Male Coronary Artery Disease Research Articles

Abstract 249: Male Mice with XX Sex Chromosome Complement Exhibit Reduced Angiotensin II-Induced Hypertension and Atherosclerosis

Objective: Hypertension and atherosclerosis exhibit sexual dimorphism, partially ascribed to effects of sex hormones. However, recent studies suggest that sex chromosome complement may also contribute to sexual dimorphism of these diseases. The renin-angiotensin system has been suggested to contribute to sexual dimorphism of hypertension and atherosclerosis. However, the relative contribution of sex hormones, versus chromosomes, in the regulation of angiotensin II (AngII)-mediated responses is unknown. We hypothesized that the presence of an XX chromosome complement in male hyperlipidemic mice would reduce AngII-induced hypertension and atherosclerosis. Methods and Results: Male Ldlr-/- mice with an Sry mutation but with an Sry transgene on autosomes were bred to Ldlr-/- females to generate XY or XX males. Male XY or XX mice were segregated to sham-operated or orchiectomized (ORC) groups and fed a high fat diet (42% kcal from fat). Two weeks later, mice were infused with AngII (1,000 ng/kg/min) for 4 weeks. In the presence of sex hormones (sham groups), systolic blood pressure (SBP) was significantly lower in AngII-infused XX than XY males (XY, 136 ± 4; XX, 119 ± 4 mmHg, p=0.024). In XY males, ORC had no significant effect on SBP compared to sham (ORC XY, 129 ± 6 mmHg; p=0.48). However, following castration of XX males, SBP significantly increased (ORC XX 135 ± 3 mmHg; p =0.002). In XY males, ORC resulted in a significant increase in atherosclerotic lesion surface area in the aortic arch (sham, 19 ± 4; ORC, 32 ± 7%; p=0.04). In contrast, ORC had no significant effect on lesion surface area in XX males (sham, 17 ± 3; ORC, 15 ± 2%; p=0.53). Moreover, in the absence of sex hormones, lesion surface area was markedly increased in XY compared to XX males (XY, 32 ± 7; XX, 15 ± 2%; p=0.002). Conclusions: These results demonstrate that effects of testosterone to regulate AngII-induced hypertension and atherosclerosis are dependent on sex chromosome complement. In XY males, testosterone protects against AngII-induced atherosclerosis. In XX males, testosterone protects against AngII-induced hypertension. Moreover, there is pronounced effect of XY chromosome complement to promote AngII-induced atherosclerosis in males.

Association of Circulating C1q/TNF-Related Protein 1 Levels with Coronary Artery Disease in Men

ObjectiveObesity is a major risk factor for cardiovascular disease. Recent evidence demonstrates that dysregulation of fat-derived hormones, also known as adipokines, is linked with the pathogenesis of obesity-related disorders including coronary artery disease (CAD). Here, we investigated whether circulating level of an adipokine C1q/TNF-related protein (CTRP) 1 is associated with the prevalence of CAD.Methods and ResultsConsecutive 76 male CAD patients were enrolled from inpatients that underwent coronary angiography. Sixty four healthy male subjects served as controls. Plasma CTRP1 concentration was determined by enzyme-linked immunosorbent assay. CTRP1 levels were correlated positively with systolic blood pressure (BP) and triglyceride levels, and negatively with HDL cholesterol levels in all subjects. Plasma levels of CTRP1 were significantly higher in CAD patients than in control subjects (CAD: 443.3±18.6 ng/ml, control: 307.8±21.5 ng/ml, p<0.001). Multiple logistic regression analysis with body mass index, systolic BP, glucose, total cholesterol, HDL cholesterol, triglyceride, adiponectin and CTRP1 revealed that CTRP1 levels, together with systolic BP and HDL cholesterol, correlated with CAD.ConclusionsOur data indicate the close association of high CTRP1 levels with CAD prevalence, suggesting that CTRP1 represents a novel biomarker for CAD.

Association of Egr3 genetic polymorphisms and coronary artery disease in the Uygur and Han of China.

BackgroundEndothelial cell activation and dysfunction are the foundation of atherosclerosis, including coronary artery disease (CAD). Endothelial cell activation is mediated by the level of gene transcription. Early growth response 3 (Egr3) is a critical determinant of vascular endothelial growth factor (VEGF) signalling in activated endothelial cells. If endothelial cells are excessively activated, it may lead to vasculopathic diseases, such as pathologic angiogenesis, inflammation, and atherosclerosis. The aim of the present study was to assess the association between the Egr3 gene polymorphisms and CAD.MethodsTwo independent case–control studies that involved the Han group (409 CAD patients and 351 control subjects) and the Uygur group (299 CAD patients and 303 control subjects) analysed the relationship between Egr3 SNPs (rs1996147 and rs1008949) and CAD. Genotyping was undertaken using the TaqMan SNP genotyping assay.ResultsThe entire Uygur group and the males in the Uygur group showed a higher frequency of the A allele (rs1996147) in CAD patients than in the control subjects (P = 0.003 and P = 0.005, respectively). Additionally, the distribution of the recessive model of rs1996147 (AA vs GG + AG) for the total sample and the males was significantly different between CAD patients and control participants (P = 0.002 and P = 0.003, respectively), and the difference remained statistically significant following multivariate adjustment (Total: OR = 1.705; 95% CI: 1.166-2.494, P = 0.006; males: OR = 1.908, 95% CI: 1.189-3.062, P = 0.007). However, for Uygur females, we did not observe a difference in the allele frequency or genotypic distribution of rs1996147 between CAD patients and control participants. Similarly, the distribution of the rs1996147 allele frequency or genotypes showed no significant difference between patients with CAD and control participants in the Han group. The distribution of rs1008949 genotypes, dominant model, recessive model, and allele frequency did not show a significant difference between patients with CAD and the control subjects in the Han and Uygur groups.Conclusionrs1996147 may be a novel polymorphism of the Egr3 gene associated with CAD in males of the Chinese Uygur population.

A Nationwide Population-Based Study of the Risk of Tuberculosis in Different Solid Organ Transplantations in Taiwan

Advances in immunosuppressants for solid organ transplantation (SOT) have improved prevention and treatment of acute rejection as well as reduced the risk of chronic graft damage. However, SOT recipients are prone to developing opportunistic infections because of their long-term immunosuppressed status. Tuberculosis (TB) is a serious opportunistic infection that is associated with increased morbidity and mortality in SOT recipients. However, nationwide population-based research specifically focused on the associations between kidney transplantation (KTx), liver transplantation (LTx), and heart transplantation (HTx), and subsequent TB infection is lacking. This study was conducted using Taiwan's National Health Insurance Research Database, which provided claims data for SOT recipients from 2000 to 2009. Clinical features, treatment, and outcomes were analyzed to determine the risk for TB after SOT. In total, 153 (3.2%) RTx, 19 (1.1%) LTx, and 26 (2.8%) HTx recipients became infected with TB. Compared with non-TB patients, HTx recipients with TB had significantly higher prevalence of older age (P = .037), hypertension (P < .001), and coronary artery disease (CAD) (P = .002). There were also greater percentages of male sex (P = .018), diabetes (P = .029), hyperlipidemia (P = .016), CAD (P < .001), and chronic obstructive pulmonary disease (COPD) (P < .001) in RTx recipients with TB than in those without. In conclusion, posttransplantation TB is a serious problem worldwide, and a high index of suspicion is warranted to ensure early diagnosis and prompt initiation of treatment for TB among SOT patients. In this preliminary study, KTx recipients had a higher risk of TB infection than LTx and HTx recipients, and the high-risk factors were male sex, diabetes, hyperlipidemia, CAD, and COPD. The use of optimal immunosuppressive agents to minimize acute rejection, monitoring of high-risk recipients, prompt diagnosis, and appropriate treatment are required for the management of TB infection in endemic areas such as Taiwan.

Activity of daily living is associated with circulating CD34+/KDR+ cells and granulocyte colony-stimulating factor levels in patients after myocardial infarction

The study aimed to investigate whether the extent of activities of daily living (ADL) of patients after myocardial infarction affect numbers of circulating CD34(+)/KDR(+) and CD45(+)/CD34(+) cells, which are supposed to protect structural and functional endothelial integrity. In a cross-sectional study, 34 male coronary artery disease patients with a history of myocardial infarction were assessed for times spent per week for specific physical ADL, including basic activities (instrumental ADL), leisure time activities, and sport activities, using a validated questionnaire. Individual specific activity times were multiplied with respective specific metabolic equivalent scores to obtain levels of specific activities. Numbers of circulating CD34(+)/KDR(+) and CD45(+)/CD34(+) cells were analyzed by flow cytometry. Furthermore, the colony-forming capacity of CD34(+) cells and the level of granulocyte colony-stimulating factor (G-CSF) in serum were measured. Analysis revealed that the extent of total activities and basic activities, as well as total activity time, were positively correlated with numbers of circulating CD34(+)/KDR(+) cells (r = 0.60, 0.56, and 0.55, P < 0.05). Higher levels of total activity were also associated with increased colony-forming capacity of CD34(+) cells (r = 0.54, P < 0.05) and with higher systemic levels of G-CSF (r = 0.44, P < 0.05). These findings indicate that even ADL-related activities of coronary artery disease patients after myocardial infarction exert stimulating effects on CD34(+)/KDR(+) cell mobilization, potentially mediated by increased G-CSF levels. This, in turn, potentially contributes to the beneficial effects of exercise on the diseased cardiovascular system.

Association between androgenetic alopecia and coronary artery disease in young male patients.

Background:Several studies have demonstrated an association between androgenetic alopecia (AGA) and cardiovascular disease. Still controversies exist regarding the association. Are they truly associated?Objective:The purpose of the present study was to assess the prevalence of AGA and establish its association in young (<45 years) Asian Indian Gujarati male patients having coronary artery disease (CAD).Materials and Methods:Case-control prospective multicentric study was carried out on 424 men. Case group consisted of 212 male subjects having CAD (Group 1) and another 212, either sibling or first degree male relative of the case subjects (having no evidence of CAD) were considered as the control group (Group 2). Age, total cholesterol, incidence of diabetes mellitus, and hypertension were similar in both groups. The degree of alopecia was assessed using the Norwood-Hamilton scale for men. Statistical analysis was performed using Chi-square test.Results:AGA was found in 80 (37.73%) young CAD patients (Group 1), whereas 44 (20.7%) of patients had alopecia in the control group (Group 2). There was statistically significant association between male AGA and CAD (P = 0.001). Odds ratio was 2.70 (95% confidence interval [CI], 1.72 ± 4.26). Statistically significant association was found between high grade baldness (Grades IV-VII) and CAD in young men (P < 0.05). Odds ratio = 2.36 (95% CI, 1.108 ± 5.033). There is statistically significant association of AGA in young Asian Gujarati male with CAD and the prevalence of AGA in young CAD patient is 37.73%.Conclusion:This study implies early onset AGA in male is independently associated with CAD, though mechanisms need to be investigated.

Interleukin 17A in Patients With Stable Coronary Artery Disease: Are There Differences According to Gender?

BackgroundCoronary artery disease (CAD) is a current major public health concern. Immunity and inflammation are involved in all phases of CAD and there is a dynamic balance between cells and molecules. Interleukin 17A (IL17A) concentrations are higher in male patients with acute myocardial infarction than in women. In this study, we evaluated if the IL17A concentrations in male CAD patients (MPs) differed from those in female patients (FPs) and male controls (MCs). Moreover, FPs were compared with female controls (FCs).MethodsThis was a cross-sectional, prospective, and analytical study conducted between March 2012 and August 2013 that enrolled 40 patients (24 men and 16 women) with stable CAD and 20 healthy volunteers (12 men and 8 women) were selected as controls and were matched with the patients (1:2) for sex and age (± 3 years). Comparative analyses of IL17A concentrations in serum and cell culture with and without stimulation were performed between MPs and MCs, MPs and FPs, and FPs and FCs. The lower detection limit was 3.91 pg/mL.ResultsThe comparison of the IL17A concentrations showed: after 48 hours of cell culture with stimulus: MP = 451.67 (99.02 - 892.58) vs. MC = 135 (3.91 - 285), P = 0.04; after 48 hours of cell culture with stimulus: MP = 451.67 (99.02 - 892.58) vs. FP = 131.21 (3.91 - 231.97), P = 0.02; after 48 hours of cell culture with stimulus: FP = 131.21 (3.91 - 231.97) vs. FC = 173.78 (3.91 - 642), P = 0.24.ConclusionThis study revealed higher IL17A concentrations in the stimulated cells isolated from the MPs than in those isolated from FPs and MCs. These findings support the hypothesis that when exposed to certain stimuli, cells isolated from MPs with chronic CAD may produce higher IL17A concentrations than those from FPs and MCs.

Association between intercellular adhesion molecule-1 K469E polymorphism and coronary heart disease in people with Uygur ethnicity, in Xinjiang

To explore the distribution on K469E single nucleotide polymorphism of ICAM-1 gene among people with Uygur ethnicity, in Xinjiang and to analyze the correlation between ICAM-1 gene polymorphism and coronary heart disease. 245 patients with coronary heart disease patients and 377 healthy controls in Xinjiang Uygur population were studied. ICAM-1 gene K469E genotype located in exon 6 were detected by polymerase chain reaction-restricted fragments length polymorphism. Distribution of genotypes in the two groups appeared to be in Hardy-Weinberg equilibrium (P > 0.05). The distribution of genotypes showed significant difference between the two groups (P = 0.039)and the distributions of K and E allele also presented statistically significant difference (P = 0.031). Significant difference was also observed in males(P = 0.029 for genotype, P = 0.025 for allele)but not in females. After adjusted for confounding factors, results from logistic regression analysis indicated that KK genotype was a risk factor for CHD in Uygur male population (OR = 2.389, 95% CI:1.458-3.915, P = 0.001). Genetic polymorphism of ICAM-1 K469E might increase the risk for coronary artery disease in males of Uygur patients in Xinjiang.

GW24-e0002 Interactive association of five candidate polymorphisms in apelin/APJ pathway with coronary artery disease among Chinese hypertensive patients

ObjectivesThe apelin/angiotensin receptor-like 1 (apelin/APJ) pathway has emerged as an essential novel mediator of cardiovascular disease. Via sequencing the genes of apelin/APJ pathway, we have recently identified and validated four...

Body fat responses to a 1‐year combined exercise training program in male coronary artery disease patients

To analyze the body fat (BF) content and distribution modifications in coronary artery disease (CAD) patients in response to a 1-year combined aerobic and resistance exercise training (CET) program. We followed two groups of CAD male patients for 12 months. One group consisted of 17 subjects (57 ± 12 years) who engaged in a CET program (CET group) and the other was a age-matched control group of 10 subjects (58 ± 11 years). BF content and distribution were measured through dual energy X-ray absorptiometry (DXA) at baseline and follow-up. We found no differences on body mass and BMI between baseline and end of follow-up in both groups but, in CET group, we found significant reductions in all analyzed BF depots, including total BF (21.60 ± 6.00 vs. 20.32 ± 5.89 kg, P < 0.01), % total BF (27.8 ± 5.5 vs. 26.4 ± 5.4%, P < 0.05), trunk fat (12.54 ± 3.99 vs. 11.77 ± 4.01 kg, P < 0.05), % trunk fat (31.1 ± 6.9 and 29.2 ± 7.1%, P < 0.05), appendicular fat (8.22 ± 2.08 vs. 7.72 ± 2.037 kg, P < 0.01), % appendicular fat (25.7 ± 4.9 and 24.5 ± 4.9%, P < 0.05), and abdominal fat (2.95 ± 1.06 vs. 2.75 ± 1.10 kg, P < 0.05). Control group showed significant increase in appendicular fat (7.63 ± 1.92 vs. 8.10 ± 2.12 kg, P < 0.05). These results confirm the positive effect of CET on body composition of CAD patients, despite no changes in body mass or BMI. In this study, we observed no alterations on BF distribution meaning similar rate of fat loss in all analyzed BF depots. These results also alert for the limitations of BMI for tracking body composition changes.

Paradoxical protective effect of central obesity in patients with suspected stable coronary artery disease

Increased body mass index (BMI) has been paradoxically inversely associated with the presence of angiographic coronary artery disease (CAD). Central obesity measures, considered to be more appropriate for assessing obesity-related cardiovascular risk, have been little studied in relation to the presence of CAD. The aim was to investigate the association of central obesity with the presence of angiographic CAD as well as the prognostic significance of obesity measures in CAD prediction when added to other cardiovascular risk factors. Patients with suspected stable CAD (n = 403, age 61 ± 10 years, 302 males) referred for diagnostic coronary angiography with documented anthropometric data were enrolled. Significant angiographic CAD was found in 51% of patients. Both BMI (OR = 0.64 per 1 SD increase, P = 0.001) and waist circumference (WC) (OR = 0.54 per 1 SD increase, P < 0.001) were inversely associated with the presence of CAD even after adjustment for cardiovascular risk factors. In subgroup analysis, BMI and WC were significantly inversely associated with the presence of CAD in males, non diabetics, patients >60 years old and patients with Framingham risk score (FRS) >20% (P < 0.01 for all). The addition of BMI or WC in FRS-based regression models improved prediction of CAD (P = 0.03 and P < 0.001 for BMI and WC respectively) without a significant difference between the two models (P = 0.08). Central and overall obesity were independently associated with a reduced prevalence of angiographic CAD, lending further credence to the existence of the 'obesity paradox'. Obesity measures may further improve risk discrimination for the presence of CAD when added in an established risk score such as FRS.

Association between C1019T polymorphism of the connexin37 gene and coronary heart disease in patients with in-stent restenosis

Studies have shown that a C1019T polymorphism of the gene encoding the gap junction protein connexin37 is associated with coronary artery disease (CAD). The aim of the present study was to explore the association between the C1019T polymorphism in the connexin37 gene and CAD patients with in-stent restenosis (ISR). A total of 532 patients who had undergone coronary stenting and coronary angiography at least three months after the procedure were divided according to a clinical diagnosis standard into two groups which were ISR (n=67) and no in-stent restenosis (NISR; n=465) groups. A further 501 healthy individuals were controls. The subjects were genotyped by DNA sequencing. The results demonstrated the following: i) connexin37 gene 1019 sites in the population were distributed by polymorphism into three genetic types (CC, TC and TT types). The distribution frequency of the healthy control, ISR and NISR groups conformed to the Hardy-Weinberg genetic balance rule; ii) in comparison with the healthy controls, the frequency of the connexin37 C allele was higher in the CAD patients (57.05% vs. 41.32%; OR, 1.89; 95% CI, 1.58–2.25; P<0.01). The frequency of the C carriers (CC+TC) was 65.47% in the healthy controls, vs. 79.32% in CAD patients (P<0.01). The CAD risk was significantly increased in the carriers of the C allele (CC+TC) compared with TT homozygotes (OR, 2.03; 95% CI, 1.53–2.80; P<0.01). Stratified analysis demonstrated that a significant difference existed in the frequency of C carriers between the male CAD patients and healthy controls (79.63% vs. 72.45%; OR, 1.48; 95% CI, 1.06–2.09, P=0.02), as well as in the female CAD patients (78.00% vs. 51.50%; OR, 3.34; 95% CI, 1.90–5.86; P<0.01). In the female and male CAD patients, the frequency of the connexin37 C allele was higher than in the healthy controls (male: χ2=12.67, P<0.01; female: χ2=50.20, P<0.01); iii) compared with the NISR group, the frequencies of the connexin37 C allele and C carriers (CC+TC) were significantly higher in the ISR group (frequency of C allele: 72.39% vs. 54.84%; P<0.01; frequency of C carriers: 89.55% vs. 77.85%; P=0.03). Compared with TT homozygotes, the restenosis risk was significantly increased in the carriers of the C allele (CC+TC; OR, 2.44; 95% CI, 1.08–5.50). Subsequent stratified analysis revealed that the frequency of the C allele was significantly higher in the male ISR group than in the male NISR group (78.57% vs. 52.66%; OR, 3.30; 95% CI, 2.05–5.29; P<0.01). The restenosis risk was ∼four-fold higher in the C carriers (CC+TC) than in the TT homozygotes (OR, 3.74; 95% CI, 1.32–10.64). However in the female population, there was no difference in the ISR risk between the carriers of the C allele (CC+TC) and the TT homozygotes (P=0.70). In summary, the C allele of the connexin37 gene is not only is associated with the susceptibility to CAD, but also associated with restenosis following coronary stenting in the population studied herein, particularly the male population.

Interactive Association of Five Candidate Polymorphisms in Apelin/APJ Pathway with Coronary Artery Disease among Chinese Hypertensive Patients

BackgroundVia sequencing the genes of apelin/angiotensin receptor-like 1 (apelin/APJ) pathway, we have recently identified and validated four common polymorphisms (rs3761581, rs56204867, rs7119375, and rs10501367) implicated in the development of hypertension. Extending these findings, we, in Chinese hypertensive patients, sought to investigate the association of these four polymorphisms and one additional promising candidate (rs9943582) from this pathway with the risk of developing coronary artery disease (CAD).Methodology/Principal FindingsGenotypes were obtained from 994 sporadic CAD patients and 708 age- and sex-matched controls. All participants were hypertensives and angiographically-confirmed. Data were analyzed by Haplo.Stats and multifactor dimensionality reduction (MDR) softwares. Genotype distributions of five examined polymorphisms satisfied Hardy-Weinberg equilibrium in controls of both genders. Single-locus analyses exhibited no significant differences in the genotype/allele frequencies of examined polymorphisms between CAD patients and controls (P>0.05), even after controlling traditional cardiovascular confounders. In haplotype analyses, low-penetrance haplotype G-A (in order of rs56204867 and rs3761581 from apelin gene) was significantly overrepresented in controls (1.73%) relative to in CAD patients (0.4%) in males (P = 0.047). Further interaction analyses suggested an overall best MDR model including rs3761581 in males (P = 0.0408) and including rs7119375 and rs9943582 in females (P<0.0001), which were further substantiated in the classical logistical regression model.ConclusionsOur findings demonstrated a contributive role of low-penetrance haplotype in apelin gene on CAD in males, and more importantly, interactive effects of genetic defects in apelin/APJ pathway might confer a potential risk in Chinese hypertensive patients.

Body Fat Responses to a 1-Year Combined Exercise Training Program in Male Coronary Artery Disease Patients

Body Fat Responses to a 1-Year Combined Exercise Training Program in Male Coronary Artery Disease Patients

Waist Circumference and Metabolic Syndrome: The Risk for Silent Coronary Artery Disease in Males

Waist circumference (WC) is a component used to define metabolic syndrome. However, its role as an independent predictor of silent coronary artery disease (CAD), above its contribution to metabolic syndrome, remains unknown. Male veterans without known CAD, undergoing cardiac stress testing for indications other than typical angina or its equivalent, were evaluated for the presence of silent CAD. High WC and metabolic syndrome were defined per the revised National Cholesterol Education Program (NCEP-R) and the International Diabetes Federation (IDF) criteria. Data on 1,071 patients (age 61±11 years) were analyzed retrospectively. On multivariable logistic regression analysis [odds ratio (OR), 95% confidence interval (CI), P value), a WC ≥94 cm (1.42, 1.04-1.93; P=0.026), metabolic syndrome by NCEP-R (1.73, 1.29-2.33; P<0.0001), and metabolic syndrome by IDF (1.57, 1.17-2.11; P=0.003) were independent predictors of silent CAD. When comparing patients meeting criteria for metabolic syndrome defined by either NCEP-R or IDF, the prevalence of silent CAD was not statistically different (P=0.86). The prevalence of silent CAD associated with a high WC was not inferior to that seen between silent CAD and metabolic syndrome as defined by either criterion. Last, among patients with metabolic syndrome defined by NCEP-R, those with a high WC as a defining component of metabolic syndrome had a higher prevalence of silent CAD (30% vs. 20%; P=0.026). A WC ≥94 cm in males is independently associated with an increased prevalence of silent CAD. In patients with metabolic syndrome, this prevalence is increased by the presence of high WC.

The role of mediastinal adipose tissue 11β-hydroxysteroid d ehydrogenase type 1 and glucocorticoid expression in the development of coronary atherosclerosis in obese patients with ischemic heart disease

BackgroundVisceral fat deposition and its associated atherogenic complications are mediated by glucocorticoids. Cardiac visceral fat comprises mediastinal adipose tissue (MAT) and epicardial adipose tissue (EAT), and MAT is a potential biomarker of risk for obese patients.AimOur objective was to evaluate the role of EAT and MAT 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) and glucocorticoid receptor (GCR) expression in comparison with subcutaneous adipose tissue (SAT) in the development of coronary atherosclerosis in obese patients with coronary artery disease (CAD), and to assess their correlations with CD68 and fatty acids from these tissues.Methods and resultsExpression of 11β-HSD-1 and GCR was measured by qRT-PCR in EAT, MAT and SAT of thirty-one obese patients undergoing coronary artery bypass grafting due to CAD (obese CAD group) and sixteen obese patients without CAD undergoing heart valve surgery (controls). 11β-HSD-1 and GCR expression in MAT were found to be significantly increased in the obese CAD group compared with controls (p < 0.05). In the obese CAD group, 11β-HSD-1 and GCR mRNA levels were strongly correlated in MAT. Stearidonic acid was significantly increased in EAT and MAT of the obese CAD group and arachidonic acid was significantly expressed in MAT of the obese male CAD group (p < 0.05).ConclusionsWe report for the first time the increased expression of 11β-HSD-1 and GCR in MAT compared with EAT and SAT, and also describe the interrelated effects of stearidonic acid, HOMA-IR, plasma cortisol and GCR mRNA levels, explaining 40.2% of the variance in 11β-HSD-1 mRNA levels in MAT of obese CAD patients. These findings support the hypothesis that MAT contributes locally to the development of coronary atherosclerosis via glucocorticoid action.

A study on risk factors of coronary artery disease in Chong Qing city

ObjectiveTo investigate the relationship between risk factors and coronary artery disease in Chong Qing city, and to provide scientific basis for preventing and intervening coronary artery disease.MethodsFour hundred and fifty...

ABCA1 impacts athero-thrombotic risk and 10-year survival in a contemporary secondary prevention setting

ObjectivesWe prospectively investigated the effects of ATP-binding cassette protein-1 (ABCA1) variants on long-term clinical outcome in patients with coronary artery disease (CAD). BackgroundABCA1 is implicated in the etiology of atherothrombosis and may offer a target to reduce cardiovascular risk. However, the impact of ABCA1 on recurrent cardiovascular disease in a secondary prevention setting is as of yet unknown. MethodsWe studied cause-specific 10-year mortality and quantitative coronary angiography data from the Regression GRowth Evaluation Statin Study (REGRESS), comprising 884 male CAD patients genotyped for promoter variants encompassing a proximal regulatory region (rs2422493, rs1800976, rs2740483 and rs1800977). Kaplan–Meier, proportional hazards and haplotype analyses were used to ascertain single-variant and multi-marker effects on absolute risk and extent of CAD. ResultsProtection from 10-year vascular death could be attributed to the rs2422493 genotype (available in 639 patients) T allele with absolute risk decreasing stepwise from 12.2% to 8.6% to 4.7% per each added allele copy, HR 0.64, p=0.03 and HR 0.53, p=0.04 in the TGCC haplotype context. The TGCC (p=0.04) and TCCT (p=0.003) haplotypes exhibited less extensive CAD. ConclusionsOn a background of contemporary secondary prevention, variation in the ABCA1 promoter influences 10-year risk of vascular death and angiographic extent of CAD in men. These insights contribute to identification of patients sharing a specific prognosis, understanding of its etiological basis and development of strategies of risk reduction in CAD.

Endogenous oestradiol but not testosterone is related to coronary artery disease in men

Men die of coronary artery disease (CAD) more often than women. There is evidence that testosterone either is neutral or has a beneficial effect on male cardiovascular disease. The role of oestrogens in male CAD has been less studied. This study was carried out with the purpose of evaluating the relationship between sex hormone levels and CAD. Case-control study. Men (aged 40-70) submitted to coronary angiography. A 70% occlusion of at least one major coronary artery defined the cases; subjects with ≤ 50% occlusion constituted the control group. Blood samples were collected for total testosterone (TT), oestradiol, luteinizing hormone, follicle-stimulating hormone, sex hormone-binding globulin, lipid profile and albumin measurements. Bioavailable and free testosterone, free androgen index (FAI) and free oestrogen index (FEI) were calculated. Oestradiol and TT levels were examined as terciles, based on the whole study population. Of the 140 patients included, 72 were cases and 68 were controls. The baseline characteristics of the two groups were similar, except for the older age and lower LDL-C in the cases. Oestradiol and FEI but not total, bioavailable and free testosterone and FAI correlated positively with CAD. After adjustments for potential confounders, oestradiol remained statistically significant. The prevalence of CAD was significantly higher in the 3rd than in the 1st tercile of oestradiol. In this study, men with CAD had higher oestradiol and FEI levels. Additional studies are needed to clarify the direction of causality and possible underlying mechanisms.

Telomere length and cardiovascular risk in hypertensive patients with left ventricular hypertrophy: the LIFE study

Short telomeres are associated with aging and age-related diseases. Our aim was to determine whether short leukocyte telomere length is associated with risk factors and cardiovascular diseases in a high-risk hypertensive population. We measured leukocyte telomere lengths at recruitment in 1271 subjects with hypertension and left ventricular hypertrophy (LVH) participating in the Lifestyle Interventions and Independence for Elders (LIFE) study. At baseline, short mean telomere length was associated with coronary artery disease in males (odds ratio (OR) 0.61, 95% confidence interval (CI) 0.39-0.95), and transient ischemic attack in females (OR 0.62 95% CI 0.39-0.99). Proportion of short telomeres (shorter than 5 kb) was associated with Framingham risk score (r=0.07, P<0.05), cerebrovascular disease (OR 1.18, 95% CI 1.01-1.15) and type 2 diabetes in men (OR 1.07, 95% CI 1.02-1.11). During follow-up, proportion of short telomeres was associated with combined cardiovascular mortality, stroke or angina pectoris (hazard ratio 1.04, 95% CI 1.01-1.07). Telomere length was not associated with smoking, body mass index, pulse pressure or self-reported use of alcohol. Our data suggest that reduced leukocyte telomere length is associated with cardiovascular risk factors and diseases as well as type 2 diabetes, and is a predictor of cardiovascular disease in elderly patients with hypertension and LVH.