Onset Of Coronary Heart Disease Research Articles

A 1H NMR based metabonomics approach to progression of coronary atherosclerosis in a rabbit model

Subtle metabolic variations precede and accompany oxidative and vascular damage, which correspond to the pathophysiological process of coronary heart disease (CHD). To investigate the progression of coronary atherosclerosis and identify potential biomarkers, the metabolic profiling in the plasma of rabbits fed a high-cholesterol diet were investigated using proton nuclear magnetic resonance spectroscopy (1H NMR) coupled with multivariate data analysis. Metabolite variations during atherogenesis showed a time-dependent development from physiological to pathophysiological status in rabbits. NMR-based plasma profiling demonstrated that low-density lipoprotein/very-low-density lipoprotein (LDL/VLDL), glutamine, phosphorylcholine, N-acetyl glycoproteins, betaine, proline, and tyrosine were the most positively corresponded metabolites of the aortic atherosclerotic lesions, whereas high-density lipoprotein (HDL), unsaturated lipids, citrate, glucose, and creatinine were the most negatively correlated metabolites. Multiple biochemical changes indicated dyslipidemia, oxidative stress, alteration of energy metabolism, and endothelial dysfunction after cholesterol overloading, and subsequently to early coronary atherosclerosis in rabbits. This study indicated that 1H NMR based metabonomics can provide valuable information for the investigation of the dynamic biochemical variations underlying complex physiopathological conditions. It also offers a promising non-invasive means to the discovery of biomarkers for monitoring the onset and progression of CHD.

Relation of Increased Prebeta-1 High-Density Lipoprotein Levels to Risk of Coronary Heart Disease

Preβ-1 high-density lipoprotein (HDL) plays a key role in reverse cholesterol transport by promoting cholesterol efflux. Our aims were (1) to test previous associations between preβ-1 HDL and coronary heart disease (CHD) and (2) to investigate whether preβ-1 HDL levels also are associated with risk of myocardial infarction (MI). Plasma preβ-1 HDL was measured by an ultrafiltration-isotope dilution technique in 1,255 subjects recruited from the University of California-San Francisco Lipid and Cardiovascular Clinics and collaborating cardiologists. Preβ-1 HDL was significantly and positively associated with CHD and MI even after adjustment for established risk factors. Inclusion of preβ-1 HDL in a multivariable model for CHD led to a modest improvement in reclassification of subjects (net reclassification index 0.15, p = 0.01; integrated discrimination improvement 0.003, p = 0.2). In contrast, incorporation of preβ-1 HDL into a risk model of MI alone significantly improved reclassification of subjects (net reclassification index 0.21, p = 0.008; integrated discrimination improvement 0.01, p = 0.02), suggesting that preβ-1 HDL has more discriminatory power for MI than for CHD in our study population. In conclusion, these results confirm previous associations between preβ-1 HDL and CHD in a large well-characterized clinical cohort. Also, this is the first study in which preβ-1 HDL was identified as a novel and independent predictor of MI above and beyond traditional CHD risk factors.

Novel association analysis between 9 short tandem repeat loci polymorphisms and coronary heart disease based on a cross-validation design

ObjectiveTo investigate genes associated with coronary heart disease (CHD) screened with a novel cross-validation design. MethodsOn the basis of age at the onset of the first episode of CHD, stratified sampling by age (<50 years, 50–59 years, 60–69 years, 70–79 years and >80 years) was performed. Alleles of the nine CODIS STR loci including D3S1358, vWA, FGA, D8S1179, D21S11, D18S51, D5S818, D13S317, and D7S820, were determined using the STR Profiler Plus PCR amplification kit. Allele frequencies were compared with a control population. The mean age of patients with and without the alleles was compared. Cross-validation was based on differences in both frequency values and ages instead of adjustment procedure for multiple testing. ResultsThere were statistical differences in frequency values between the CHD group and the control population for three alleles, and also statistical differences in the age at first onset of CHD for two alleles; at least one allele, D21S11-28.2, was statistically different with regards to both frequency values and age. It was confirmed that D21S11-28.2 is truly related with CHD. ConclusionsA single true CHD-related allele could be discriminated from the sampling errors through cross-validation. It appears that CHD-related genes may be located near to loci D21S11.

Participating in cardiac rehabilitation: a systematic review and meta-synthesis of qualitative data

Participation in cardiac rehabilitation (CR) benefits patients with coronary heart disease (CHD), yet worldwide only some 15–30% of those eligible attend. To improve understanding of the reasons for poor participation we undertook a systematic review and meta-synthesis of the qualitative literature. Qualitative studies identifying patient barriers and enablers to attendance at CR were identified by searching multiple electronic databases, reference lists, relevant conference lists, grey literature, and keyword searching of the Internet (1990–2010). Studies were selected if they included patients with CHD and reviewed experience or understanding about CR. Meta-synthesis was used to review the papers and to synthesize the data. From 1165 papers, 34 unique studies were included after screening. These included 1213 patients from eight countries. Study methodology included interviews (n = 25), focus groups (n = 5), and mixed-methods (n = 4). Key reasons for not attending CR were physical barriers, such as lack of transport, or financial cost, and personal barriers, such as embarrassment about participation, or misunderstanding the reasons for onset of CHD or the purpose of CR. There is a vast amount of qualitative research which investigates patients’ reasons for non-attendance at CR. Key issues include system-level and patient-level barriers, which are potentially modifiable. Future research would best be directed at investigating strategies to overcome these barriers.

Transcatheter closure of coronary artery fistula with an Amplatzer Duct Occluder II in a symptomatic infant

induced platelet aggregation (8), others documented increased aggregation of platelets in the presence of THC (9). Increased myocardial oxygen demand, decreased blood supply, marked vasoconstriction of the coronary arteries and platelet activation all contribute to the development of acute event. In our case, probably, he has had early onset coronary heart disease in whom the cigarette smoking was the single risk factor and cannabis smoking triggered the plaque rupture and induced thrombosis.

The Relationship Between Polymorphisms on Chromosome 9p21 and Age of Onset of Coronary Heart Disease in Black and White Women

Genome-wide association studies have identified variants on chromosome 9p21 that are associated with coronary heart disease (CHD). The relationship between these variants and the age of onset of CHD is less clear. The aim of this study was to examine the allelic frequencies and haplotype structure of eight single-nucleotide polymorphisms (SNPs) on chromosome 9p21 in ethnically diverse women. We also explored the relationship between 9p21 SNPs and the age of CHD onset. There was considerable interethnic allelic and haplotype diversity across the 9p21 locus with only two SNPs (rs10757274 and rs4977574) in perfect linkage disequilibrium in both races, and only a small proportion of the haplotypes shared between the racial groups. With the exception of rs1333040, whites with at least one copy of the 9p21 SNP risk alleles were found to have CHD from 1.45 (rs10116277) to 4.77 (rs2383206) years earlier than those with the wild-type alleles. Blacks carrying at least one copy of the risk allele (92%) for rs1333040 had a CHD age of onset that was 6.5 years earlier than those with the wild-type alleles. Different variants on chromosome 9p21 may influence CHD age of onset in whites and blacks.

Importance of psychosocial status in secondary prevention and rehabilitation of coronary artery disease

Lifestyle and behavioral factors play a major part in the development of coronary heart disease (CHD). Rehabilitation and secondary prevention of CHD must likewise consider behavioral and lifestyle change as adjuncts to other therapies. Principal among the psychosocial factors are depression, anxiety and anger/hostility. Related to these negative emotions, a distressed personality style (type-D) in which both negative emotion and social inhibition are present represents a psychosocial risk factor. In addition, social experience, both in the resources available through social networks and the subjective experience of isolation, is related to both the onset and course of CHD. Psychosocial interventions have been found to be effective in rehabilitation and secondary prevention. Finally, a case is made that all professionals working in cardiac rehabilitation and secondary prevention should be knowledgeable in the psychological constructs of motivation and readiness for behavioral change. The widely employed transtheoretical model of change is presented as an example of the need for interventions to be developed that recognize patients' difference in the readiness for change.

Gender differences in the association between education and the incidence of cardiovascular events in Northern Italy

The educational differences in the incidence of major cardiovascular events are under-studied in Southern Europe and among women. The study sample includes n = 5084 participants to 4 population-based Northern Italian cohorts, aged 35-74 at baseline and with no previous cardiovascular events. The follow-up to ascertain the first onset of coronary heart disease (CHD) or ischaemic stroke ended in 2002. At baseline, major cardiovascular risk factors were investigated adopting the standardized MONICA procedures. Two educational classes were obtained from years of schooling. Age- and risk factors-adjusted hazard ratios of first CHD or ischaemic stroke were estimated through sex-specific separate Cox models (high education as reference). Median follow-up time was 12 years. Event rates were 6.38 (CHD) and 2.12 (ischaemic stroke) per 1000 person-years in men; and 1.59 and 0.94 in women. In men, low education was associated with higher mean Body Mass Index and prevalence of diabetes and cigarette smokers; but also with higher HDL cholesterol and a more favourable alcohol intake pattern. Less-educated women had higher mean systolic blood pressure, Body Mass Index and HDL cholesterol and were more likely to have diabetes. Men and women in the low educational class had a 2-fold increase in ischaemic stroke and CHD incidence, respectively, after controlling for major risk factors. Education was not associated with CHD incidence in men. Higher ischaemic stroke rates were observed among more educated women. In this northern Italian population, the association between education and cardiovascular risk seems to vary by gender.

Evaluation of subclinical atherosclerosis by computed tomography coronary angiography and its association with risk factors in familial hypercholesterolemia

Background Increasing age and cholesterol levels, male gender, and family history of early coronary heart disease (CHD) are associated with early onset of CHD in familial hypercholesterolemia (FH). Objective Assess subclinical atherosclerosis by computed tomography coronary angiography (CTCA) and its association with clinical and laboratorial parameters in asymptomatic FH subjects. Methods 102 FH subjects (36% male, 45 ± 13 years, LDL-c 280 ± 54 mg/dL) and 35 controls (40% male, 46 ± 12 years, LDL-c 103 ±18 mg/dL) were submitted to CTCA. Plaques were divided into calcified, mixed and non-calcified; luminal stenosis was characterized as >50% obstruction. Results FH had a greater atherosclerotic burden represented by higher number of patients with: plaques (48% vs. 14%, p = 0.0005), stenosis (19% vs. 3%, p = 0.015), segments with plaques (2.05 ± 2.85 vs.0.43 ± 1.33, p = 0.0016) and calcium scores (55 ± 129 vs. 38 ± 140, p = 0.0028). After multivariate analysis, determinants of plaque presence were increasing age (OR = 2.06, for age change of 10 years, CI95%: 1.38–3.07, p < 0.001) and total cholesterol (OR = 1.86, for cholesterol change by 1 standard deviation, CI95%: 1.09–3.15, p = 0.027). Coronary calcium score was associated with the presence of stenosis (OR = 1.54; CI95%: 1.27–1.86, p < 0.001, for doubling the calcium score). Male gender was directly associated with the presence of non-calcified plaques (OR: 15.45, CI95% 1.72–138.23, p = 0.014) and inversely with calcified plaques (OR = 0.21, CI95%: 0.05–0.84, p = 0.027). Family history of early CHD was associated with the presence of mixed plaques (OR = 4.90, CI95%: 1.32–18.21, p = 0.018). Conclusions Patients with FH had an increased burden of coronary atherosclerosis by CTCA. The burden of atherosclerosis and individual plaque subtypes differed with the presence of other associated risk factors, with age and cholesterol being most important. A coronary calcium score of zero ruled out obstructive disease in this higher risk population.

The association of "three high" factors with the onset of coronary artery disease

Objective To explore the association of hypertension and higher levels of blood lipids and sugar (three high factors) with the onset of coronary artery disease.Methods From June 2005 to January 2009,276 hospitalized patients with suspected coronary heart disease underwent coronary angiography by sixteen-slice spiral CT. The patients were divided into two groups with or without coronary artery disease according to the findings of cardiac CTA. Chi square test,binary logistic regression,mean comparison and receiver operating characteristic (ROC) curves were used to analyze the association of three high factors with the onset of coronary artery disease. Results Chi square test showed that the onset of coronary heart disease was affected by age (χ2=13.560,P=0.001),total cholesterol (TC) (χ2=8.260,P=0.004),triglyceride (TG) (χ2=5.718,P=0.017),and low density lipoprotein (LDL) (χ2=6.375,P=0.012).Logistic regression exhibited that the onset of coronary heart disease closely correlated to TC (OR=1.967,P=0.000) and age (OR=1.046,P=0.004). Serum levels of TC (t=3.387,P=0.001) and LDL (t=3.662,P=0.000) increased significantly in patients with coronary heart disease compared with those without coronary heart disease. The areas under the ROC cures of TC,TG,HDL and LDL to predict the onset of coronary heart disease was 0.655,0.473,0.569,and 0.640,respectively. Conclusions Among the three high factors,serum TC level shows the closest association with the onset of coronary artery disease,followed by LDL level; blood presure and sugar don't show any association. However,serum levels of TC and LDL could hardly predict the onset of coronary heart disease. Key words: Coronary artery disease; Hypertension; Blood lipids; Blood sugar

A Cloned Pig Model for Examining Atherosclerosis Induced by High Fat, High Cholesterol Diets

The pig is a recognized model for the onset of coronary heart disease and heart attacks. Previous studies have shown that serum cholesterol levels in the pig can be elevated using a high fat, high cholesterol (HFHC) diet. What has been lacking is a genetically defined model corresponding to human ApoE4 susceptibility that can be linked to diets capable of inducing atherosclerosis. This study used a cloned pig model to examine the impact of cholesterol levels with the development of aorta fatty deposits leading to atherosclerosis. Diets were formulated using vegetable sources of protein to provide similar intakes of metabolizable energy, calcium, phosphorous and principal amino acids in both control and HFHC groups. After 60 days, the HFHC group demonstrated a 40-fold increase in aortic fatty streak lesion area combined with 6- and 11-fold increases in total and LDL cholesterol, respectively, over control diet fed cloned pigs. Previous studies have suffered from either imbalanced total caloric intake, an overall imbalance in the nutrition of the control versus HFHC groups or genetic heterogeneity when evaluating dietary constraints related to atherosclerosis. This study demonstrated that cloned, genetically-defined ApoE4 pigs provided balanced nutrition diets provide an experimental system ideally suited to examining atherosclerosis and the onset of coronary heart disease.

Review: Plasma renin and the incidence of cardiovascular disease

Whether renin is involved in the onset of coronary heart disease (CHD) remains unclear. A case-control study in 1972, suggesting a causal association between renin and CHD, has now been followed by three prospective studies. One was based on 1,717 hypertensive subjects in a Work-Site Program in New York. The main results showed an increased risk of CHD the higher the renin level. A second study in occupational groups in North West London, UK, recruited 803 white men not selected according to blood pressure, and found no association. A possible exception was in the minority of those with similar blood pressure levels to participants in the Work-Site Program, in whom the incidence of CHD was higher according to the renin level, but not significantly so. The third study was in Framingham Offspring and included 3,532 participants also not selected according to blood pressure. As in the UK study, there was no clear association between renin and risk of CHD in all participants, or in this study in those with raised blood pressure. The authors considered their results consistent with those of the UK study in finding "no association of renin with overall risk of CHD". Besides the three epidemiological studies, dealing explicitly with renin, other studies in which it has been one of several variables considered have also not found convincing evidence of its involvement in CHD. There is, therefore, little support for the hypothesis that high renin levels increase the risk of CHD, with the possible but uncertain exception of those with raised blood pressure.

Identification of a recurrent insertion mutation in the LDLR gene in a Pakistani family with autosomal dominant hypercholesterolemia

Familial Hypercholesterolemia (FH) results in elevated levels of blood lipids including total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) with normal triglycerides (TG). This disease is one of the major contributors towards an early onset of coronary heart disease (CHD). The aim of the present study was to identify the genes responsible for causing FH in Pakistani population, for this purpose a large consanguineous FH family was selected for genetic analysis. Serum lipid levels, including TC, TG, LDL-C and high density lipoprotein cholesterol (HDL-C), were determined in patients and healthy controls. In order to find the causative mutation in this family, direct sequencing of the low density lipoprotein receptor (LDLR) gene was performed. In addition the part of the Apolipoprotein-B (APOB) gene containing the mutations R3500Q and R3500W was also sequenced. Affected individuals of the family were found to have raised TC and LDL-C levels. Sequencing revealed an insertion mutation (c.2416_2417InsG) in exon 17 of the LDLR gene in all the affected individuals of the family. Common FH causing APOB mutations were not present in this family. Heterozygous individuals had TC levels ranging from ~300-500 mg/dl and the only homozygous individual with typical xanthomas had TC levels exceeding 900 mg/dl. This is the first report of a known LDLR gene mutation causing FH in the Pakistani population. Despite a large heterogeneity of LDLR mutations there are still some common mutations which are responsible for FH throughout the world.

Complement factor H Y402H gene polymorphism and coronary heart disease susceptibility: a meta-analysis

The complement factor H (CFH) Y402H (T1277C) gene polymorphism has been reported to be associated with coronary heart disease (CHD), but results were conflicting. To evaluate the role of the variant in CHD, we performed meta-analyses of all available data. Both electronic and manual searches were performed, all relevant studies were identified. ORs with 95% confidential intervals (CI) under codominant (CC versus TT, TC versus TT), dominant (CC + TC versus TT) and recessive (CC versus TT + TC) models were calculated. Publication bias was addressed. Ten studies including 11 cohorts comprising of 29,764 participants were included. No association between the CFH T1227C polymorphism and CHD could be found. (For overall analysis: dominant model, OR = 1.04, 95%CI: 0.97-1.11; recessive model, OR = 1.04, 95%CI: 0.97-1.11; for Caucasian subgroup: OR = 1.08 95%CI: 0.92-1.27; recessive model, OR = 1.03, 95%CI: 0.96-1.11). Two studies reported positive results in separate population (Caucasian study: recessive model, OR = 0.51, 95%CI: 0.30-0.86; Asians study: dominant model, OR = 2.37, 95%CI: 1.13-4.96). Current evidence do not support the association between the CFH T1277C polymorphism and CHD risk among common population. The association, which could be influenced by CHD onset age, CHD risk factors status and genetics backgrounds, might be significant in some population. More studies on different CHD onset ages and risk factor status should be encouraged.

Radial Arterial Wave Reflection is Associated with the MEGA Risk Prediction Score, an Indicator of Coronary Heart Disease Risk, in Middle-Aged Men with Mild to Moderate Hypercholesterolemia

The present study examined the association between the radial augmentation index (AI), a marker of arterial wave reflection, and the MEGA risk prediction score (MEGA score), an indicator of coronary heart disease (CHD) risk, in middle-aged men with mild to moderate hypercholesterolemia. Radial AI was measured during a company health examination in 266 men (age: 47+/-5 years) with total cholesterol levels ranging 220-270 mg/dL who were not taking antihypertensive, lipid-lowering, or antidiabetic agents. The MEGA score was calculated based on sex, age, low- and high-density lipoprotein cholesterol, blood pressure, glucose level, and smoking status. The higher MEGA score indicates increased CHD risk. A MEGA score > or = 22 corresponds to a 5-year CHD risk > or = 2.5% and we defined a MEGA score > or = 22 as a high estimated CHD risk. The mean AI was 74.4+/-12.6%. A high estimated CHD risk was seen in 32 subjects (12.0%). After adjusting for height and heart rate, the AI was higher in subjects with a high estimated CHD risk (81.5+/-10.6%) than in those without (73.4+/-10.4%, p<0.001). The odds ratio for high estimated CHD risk in the highest tertile of AI was 8.14 (p=0.002) in comparison to the lowest tertile, after adjusting for multiple potential confounders which did not constitute the MEGA score. The radial AI was positively associated with the estimated risk of CHD. These results suggest the usefulness of radial AI as a risk marker for future onset of CHD in middle-aged men with mild to moderate hypercholesterolemia.

Genetic and environmental determinants of total and high-molecular weight adiponectin in families with low HDL-cholesterol and early onset coronary heart disease

ObjectivePlasma adiponectin and high-density lipoprotein cholesterol (HDL-C) exhibit a well-known positive metabolic correlation. Neither heritability nor genome-wide linkage analysis for the high-molecular weight (HMW) adiponectin is available. This work estimates the genetic and environmental determinants and the heritabilities of the adiponectins and lipid traits in Finnish families with early onset coronary heart disease (CHD) and low HDL-C. MethodsHeritability and genome-wide univariate linkage analysis was performed for total and HMW adiponectin in extended families from Northern Finland with early onset CHD and low HDL-C using a variance components approach. The genetic and environmental correlations between the plasma adiponectins and various lipid traits were also studied and a bivariate analysis for HDL-C and the adiponectins carried out. ResultsIn the partial correlation analysis (adjusted for sex, age, BMI and statin use) the adiponectins showed a stronger correlation with HDL-C (total 0.57, p=0.001, HMW 0.51, p<0.005) than with any other lipid trait in unrelated subjects. Our estimates detected strong heritability for total (0.53±0.10), HMW (0.51±0.10) and the HMW/total adiponectin ratio (0.68±0.11). Univariate linkage analysis showed suggestive evidence of linkage on chromosome 11p15 for total adiponectin and on 3q13.2-q24 and 6p21 for the HMW adiponectin. The strongest environmental cross-correlation between the adiponectins and lipids was seen between HDL-C and total adiponectin (ρe=0.64, p<0.05), whereas the strongest genetic correlation was detected between low-density lipoprotein cholesterol and the HMW adiponectin (ρg=−0.48, p<0.05). ConclusionNo significant genetic correlations between HDL-C and the adiponectins were observed. Therefore, the metabolic association between HDL-C and adiponectin is most likely regulated by complex genetic pathways and environmental factors.

The burden of coronary heart disease in Māori: population‐based estimates for 2000‐02

To estimate coronary heart disease (CHD) incidence, prevalence, survival, case fatality and mortality for Māori, in order to support service planning and resource allocation. Incidence was defined as first occurrence of a major coronary event, i.e. the sum of first CHD hospital admissions and out-of-hospital CHD deaths in people without a hospital admission for CHD in the preceding five years. Data for the years 2000-02 were sourced from the New Zealand Health Information Service and record linkage was carried out using a unique national identifier, the national health index. Compared to the non-Māori population, Māori had both elevated CHD incidence and higher case fatality. Median age at onset of CHD was younger for Māori, reflecting both higher age specific risks and younger population age structure. The lifetable risk of CHD for Māori was estimated at 37% (males) and 34% (females), only moderately higher than the corresponding estimates for the non-Māori population, despite higher Māori CHD incidence. This reflects the offsetting effect of the higher 'other cause' mortality experienced by Māori. Median duration of survival with CHD was similar to that of the non-Māori population for Māori males but longer for Māori females, which is most likely related to the earlier age of onset. This study has generated consistent estimates of CHD incidence, prevalence, survival, case fatality and mortality for Māori in 2000-02. The inequality identified in CHD incidence calls for a renewed effort in primary prevention. The inequality in CHD case fatality calls for improvement in access for Māori to secondary care services.

Erectile dysfunction and CHD: Related risk factors and implications for nursing practice

Erectile dysfunction needs further attention in nursing. The purpose of this article is to raise nurses’ awareness about the link between erectile dysfunction (ED) and coronary heart disease (CHD). This paper considers ED as a risk factor for CHD, discusses the pathophysiology and prevalence of ED and reviews the shared risk factors for ED and CHD. Knowing that ED can occur before the onset of CHD may further encourage nurses to ask questions about sexual function. Understanding the link between ED and CHD may equip nurses in primary and secondary care settings to educate and empower patients to initiate lifestyle changes to improve both their sexual health and general wellbeing. This may potentially delay the onset or reduce the risk of other acute and chronic vascular conditions in their patients.

Job Stress and Coronary Heart Disease: A Case‐control Study using a Chinese Population

This study was to examine the association between job stress and coronary heart disease (CHD) in a Chinese population. The 388 participants aged 30 to 70 yr who received coronary angiography for suspected or known ischemic heart disease were enrolled in this series, which included 292 CHD cases and 96 controls. The job stress before CHD onset was measured by the effort-reward imbalance (ERI) model. In the results, compared with the baseline, high ERI, high extrinsic effort or high overcommitment increased the risk of CHD with odds ratios (OR) of 2.8, 2.7 and 2.8 respectively after adjustment for the traditional CHD risk factors, such as age, gender, primary hypertension, diabetes mellitus, hyperlipidemia, smoking, body mass index, CHD family history, educational level, and marital status. The combination of high ERI and high overcommitment led to the highest risk of CHD with adjusted OR 5.5. However, high reward reduced the risk of CHD with an adjusted OR of 0.4 in comparison to low reward. Dose-response relationships were also observed. Job stress evaluated by the ERI model significantly increased the risk of CHD, and it may be an important risk factor independent of the traditional risk factors of CHD in the Chinese population.

Independent Association of HbA1c and Incident Cardiovascular Disease in People Without Diabetes

Recent studies have reported no association between elevated glycated hemoglobin (HbA(1c)) and incident cardiovascular disease (CVD) among women without diabetes. This study describes associations between HbA(1c) and new onset CVD in a representative adult population cohort. Assessment of participants in The North West Adelaide Health Study (NWAHS), a population study of randomly selected adults (age > or =18 years, n = 4,060), included measurement of height, weight, blood pressure, fasting lipids, glucose, and HbA(1c). A self-completed questionnaire assessed doctor-diagnosed diabetes, CVD and stroke, smoking status, and demographics. The cohort was followed for an average 3.5 years. Of the 2,913 adults free of diabetes at baseline and follow-up, 94 (3.5%) reported new onset coronary heart disease (CHD) and/or stroke. Compared with those with an HbA(1c) < or =5.0%, risk of new onset CVD was increased in those with HbA(1c) 5.4-5.6% (odds ratio (OR) 2.5, 95% confidence interval (CI) 1.4, 4.6), and > or =5.7% (OR 1.9, 95% CI 1.1, 3.4), after adjustment for other risk factors. The association was stronger in women than men (P = 0.03), and attenuated to only a small degree by addition of impaired fasting glucose (IFG), hypertension, hypercholesterolemia, BMI, waist circumference, or smoking to the model. Elevated HbA(1c) is related to new onset CVD over a relatively short follow-up period in both men and women without diabetes and who do not develop diabetes, after adjustment for other major risk factors. Unlike previous studies, this relationship was not substantially attenuated by other traditional risk factors.