Risk Of Coronary Artery Disease In Women Research Articles

Sex differences in the associations of HDL particle concentration and cholesterol efflux capacity with incident coronary artery disease in type 1 diabetes: The RETRO HDLc cohort study

In type 1 diabetes, women lose their relative protection (compared to men) against coronary artery disease (CAD), while high-density lipoprotein cholesterol (HDL-C) is less strongly associated with lower CAD risk in women. We aimed to assess whether sex differences in the HDL particle concentration (HDL-P) and cholesterol efflux capacity (CEC) association with CAD may explain these findings. HDL-P (calibrated differential ion mobility analysis) and total and ATP binding cassette transporter A1 (ABCA1)-specific CEC were quantified among 279 men and 271 women with type 1 diabetes (baseline mean age 27·8 years; diabetes duration, 19·6 years). Clinical CAD was defined as CAD death, myocardial infarction and/or coronary revascularization. Women had higher large HDL-P levels and marginally lower concentrations of small HDL-P and ABCA1-specific CEC than men. No sex differences were observed in extra-small HDL-P, medium HDL-P and total CEC. During a median follow-up of 26 years, 37·6 % of men and 35·8 % of women developed CAD (p = 0·72). In multivariable Cox models stratified by sex (pTotal HDL-P x sex interaction=0·01), HDL-P was negatively associated with CAD incidence in both sexes. However, associations were stronger in men, particularly for extra-small HDL-P (hazard ratio (HR)men=0·11, 95 % confidence interval (CI): 0·04-0·30; HRwomen=0·68, 95 % CI: 0·28-1·66; pinteraction=0·001). CEC did not independently predict CAD in either sex. Despite few absolute differences in HDL-P concentrations by sex, the HDL-P - CAD association was weaker in women, particularly for extra-small HDL-P, suggesting that HDL-P may be less efficient in providing atheroprotection in women and perhaps explaining the lack of a sex difference in CAD in type 1 diabetes.

A Correlative Study of Vitamin D Receptor Variants Fok1, Apa1, Bsm1, and Taq1 Polymorphism and Vitamin D Deficiency with Higher Risk Ratio of Coronary Artery Disease in Female Population

Abstract No studies are available on single nucleotide polymorphisms (SNPs) of the VDR gene in association with coronary artery disease (CAD) in women. The study aimed to investigate the association between SNPs in the VDR regions Fok I (rs10735810), Bsm I (rs1544410), Apa I (rs7975232), and Taq I (rs731236) and its associated risk of CAD in female patients. This prospective case-control study included 100 women diagnosed with CAD and age-matched healthy controls. The association between 1,25-dihydroxy vitamin D levels and VDR polymorph was assessed. In cases, the genotype ‘ff’ was reduced (14%) in co-dominant (OR, 0.13; CI, 0.03–0.65, p=0.0018) and recessive (OR, 0.11; CI, 0.02–0.54, p=0.0018) models. The ‘Ff’ genotype frequency in the over-dominant model was significantly higher (15%) in some cases (OR, 2.58; CI, 1.04–6.41, p=0.031). The frequency of genotype ‘Bb’ was increased (14%) in co-dominant (OR, 2.24; CI, 0.83–6.01, p=0.029) and over-dominant (OR, 2.65; CI, 1.01–6.94, p=0.035) cases. Women with CAD had a significantly lower frequency (14%) of the ‘bb’ genotype in both co-dominant (OR, 0.48; CI, 0.19–1.17, p=0.029) and recessive models (OR, 0.40; CI, 0.17–0.95, p=0.039). VDR genotypes such as Aa+aa, BB+Bb, Aa, Bb, FF+Ff, Tt+tt, aa, Ff, and tt were associated with an increased risk of CAD, and serum vitamin D levels were lower. Alleles ‘a’, ‘B’, and ‘t’ increase CAD risk in women. Subjects with genotypes (BB/Bb), (Tt/tt), and (FF) have a 2-fold, 2.6-fold, and 3-fold increased risk of low 25(OH)D3 levels. We found a statistically significant association between VDR polymorphisms and 25(OH)D3 levels for Taq I and Bsm I genotypes in females with CAD.

Gender Disparities on Access to Care and Coronary Disease Management.

Mortality decline in women to a lesser extent than in men with coronary artery disease (CAD) has provoked a bigger interest in some already existing dilemmas and questions. Many studies carried out in the past three decades did not provide us with precise conclusions. Moreover, various challenges in the prevention, diagnosis, treatment and outcome of CAD in women are still remaining. The meta-analysis and the systematic review conducted in the last years have offered novel approaches to understanding CAD gender disparities in access to care and coronary disease management in women, but women are more likely to experience less favorable short- and long-term outcomes than men do. The reasons for these findings should lie in several known segments in the CAD pathophysiological mechanisms different in women and ultimately leading to a lower quality of care. Clinical presentation in women, which is often characterized by atypical chest pain and a higher prevalence of non-obstructive CAD when evaluated invasively, places women to the false-negative diagnosis of CAD and influences inadequate access to care. Clinical presentation and diagnostic methods, as well as the appropriate treatment options insufficiently examined in women, need to be better defined. The traditional CAD risk factors have a greater impact on women than on men. Unique CAD risk factors only seen in women, have recently been recognized with more attention. However, it is important to note that even in women with obstructive CAD and typical clinical presentation, invasive therapy and pharmacologic therapy are not always implemented as recommended by guidelines as in men. Women are underrepresented in CAD trials, and in current guidelines, gender differences in CAD management have not yet been justified. The underestimation of the risk of CAD in women, followed by its underdiagnosis and undertreatment, might be one of the reasons for a worse prognosis in women in comparison with men.

Abstract 13648: Sex Differences in Modifiable Risk Factors and Severity of Coronary Artery Disease

Introduction: It is still unknown whether traditional risk factors may have a sex specific impact on coronary artery disease (CAD) burden. Hypothesis: We sought to investigate at individual level whether there are sex differences in the four modifiable traditional cardiovascular risk factors and how these differences may impact the CAD and outcomes in ACS. Methods: We identified 14,793 patients who underwent coronary angiography for acute coronary syndromes in the ISACS-TC registry (NCT01218776) from 2010 to 2019. Main outcome measure was the association between traditional risk factors and severity of CAD and its relationship with 30-day mortality. The relative risk (RR) ratios and 95% CI were calculated from the ratio of the absolute risks of women versus men using inverse probability of weighting. Estimates were compared by test of interaction on the log scale. Severity of CAD was categorized as obstructive (≥50% stenosis) versus nonobstructive CAD. Results: The RR ratios for obstructive CAD in women versus men among nondiabetic people was 0.49 (95%CI 0.41-0.60) and diabetic people was 0.89 (95%CI 0.62-1.29); interaction by diabetes status: p=0.018. Exposure to smoking shifted the RR ratios from 0.50 (95%CI 0.4 -0.61) in nonsmokers to 0.75 (95%CI 0.54-1.03) in current smokers; interaction by smoking status: p=0.018. There were no significant sex-related interactions with hypercholesterolemia and hypertension. Women with obstructive CAD had higher 30-day mortality rates than men (RR 1.75, 95%CI 1.48-2.07). No sex differences in mortality were observed in patients with nonobstructive CAD. Conclusions: Obstructive CAD in women signifies a higher risk for mortality compared with men. Current smoking and diabetes disproportionally increase the risk of obstructive CAD in women. Achieving the goal of improving cardiovascular health in women still require intensive efforts toward further implementation of lifestyle and treatment interventions.

Analysis of selected promoter polymorphisms and haplotypes of the CYBA gene encoding the p22phox, subunit of NADPH oxidases, in patients with coronary artery disease

The p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA gene. It was shown that functionally relevant polymorphisms of the CYBA gene −930A > G, −852C > G, −675A > T, −536C > T, 214C > T (previously described as 242C > T), *24A > G (previously described as 640A > G), and *49A > G modulate generation of reactive oxygen species (ROS). To analyse whether the CYBA gene polymorphisms −852C > G, −675A > T, and −536C > T were associated with coronary artery disease (CAD), and to designate haplotype blocks. Four hundred and ninety subjects: 245 patients with CAD and 245 age and sex-matched controls. The polymorphisms were genotyped using the PCR-RFLP method and the TagMan® Pre-designed SNP Genotyping Assay. The analysed polymorphisms do not form haplotype blocks. Case–control study revealed that the −930 G/-675T and −930G/*49G diplotypes were a CAD risk factor. The 675T/*49G diplotype can modulate CAD risk in women. The protective effect reducing CAD risk in women was related to the −930A/−675T and −930A/*49A diplotypes. Carrier state of the −852C allele (−852C > G) was associated with multivessel stenosis while the CC genotype of the −536C > T polymorphism was more frequent in patients with peripheral artery disease. Hypercholesterolemic, cigarette smokers had an increased risk of CAD, especially C − 852 allele (−852C > G) carriers (SIM = 3.54; odds ratios (OR) = 10.01, p < 0.000). The CYBA gene polymorphisms modulate the risk of CAD but do not form a haplotype blocks.

A Novel Polymorphism in the Promoter of the CYP4A11 Gene Is Associated with Susceptibility to Coronary Artery Disease.

Enzymes CYP4A11 and CYP4F2 are involved in biosynthesis of vasoactive 20-hydroxyeicosatetraenoic acid and may contribute to pathogenesis of coronary artery disease (CAD). We investigated whether polymorphisms of the CYP4A11 and CYP4F2 genes are associated with the risk of CAD in Russian population. DNA samples from 1323 unrelated subjects (637 angiographically confirmed CAD patients and 686 age- and sex-matched healthy individuals) were genotyped for polymorphisms rs3890011, rs9332978, and rs9333029 of CYP4A11 and rs3093098 and rs1558139 of CYP4F2 by using the Mass-ARRAY 4 system. SNPs rs3890011 and rs9332978 of CYP4A11 were associated with increased risk of CAD in women: OR = 1.26, 95% CI: 1.02–1.57, P = 0.004, and Q = 0.01 and OR = 1.45, 95% CI: 1.13–1.87, P = 0.004, and Q = 0.01, respectively. Haplotype G-C-A of CYP4A11 was associated with increased risk of CAD (adjusted OR = 1.41, 95% CI: 1.12–1.78, and P = 0.0036). Epistatic interactions were found between rs9332978 of CYP4A11 and rs1558139 of CYP4F2 (P interaction = 0.025). In silico analysis allowed identifying that SNP rs9332978 is located at a binding site for multiple transcription factors; many of them are known to regulate the pathways involved in the pathogenesis of CAD. This is the first study in Europeans that reported association between polymorphism rs9332978 of CYP4A11 and susceptibility to coronary artery disease.

Sex-specific association of SH2B3 and SMARCA4 polymorphisms with coronary artery disease susceptibility.

To determine whether sex differences affect the association between genetic polymorphisms and coronary artery disease (CAD) in the Chinese Han population, we conducted a study comparing the frequency of SH2B3 and SMARCA4 variants in 456 CAD patients (291 men, 165 women) and 685 age-matched controls (385 men, 300 women). Ten single nucleotide polymorphisms (SNPs) in SH2B3 and SMARCA4 were genotyped using MassARRAY technology. Allelic and genotypic models and haplotype frequencies were compared between groups. Logistic regression was used to estimate the CAD risk associated with the genotypes. We found that the “A” alleles in both rs11879293 and rs12232780 of SMARCA4 were associated with CAD risk in men (p = 0.036 and p = 0.001, respectively). The genetic model showed that SH2B3 was associated with CAD susceptibility in both women and men, while SMARCA4 was associated with reduced odds of CAD in men. SH2B3 haplotypes were associated with decreased CAD risk in women (p = 0.007) and increased CAD risk in men (p = 0.047). By providing evidence for the sex-related association between SH2B3 and SMARCA4 gene variants and CAD susceptibility in the Chinese Han population, this study may help define useful diagnostic and preventive markers for these patients.

Variants in the CXCL12 gene was associated with coronary artery disease susceptibility in Chinese Han population.

BackgroundCoronary artery disease (CAD) is one of the most serious diseases all around the world. Previous studies have shown the function of CXCL12 in the process of atherosclerosis. The aim of this research is to examine whether variants of CXCL12 contribute to CAD.Materials and MethodsTo examine whether variants of CXCL12 contribute to CAD, we selected 6 single nucleotide polymorphisms (SNPs) of CXCL12, and genotyped by Sequenom MassARRAY technology in 597 CAD patients and 685 healthy control. Odds ratio (OR) and 95% confidence intervals (CIs) were calculated by unconditional logistic regression adjusted for age and gender. We also analysis the differences in continuous variables among the subjects with three genotypes of related genes were assessed using the ANOVA.ResultsWe found significant differences in apoB concentrations with rs1065297 and rs10793538 different genotype. In the allele model, rs1065297, rs266089 and rs10793538 in CXCL12 gene associated with the risk of CAD. Stratified according to gender, rs266089 and rs2839693 in CXCL12 gene were associated with the risk of CAD in men, while rs1065297 and rs10793538 in CXCL12 gene were associated with the risk of CAD in women. Stratified according to age, rs197452 decreased the risk of CAD in less than 50 years old group. While in more than 50 years old group, not find significant results. Haplotype analysis shown that haplotype “TGCC” in the block increased CAD risk (OR=1.26, 95%CI: 1.00-1.58, p=0.046).ConclusionThis study provides an evidence for polymorphism of CXCL12 gene associated with CAD development in Chinese Han population.

Gender differences in impact of CYP2C19 polymorphism on development of coronary artery disease.

The aim was to clarify whether CYP2C19 polymorphism is associated with the development of coronary artery disease (CAD). This study enrolled 723 patients with CAD (men 71%, 70 years) and healthy subjects undergoing a medical checkup (n = 453) as controls (men 69%, 53 years). We analyzed the incidence of CYP2C19 polymorphism and its association with the development of CAD in the absence of diabetes, dyslipidemia, and chronic kidney disease to minimize the influence of conventional coronary risk factors. In the analysis without risk factors, there was no difference in the incidence of the CYP2C19 genotype between CAD (n = 115) and control (n = 194) groups [extensive metabolizer, intermediate metabolizer, poor metabolizer (PM) in non-risk CAD: 33%, 46%, 21%, respectively; in non-risk control: 31%, 52%, 17%, respectively]. Analysis between CAD and control groups by the χ test showed that there was significant difference in distribution of CYP2C19 genotype in women alone (P = 0.025) but not in total subjects (P = 0.471) or men (P = 0.678), respectively. CYP2C19 PM was an independent predictor of CAD risk in women alone (odds ratio, 10.717; 95% confidence interval, 1.753-65.505; P = 0.010) but not in men. CYP2C19 PM status might be associated with the development of CAD as a disease susceptibility gene, especially in women.

Genetic Variants in PCSK1 Gene Are Associated with the Risk of Coronary Artery Disease in Type 2 Diabetes in a Chinese Han Population: A Case Control Study

BackgroundInsulin and glucagon-like peptide 1 (GLP-1), converted by proprotein convertase 1 (PC1/3) from proinsulin and proglucagon, are associated with type 2 diabetes (T2DM) and coronary artery disease (CAD). The aim of this study is to investigate the association of PCSK1 gene, which encodes PC1/3, with the risk of CAD in Chinese patients with T2DM.MethodsWe selected and genotyped 5 haplotype-tagging single nucleotide polymorphisms (SNPs) at PCSK1 gene (across 39873bp locus) in a case-control study of Chinese Han population involving 425 diabetic patients (62.1% male, mean age 63.2 years) with CAD as positive cases and 258 diabetic patients (44.2% male, mean age 62.0 years) without CAD as controls.ResultsThe allele frequencies at rs3811951 were significantly different between cases and controls (30.7% vs. 37.2%), with the allele G associated with decreased risk for CAD (OR = 0.75, 95% CI = 0.59–0.94, p = 0.013). In recessive inheritance mode, the carriers of GG had a lower risk (OR = 0.50, 95%CI = 0.31–0.82, p = 0.005), even after adjusted for gender, age, BMI and smoking (OR = 0.43, 95%CI = 0.24–0.77, p = 0.004). The carriers of the minor allele A at rs156019 had a higher risk (OR = 1.66, 95%CI = 1.10–2.50, p = 0.016 after adjustment) in dominant inheritance mode. The SNP rs6234 was also significantly associated with CAD risk in women, with the carriers of the minor allele G at rs6234 associated with a reduced CAD risk in recessive inheritance mode (OR = 0.42, 95% CI = 0.18–0.95, p = 0.036 after adjustment).ConclusionsOur results found that common genetic variants in PCSK1 were associated with CAD in Chinese patients with T2DM.

Angiographically-assessed coronary artery disease associates with HDL particle size in women

It has been suggested that a reduced HDL particle size could be another feature of the atherogenic dyslipidemia found among viscerally obese subjects. ObjectiveTo investigate, in women, the relationship between HDL particle size and coronary artery disease (CAD). MethodsAverage HDL particle size was measured in a sample of 239 women on whom CAD was assessed by angiography. ResultsOverall, women who had CAD were characterized by a deteriorated fasting metabolic risk profile, which was accompanied by smaller HDL particles compared to women without CAD (80.4 ± 2.2 Å vs. 81.5 ± 2.7 Å, p < 0.01). In addition, a reduced HDL particle size was a significant correlate of several features of the atherogenic metabolic profile of abdominal obesity such as increased triglyceride and apolipoprotein B concentrations, decreased HDL cholesterol levels, an elevated cholesterol/HDL cholesterol ratio and hyperinsulinemia and was also associated with an increased waist circumference (0.13≤|r|≤0.21, p < 0.05). Odds ratio of being affected by CAD was increased by 2.5-fold (95% CI: 1.4–4.5; p < 0.01) among women with smaller HDL particles compared to women with larger HDL particles. Finally, women characterized by the presence of the NCEP-ATP III clinical criteria or by hypertriglyceridemic waist were characterized by smaller HDL particles compared to women without these clinical phenotypes (p < 0.05). ConclusionHDL particle size appears to be another relevant feature of a dysmetabolic state which is related to CAD risk in women.

Plasma lecithin:cholesterol acyltransferase and carotid intima-media thickness in European individuals at high cardiovascular risk

Lecithin:cholesterol acyltransferase (LCAT) is the enzyme responsible for cholesterol esterification in plasma. LCAT is a major factor in HDL remodeling and metabolism, and it has long been believed to play a critical role in macrophage reverse cholesterol transport (RCT). The effect of LCAT on human atherogenesis is still controversial. In the present study, the plasma LCAT concentration was measured in all subjects (n = 540) not on drug treatment at the time of enrollment in the multicenter, longitudinal, observational IMPROVE study. Mean and maximum intima-media thickness (IMT) of the whole carotid tree was measured by B-mode ultrasonography in all subjects. In the entire cohort, LCAT quartiles were not associated with carotid mean and maximum IMT (P for trend 0.95 and 0.18, respectively), also after adjustment for age, gender, HDL-cholesterol (HDL-C), and triglycerides. No association between carotid IMT and LCAT quartiles was observed in men (P=0.30 and P=0.99 for mean and maximum IMT, respectively), whereas carotid IMT increased with LCAT quartiles in women (P for trend 0.14 and 0.019 for mean and maximum IMT, respectively). The present findings support the concept that LCAT is not required for an efficient reverse cholesterol transport and that a low plasma LCAT concentration and activity is not associated with increased atherosclerosis.

High-density lipoprotein cholesterol in diabetes: Is higher always better?

Recent data suggest that highly elevated high-density lipoprotein cholesterol (HDL-C) may not always protect against cardiovascular disease. To what degree this is true in type 1 diabetes is unknown, although cardiovascular risk is increased despite elevated mean HDL-C. To reassess the association between HDL-C and its subfractions with coronary artery disease (CAD) in childhood-onset type 1 diabetes. Epidemiology of Diabetes Complications study participants free of CAD at baseline (301 men, 298 women; mean age, 27.1 and diabetes duration, 18.9 years) were studied. CAD was defined as angina, ischemic electrocardiogram changes, confirmed myocardial infarction, angiographic stenosis ≥50%, revascularization, or CAD death. Cholesterol in the HDL fraction and HDL3 cholesterol subfraction was measured enzymatically after precipitation with heparin/manganese and dextran sulfate, respectively. During 18 years of follow-up, 29.5% of men and 25.5% of women developed CAD. Although a linear decrease in incidence was observed with increasing HDL-C concentration in men, incidence increased in women at less than 47 mg/dL and greater than 80 mg/dL. These patterns largely reflected the HDL3 cholesterol-CAD association. After multivariable adjustment, the linear, inverse, HDL-C/CAD association persisted in men (hazard ratio [HR] 0.97, 95% confidence interval [CI] 0.94-0.99); in women, the U-shaped relationship lost significance. HDL3 cholesterol remained multivariably associated with CAD in both men (linear association, P= .03) and women (HR 2.31 (95% CI 1.31-4.08) and HR 1.80 (95% CI 1.01-3.23) for the lowest and highest versus the middle quintiles, respectively). The increased CAD risk in women for an HDL-C >80 mg/dL in type 1 diabetes merits further study. Gender specificity could not be determined as only two men had HDL-C >80 mg/dL.

Plasma levels of lecithin:cholesterol acyltransferase and risk offuture coronary artery disease in apparently healthy men and women: aprospective case-control analysis nested in the EPIC-Norfolk populationstudy

LCAT plays a key role in the maturation of HDL, as evidenced by low HDL-cholesterol levels in carriers of deleterious mutations in LCAT. However, the role of LCAT in atherosclerosis is unclear. We set out to study this in a prospective study. Plasma LCAT levels, which strongly correlate with LCAT activity, were measured in baseline nonfasting samples of 933 apparently healthy men and women who developed coronary artery disease (CAD) and 1,852 matched controls who remained free of CAD during 6 year follow-up. LCAT levels did not differ between cases and controls but were higher in women than men. Stratification into LCAT quartiles revealed a positive association with plasma LDL-cholesterol and triglyceride levels in the unexpected absence of an association with HDL-cholesterol. In mixed-gender analyses, the odds ratio (OR) for future CAD in the highest LCAT quartile versus the lowest was 1.00 [confidence interval (CI): 0.76-1.29, P for linearity = 0.902], although opposite trends were observed in men and women. In fact, high LCAT levels were associated with an increased CAD risk in women (unadjusted OR 1.45, CI: 0.94-2.22, P for linearity = 0.036). In contrast to our studies in carriers of LCAT mutations, the current data show that low LCAT plasma levels are not associated with increased atherosclerosis in the general population.

A lack of association between adiponectin polymorphisms and coronary artery disease in a Chinese population

We investigated the association between two single nucleotide polymorphisms (SNPs) in the adiponectin gene (rs822395 and rs266729) and coronary artery disease (CAD) in a case-control study of 198 unrelated Chinese CAD patients (with ≥ 70% coronary stenosis or previous myocardial infarction) and 237 non-CAD controls. The ligase reaction was used to detect SNPs rs822395 and rs266729, and the allelic association of these SNPs with the occurrence and severity of CAD was assessed. There were no significant differences in the genotypic or allelic frequencies of the two SNPs between control and CAD individuals. In addition, there was no association between the two SNPs and the severity of CAD based on the number of diseased vessels. The frequencies of alleles C and G at rs266729 differed significantly between females in the CAD and control groups, but not between males. Female carriers of allele G at rs266729 had a higher risk of CAD compared with allele C carriers (OR = 1.30, 95% CI: 1.09-2.64, p = 0.02). These results indicate a gender-specific effect of the adiponectin gene rs266729 variant in modulating the risk of CAD in women.

Retinal Vessel Diameter and the Incidence of Coronary Artery Disease in Type 1 Diabetes

To examine the relationship between retinal vessel diameter and coronary artery disease (CAD) incidence in type 1 diabetes (T1D) using data from the Pittsburgh Epidemiology of Diabetes Complications (EDC) Study. Prospective cohort study of childhood-onset T1D. Data are from 448 participants who had retinal photographs taken at baseline examination (May 1986 to November 1988) and no history of laser photocoagulation. Computer-assisted grading was used to measure retinal arteriolar and venular caliber. CAD incidence (CAD death, myocardial infarction, revascularization/stenosis > or =50%, ischemic electrocardiogram, or physician-diagnosed angina) was ascertained over a median follow-up time of 18 years (range, 2 months to 20.5 years). Mean baseline arteriolar and venular caliber were 180.0 microm (standard deviation [SD], 15.2 microm) and 273.3 microm (SD, 28.0 microm), respectively; 80 (17.9%) CAD events occurred during follow-up. After covariate adjustment for T1D duration, gender, hypertension, serum lipids, and smoking status, smaller arteriolar caliber was significantly associated with CAD (hazard ratio [HR], 1.42; P = .03), but larger venular caliber was not. A vessel diameter-gender interaction term was significant for arteriolar caliber (P = .006). Stratified by gender, smaller arteriolar caliber was significantly associated with the incidence of CAD in women (HR, 1.92; P = .004), but not men. Venular caliber was not associated with CAD in either gender. Smaller arteriolar caliber may indicate an increased risk of CAD in women, but not men, with T1D. Additional studies are needed to further examine the role of microvascular disease in the pathogenesis of CAD in women with T1D.

Women with coronary artery disease and depression: A neglected risk group

Coronary artery disease (CAD) has been held to be a “male” disease due to men's higher absolute risk compared to women, but the relative risk of women for CAD morbidity and mortality is actually higher. The purpose of this article is to review research evidence for gender differences in CAD and depression with special emphasis on women. Current knowledge points to important gender differences in age of onset, symptom presentation, management, outcome as well as traditional and psychosocial risk factors. Compared to men, CAD risk in women is more strongly increased by some traditional factors (diabetes, hypertension, hypercholesterolemia, obesity), and socioeconomic and psychosocial factors seem to have a higher impact on CAD in women as well. With respect to differences in CAD management, a gender-bias in favour of men has to be taken into account in spite of older age and higher comorbidity in women, possibly contributing to a poorer outcome. Depression was shown to be an independent risk factor and consequence of CAD; however, concerning gender differences, the results have been inconsistent. Current evidence suggests that depression causes a greater increase in CAD incidence in women, and that female CAD patients experience higher levels of depression than men. Gender aspects should be more intensively considered both in further research on gender differences in comorbid depression and in cardiac treatment and rehabilitation with the goal of making secondary prevention for women more effective.

Dietary carotenoids and risk of coronary artery disease in women

Numerous studies have shown that higher intakes or higher blood concentrations of carotenes are associated with a lower risk of coronary artery disease (CAD). Given the null results in trials of beta-carotene supplementation, considerable attention has focused on the potential role of other dietary carotenoids in the prevention of CAD. Our objective was to prospectively examine the relation between dietary intakes of specific carotenoids and risk of CAD in women. In 1984, 73 286 female nurses completed a semiquantitative food-frequency questionnaire that assessed their consumption of carotenoids and various other nutrients. The women were followed for 12 y for the development of incident CAD (nonfatal myocardial infarction and fatal CAD), and dietary information was updated in 1986, 1990, and 1994. During 12 y of follow-up (803 590 person-years), we identified 998 incident cases of CAD. After adjustment for age, smoking, and other CAD risk factors, we observed modest but significant inverse associations between the highest quintiles of intake of beta-carotene and alpha-carotene and risk of CAD but no significant relation with intakes of lutein/zeaxanthin, lycopene, or beta-cryptoxanthin. For women in the highest compared with the respective lowest quintile of intake, the relative risks for beta-carotene and alpha-carotene were 0.74 (95% CI: 0.59, 0.93) and 0.80 (95% CI: 0.65, 0.99), respectively. The association between the specific carotenoids and CAD risk did not vary significantly by current smoking status. Higher intakes of foods rich in alpha-carotene or beta-carotene are associated with a reduction in risk of CAD.