPI involvement is related to CAD risk in these patients. Thus elevated plasma levels of total TFPI may be considered as useful diagnostic and prognostic markers in patients with CAD.

Screening for the Presence of Coronary Artery Disease

Screening for the Presence of Coronary Artery Disease

Implication of Progranulin and C1q/TNF-Related Protein-3 (CTRP3) on Inflammation and Atherosclerosis in Subjects with or without Metabolic Syndrome

ObjectiveProgranulin and C1q/TNF-related protein-3 (CTRP3) were recently discovered as novel adipokines which may link obesity with altered regulation of glucose metabolism, chronic inflammation and insulin resistance.Research Design and MethodsWe examined circulating progranulin and CTRP3 concentrations in 127 subjects with (n = 44) or without metabolic syndrome (n = 83). Furthermore, we evaluated the relationship of progranulin and CTRP3 levels with inflammatory markers and cardiometabolic risk factors, including high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), estimated glomerular filtration rate (eGFR), and adiponectin serum concentrations, as well as carotid intima-media thickness (CIMT).ResultsCirculating progranulin levels are significantly related with inflammatory markers, hsCRP (r = 0.30, P = 0.001) and IL-6 (r = 0.30, P = 0.001), whereas CTRP3 concentrations exhibit a significant association with cardiometabolic risk factors, including waist circumference (r = −0.21), diastolic blood pressure (r = −0.21), fasting glucose (r = −0.20), triglyceride (r = −0.34), total cholesterol (r = −0.25), eGFR (r = 0.39) and adiponectin (r = 0.26) levels. Serum progranulin concentrations were higher in patients with metabolic syndrome than those of the control group (199.55 [179.33, 215.53] vs. 185.10 [160.30, 204.90], P = 0.051) and the number of metabolic syndrome components had a significant positive correlation with progranulin levels (r = 0.227, P = 0.010). In multiple regression analysis, IL-6 and triglyceride levels were significant predictors of serum progranulin levels (R 2 = 0.251). Furthermore, serum progranulin level was an independent predictor for increased CIMT in subjects without metabolic syndrome after adjusting for other cardiovascular risk factors (R 2 = 0.365).ConclusionsSerum progranulin levels are significantly associated with systemic inflammatory markers and were an independent predictor for atherosclerosis in subjects without metabolic syndrome.Trial RegistrationClinicalTrials.gov NCT01668888

Assessment of the 9p21.3 locus in severity of coronary artery disease in the presence and absence of type 2 diabetes

BackgroundThe 9p21.3 locus is strongly associated with the risk of coronary artery disease (CAD) and with type 2 diabetes (T2D). We investigated the association of 9p21.3 variants with severity of CAD (defined by the number of vessel diseased [VD]) in the presence and absence of T2D.MethodsWe tested 11 9p21.3-variants for association in a white Italian study (N = 2,908), and carried out replication in 2 independent white populations, a German study (N = 2,028) and a Canadian Study (N=950). SNP association and permutation analyses were conducted.ResultsWe identified two 9p21.3-variants, rs4977574 (P < 4×10-4) and rs2383207 (P < 1.5×10-3) that were associated with severity of CAD in subjects without T2D. Association of rs4977574 with severity of CAD was confirmed in the Canadian Study. Results from subgroup analysis among patients with T2D showed an interaction between rs10738610 and T2D with P = 4.82×10-2. Further investigation showed that rs10738610 (P < 1.99×10-2) was found to be significantly associated with severity of CAD in subjects with T2D.ConclusionsThe 9p21.3 locus is significantly associated with severity of CAD. The number of associations of 9p21.3 variants with severity of CAD is variable to the presence and absence of T2D. In a CAD-susceptible region of 115 kb, there is only one variant associated with the severity of coronary vessel disease in the presence of type 2 diabetes.

Correlation of Glu298Asp eNOS Polymorphism with Serum NO Levels in Egyptian Patients with Coronary Artery Disease

Background: Nitric oxide (NO) is a potent vasodilator synthesized by the vascular endothelium. It has been reported that endothelial nitric oxide synthase (eNOS) Glu298Asp gene polymorphism is associated withcoronary artery disease (CAD). Methodology: In this study, we investigated Glu298Asp eNOS polymorphism and serum NO in a group of 146 age-matched male subjects; 77 patients with coronary artery disease (CAD) classified according to the severity of coronary insufficiency and 69 normal male controls. Results: The obtained frequencies of the eNOS Glu298Asp genotypes for the CAD subjects were GG (54.5%), GT (31.20%), and TT (14.3%).The allele distributions of G and T were 70.1 and 29.9%, respectively. In the control group, the genotype frequencies were 53.6% for GG, 36.2% for GT, and 10.2% for TT, and the frequencies of the G and T alleles were 71.7% and 28.3%, respectively. There we re no significant differences in genotype and allele frequencies between the CAD patients and the control group. The mean serum NO levels in CAD patients was significantly higher than that of healthy subjects (p=0.0139). Conclusion: No significant associa tion was detected when CAD severity, genotypes and NO serum levels were correlated.

A1c Variability Can Predict Coronary Artery Disease in Patients with Type 2 Diabetes with Mean A1c Levels Greater than 7

BackgroundRecent studies suggested that the association of acute glucose variability and diabetic complications was not consistent, and that A1c variability representing long term glucose fluctuation may be related to coronary atherosclerosis in patients with type 1 diabetes. In this study, we attempt to determine whether or not A1c variability can predict coronary artery disease (CAD) in patients with type 2 diabetes.MethodsWe reviewed data of patients with type 2 diabetes who had undergone coronary angiography (CAG) and had been followed up with for 5 years. The intrapersonal standard deviation (SD) of serially-measured A1c levels adjusted by the different number of assessments among patients (adj-A1c-SD) was considered to be a measure of the variability of A1c.ResultsAmong the 269 patients, 121 of them had type 2 diabetes with CAD. In patients with A1c ≥7%, the mean A1c levels and A1c levels at the time of CAG among the three groups were significantly different. The ratio of patients with CAD was the highest in the high adj-A1c-SD group and the lowest in the low adj-A1c-SD group (P=0.017). In multiple regression analysis, adj-A1c-SD was an independent predictor for CAD in subjects with A1c ≥7% (odds ratio, 2.140; P=0.036).ConclusionPatients with higher A1c variability for several years showed higher mean A1c levels. A1c variability can be an independent predictor for CAD as seen in angiographs of patients with type 2 diabetes with mean A1c levels over 7%.

Increased Levels of Endotoxin Core Antibodies and Decreased Levels of sCD 14 Indicate Chronic Endotoxemia in Coronary Artery Disease (CURES-127)

Introduction: Endotoxin is hypothesized to play an important role in chronic inflammation associated with coronary artery disease (CAD). The activity of the endotoxin is determined by the relative levels of endotoxin core antibodies (EndoCab), LPS binding protein (LBP) and soluble CD14 (sCD14). Towards this end, we estimated EndoCab, LBP and sCD14 levels in subjects with CAD and correlated them with clinical parameters, serum hormones and cytokine levels. Methods: The study subjects were recruited from Chennai Urban Rural Epidemiology Study (CURES). Age and gender matched subjects with (n=46) and without (n=45) CAD were selected from Phase III of the study. The levels of serum lipopolysaccharide (LPS), EndoCab and its translocation markers (sCD14 and LBP) along with insulin, glucagon, adiponectin and leptin and pro-inflammatory cytokines such as TNF-α, IL-6 and IL-1β were measured by immuno-assays. Results: Quartile analysis showed significantly higher percentage of CAD subjects in the highest quartile of EndoCab (>26.6 EMU/ml) (CAD-24% Vs Controls 0%) and LPS (>65.05 EU/ml) (CAD-21% vs. Controls 4%), while a reverse trend was seen for sCD14 (>2198398.7 ng/ml) (CAD-1% vs. Control-24%) (p<0.01). LBP levels were not statistically different between the groups. While EndoCab levels showed positive association with LPS, LBP, sCD14, hsCRP, HOMA-IR and glucagon, sCD14 showed a negative association with most of these markers. Significant increase in the levels of pro inflammatory cytokines TNFα, IL-6 and IL-1β, was also observed in the CAD group when compared to the control. Conclusions: Significantly elevated levels of EndoCab and decreased levels of sCD14 indicate chronic endotoxin exposure in CAD subjects.

Comparison of Cardiovascular Risk Factors for Peripheral Artery Disease and Coronary Artery Disease in the Korean Population

Background and ObjectivesThe objective of this study was to analyze and compare risk factors for peripheral artery disease (PAD) and coronary artery disease (CAD).Subjects and MethodsThe sample included 7936 Korean patients aged ≥20 years who were hospitalized from 1994 to 2004. Of the 7936 subjects, PAD (n=415), CAD (n=3686), and normal controls (Control) (n=3835) were examined at the Health Promotion Center, Samsung Medical Center.ResultsThe mean age (years) of PAD subjects was 64.4 (±9.3), while CAD subjects was 61.2 (±9.9), and Control subjects was 59.9 (±9.1) (p<0.01). The proportion of males was 90.6% for PAD, 71.4% for CAD, and 75.5% for Control subjects (p<0.01). The adjusted odds ratios (ORs) for hypertension, diabetes mellitus, hypercholesterolemia, smoking, metabolic syndrome and chronic kidney disease were significantly higher in subjects with PAD or CAD compared to those in Control. However, the ORs for high density lipoprotein, being overweight, and being obese were significantly lower in PAD subjects compared to those in Control.ConclusionWe found that cardiovascular risk factors were in fact risk factors for both PAD and CAD.

Effects of ACE polymorphisms and other risk factors on the severity of coronary artery disease

Coronary artery disease (CAD) is a multifactorial disease influenced by genetic and environmental factors. Major risk factors of CAD are hypertension, hyperlipidemia, smoking, family history and obesity. Also polymorphisms in the angiotensin-I converting enzyme (ACE) gene can associate with CAD. The relationship between ACE polymorphisms and other risk factors is not well understood in CAD, likely due to the complex interrelation of genetic and environmental risk factors. The aim of this study was to investigate the associations of CAD risk factors and ACE polymorphisms in patients with CAD. We enrolled 203 consecutive patients and 140 healthy subjects in the study. The severity of CAD was evaluated according to the number of vessels with significant stenosis. ACE insertion (I)/deletion (D) genotype was determined by PCR. The frequency of the DD genotype was significantly higher in patients. D allele frequency was higher among CAD subjects when compared to the control group. The number of stenotic vessels were found to be statistically associated with a high frequency of DD polymorphism and D allele and a low frequency of I allele in patients, especially in male patients. The control group displayed II and ID genotypes more frequently than did the patients. The ACE I/D genotype was associated with hyperlipidemia and smoking history. We consider that the DD polymorphism and D allele may affect the severity of CAD, while I allele may have a protective effect. In conclusion, the ACE I/D genotype may interact with conventional risk criteria in determining the risk of CAD.

The association between non-alcoholic fatty liver disease and carotid atherosclerosis in subjects with within-reference range alanine aminotransferase levels

Our aim was to investigate whether the evaluation of non-alcoholic fatty liver disease (NAFLD) by ultrasound provides additional benefit in assessing carotid atherosclerotic burden in subjects with alanine aminotransferase (ALT) concentrations within the reference range. This was a cross-sectional analysis of 769 healthy individuals (326 men and 443 women) with an ALT concentration ≤ 40 IU/L and alcohol consumption < 140 g/week. Mean carotid artery intima-media thickness (C-IMT) was measured using ultrasound. NAFLD was defined as a mild or greater degree of hepatic steatosis on ultrasound. Although all subjects had an ALT concentration within the reference range, the prevalence of NAFLD increased with increasing quartiles of ALT concentration (27.1%, 40.0%, 54.7%, 75.3% in men, P for trend < 0.001; 22.0%, 34.4%, 35.7%, 55.0% in women, P for trend < 0.001). In the 3rd and 4th quartiles of ALT concentration, women with NAFLD had a significantly higher C-IMT than those without NAFLD (0.671±0.019 mm vs. 0.742±0.025 mm, P=0.023 in Q3; 0.651±0.023 mm vs. 0.737±0.021 mm, P=0.005 in Q4). These differences remained significant even after adjusting for a broad spectrum of potential confounders. In contrast, although men with NAFLD tended to have a higher C-IMT than those without NAFLD in each quartile, these differences were not statistically significant. Women with an upper normal range ALT concentration showed increased C-IMT only when they had NAFLD. Therefore, in women with an elevated ALT level within the reference range, further evaluation for NAFLD, such as liver ultrasound, could potentially identify those patients at high risk for cardiovascular disease.