Increased Incidence Of Cardiovascular Disease Research Articles

Usefulness of Low-Density Lipoprotein Cholesterol and Non–High-Density Lipoprotein Cholesterol as Predictors of Cardiovascular Disease in Chinese

The predictive effect of non-high-density lipoprotein cholesterol (non-HDL-C) for cardiovascular disease (CVD) in Chinese general population has not been well demonstrated. The aim of our study was to examine the relation between non-HDL-C and CVD and compare the predictive effect of non-HDL-C and low-density lipoprotein cholesterol (LDL-C) for CVD in Chinese population. The baseline examination of 27,020 participants aged 35 to 74years from the China Cardiovascular Health Study and the China Multicenter Collaborative Study of Cardiovascular Epidemiology was conducted in 1998 to 2001. Follow-up evaluation was conducted in 2007 to 2008 with a response rate of 79.8%. Cox proportional hazards regression models were used to obtain the multivariable-adjusted hazard ratios and 95% confidence intervals (CIs) for CVD. Compared with those with non-HDL-C level of <130mg/dl, multivariable-adjusted hazard ratios of CVD were 1.30 (95% CI 1.04 to 1.62) and 1.93 (95% CI 1.50 to 2.47) in participants with non-HDL-C levels of 160 to 189.9 and ≥190mg/dl, respectively. An increase of 30mg/dl in non-HDL-C level would correspond to 15%, 24%, and 12% increase in risk of CVD, coronary heart disease, and stroke, respectively. Using likelihood ratio tests, non-HDL-C appeared to be a similar predictor for CVD incidence as LDL-C (chi-square for non-HDL-C, 18.02, p <0.001; chi-square for LDL-C, 18.90, p <0.001). In conclusion, higher non-HDL-C level is associated with the increased CVD incidence and has a similar effect as LDL-C on predicting CVD risk in Chinese.

The chromosome 9p21 variant interacts with vegetable and wine intake to influence the risk of cardiovascular disease: a population based cohort study.

BackgroundChromosome 9p21 variants are associated with cardiovascular disease (CVD) but not with any of its known risk markers. However, recent studies have suggested that the risk associated with 9p21 variation is modified by a prudent dietary pattern and smoking. We tested if the increased risk of CVD by the 9p21 single nucleotide polymorphism rs4977574 is modified by intakes of vegetables, fruits, alcohol, or wine, and if rs4977574 interacts with environmental factors on known CVD risk markers.MethodsMultivariable Cox regression analyses were performed in 23,949 individuals from the population-based prospective Malmö Diet and Cancer Study (MDCS), of whom 3,164 developed CVD during 15 years of follow-up. The rs4977574 variant (major allele: A; minor allele: G) was genotyped using TaqMan® Assay Design probes. Dietary data were collected at baseline using a modified diet history method. Cross-sectional analyses were performed in 4,828 MDCS participants with fasting blood levels of circulating risk factors measured at baseline.ResultsEach rs4977574 G allele was associated with a 16% increased incidence of CVD (95% confidence interval (CI), 1.10–1.22). Higher vegetable intake (hazard ratio (HR), 0.95 [CI: 0.91–0.996]), wine intake (HR, 0.91 [CI: 0.86–0.96]), and total alcohol consumption (HR, 0.92 [CI: 0.86–0.98]) were associated with lower CVD incidence. The increased CVD incidence by the G allele was restricted to individuals with medium or high vegetable intake (Pinteraction = 0.043), and to non- and low consumers of wine (Pinteraction = 0.029). Although rs4977574 did not associate with any known risk markers, stratification by vegetable intake and smoking suggested an interaction with rs4977574 on glycated hemoglobin and high-density lipoprotein cholesterol (Pinteraction = 0.015 and 0.049, respectively).ConclusionsOur results indicate that rs4977574 interacts with vegetable and wine intake to affect the incidence of CVD, and suggest that an interaction may exist between environmental risk factors and rs4977574 on known risk markers of CVD.Electronic supplementary materialThe online version of this article (doi:10.1186/s12881-014-0138-x) contains supplementary material, which is available to authorized users.

Depression, anxiety and 6-year risk of cardiovascular disease

ObjectiveDepression and anxiety are considered etiological factors in cardiovascular disease (CVD), though their relative contribution and differentiation by clinical characteristics have not been studied intensively. We examined 6-year associations between depressive and anxiety disorders, clinical characteristics and newly-developed CVD. MethodsDSM-IV diagnoses were established in 2510 CVD-free participants of the Netherlands Study of Depression and Anxiety. Data on subtype, severity, and psychoactive medication were collected. The 6-year incidence of CVD was assessed using Cox regression analyses adjusted for sociodemographic, health and lifestyle factors. ResultsOne-hundred-six subjects (4.2%) developed CVD. Having both current depressive and anxiety disorders (HR=2.86, 95%CI 1.49–5.49) or current depression only (HR=2.30; 95%CI 1.10–4.80) was significantly associated with increased CVD incidence, whereas current anxiety only (HR=1.48; 95%CI 0.74–2.96) and remitted disorders (HR=1.48; 95%CI 0.80–2.75) were not associated. Symptom severity was associated with increased CVD onset (e.g., Inventory of Depressive Symptomatology per SD increase: HR=1.51; 95%CI 1.25–1.83). Benzodiazepine use was associated with additional CVD risk (HR=1.95; 95%CI 1.16–3.31). ConclusionsCurrent depressive (but not anxiety) disorder independently contributed to CVD in our sample of initially CVD-free participants. CVD incidence over 6years of follow-up was particularly increased in subjects with more symptoms, and in those using benzodiazepines.

Évaluation de la fonction endothéliale au cours des maladies auto-immunes

Numerous autoimmune-inflammatory rheumatic diseases have been associated with accelerated atherosclerosis or other types of vasculopathy leading to an increase in cardiovascular disease incidence. In addition to traditional cardiovascular risk factors, endothelial dysfunction is an important early event in the pathogenesis of atherosclerosis, contributing to plaque initiation and progression. Endothelial dysfunction is characterized by a shift of the actions of the endothelium toward reduced vasodilation, a proinflammatory and a proadhesive state, and prothrombic properties. Therefore, assessment of endothelial dysfunction targets this vascular phenotype using several biological markers as indicators of endothelial dysfunction. Measurements of soluble adhesion molecules (ICAM-1, VCAM-1, E-selectin), pro-thrombotic factors (thrombomodulin, von Willebrand factor, plasminogen activator inhibitor-1) and inflammatory cytokines are most often performed. Regarding the functional assessment of the endothelium, the flow-mediated dilatation of conduit arteries is a non-invasive method widely used in pathophysiological and interventional studies. In this review, we will briefly review the most relevant information upon endothelial dysfunction mechanisms and explorations. We will summarize the similarities and differences in the biological and functional assessments of the endothelium in different autoimmune diseases.

Acarbose treatment and the risk of cardiovascular disease in type 2 diabetic patients: a nationwide seven-year follow-up study.

Objective. To investigate the potential benefits of acarbose treatment on cardiovascular disease (CVD) in patients with type 2 diabetes by using nationwide insurance claim dataset. Research Design and Methods. Among 644,792 newly diagnosed type 2 diabetic patients without preexisting CVD in a nationwide cohort study, 109,139 (16.9%) who had received acarbose treatment were analyzed for CVD risk. Those with CVD followed by acarbose therapy were also subjected to analysis. Result. During 7 years of follow-up, 5,081 patients (4.7%) developed CVD. The crude hazard ratio (HR) and adjusted HR were 0.66 and 0.99, respectively. The adjusted HR of CVD was 1.19, 0.70, and 0.38 when the duration of acarbose use was <12 months, 12–24 months, and >24 months, respectively. Adjusted HR was 1.14, 0.64, and 0.41 with acarbose cumulative doses <54,750 mg, 54,751 to 109,500 mg, and >109,500 mg, respectively. Conclusion. In patients with type 2 diabetes without preexisting CVD, treatment with acarbose showed a transient increase in incidence of CVD in the initial 12 months followed by significant reductions of CVD in prolonged acarbose users. After the first CVD events, continuous use of acarbose revealed neutral effect within the first 12 months. The underlying mechanisms require further investigations.

Body Fat Distribution After Menopause and Cardiovascular Disease Risk Factors: Korean National Health and Nutrition Examination Survey 2010

The prevalence of cardiovascular disease in women increases sharply after menopause. The purpose of this study was to clarify the relationship between menopause and body fat distribution and to investigate their association with cardiovascular disease risk factors. We analyzed 2035 women 20-79 years of age using the National Health and Nutrition Examination Survey (KNHANES) 2010 database. Body fat was measured using dual-energy X-ray absorptiometry. The percentage of total body fat and the body fat distribution (BFD) index (the ratio of the trunk fat mass to leg fat mass) are significantly higher in postmenopausal women than in premenopausal women (all p<0.001). When adjusted for age, menopause was associated with higher total body fat percentage (adjusted β=1.082, 95% confidence interval [CI] 0.074-2.090, p=0.035). In women with a body mass index<25 kg/m(2), the higher BFD index was also independently associated with menopause (adjusted β=14.408, 95% CI 1.672-27.145, p=0.027). After adjusting for age and body fat percentage, the BFD index showed significant and independent associations with systolic and diastolic blood pressure (adjusted β=0.060 and 0.042, all p<0.001, respectively), fasting glucose (adjusted β=0.007, p<0.001), total and high density lipoprotein cholesterol (adjusted β=0.001 and -0.002, p<0.05 and p<0.001, respectively), and triglyceride levels (adjusted β=0.007, p<0.001- except for low density lipoprotein cholesterol. After menopause, women have not only higher total body fat percentage but also its different distribution, which independently correlates with cardiovascular disease risk factors. Therefore, this change in body fat may cause the sharp increase in cardiovascular disease incidence in middle-aged women, especially after menopause.

J-curve for DBP and cardiovascular mortality in coronary artery disease patients

J-curve for DBP and cardiovascular mortality in coronary artery disease patients

54 DOES ERECTILE DYSFUNCTION IMPROVE CARDIOVASCULAR DISEASE RISK PREDICTION?

You have accessJournal of UrologyGeneral & Epidemiological Trends & Socioeconomics: Evidence-based Medicine & Outcomes II1 Apr 201054 DOES ERECTILE DYSFUNCTION IMPROVE CARDIOVASCULAR DISEASE RISK PREDICTION? Andre Araujo, Susan Hall, Peter Ganz, Gretchen Chiu, Raymond Rosen, Varant Kupelian, and John McKinlay Andre AraujoAndre Araujo Watertown, MA More articles by this author , Susan HallSusan Hall Watertown, MA More articles by this author , Peter GanzPeter Ganz San Francisco, CA More articles by this author , Gretchen ChiuGretchen Chiu Watertown, MA More articles by this author , Raymond RosenRaymond Rosen Watertown, MA More articles by this author , Varant KupelianVarant Kupelian Watertown, MA More articles by this author , and John McKinlayJohn McKinlay Watertown, MA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2010.02.100AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Erectile dysfunction (ED) and cardiovascular disease (CVD) share pathophysiological mechanisms and often co-occur. It is unknown whether ED improves the prediction of CVD beyond traditional risk factors. We sought to determine whether ED predicts CVD beyond traditional risk factors METHODS The Massachusetts Male Aging Study (MMAS) is a population-based, prospective study of 1,709 men aged 40-70 y. ED was measured by self-report. Data on CVD were obtained from 3 sources: questionnaire, linkage of the MMAS database with the National Death Index (NDI), and medical records. CVD was defined by ICD-9/ICD-10 codes 390-459/I00-I99. Subjects were followed for CVD for an average follow-up of 11.7 years. The association between ED and CVD was examined using the Cox proportional hazards regression model. The reclassification of CVD risk associated with ED was assessed using a method that quantifies net reclassification improvement (NRI). This involved the fitting of two statistical models with CVD as the outcome: one including age and Framingham risk score, and a second that added ED. Based on this, we evaluated changes in risk category classification separately for CVD cases and non-cases that occurred during the first 10 years of follow-up, with results expressed in the NRI. RESULTS 1,057 men with complete data who were free of CVD and diabetes at baseline were included. During follow-up, 261 new cases of CVD occurred (200 of these were confirmed by NDI or medical record). ED was associated with CVD incidence controlling for age (Hazard Ratio (HR): 1.42 (95% Confidence Interval (CI)): 1.05, 1.90), age and traditional CVD risk factors (HR: 1.41, 95% CI: 1.05, 1.90), as well as age and Framingham risk score (HR: 1.40, 95% CI: 1.04-1.88). Despite these significant findings, ED did not significantly improve the prediction of CVD incidence beyond traditional risk factors. Specifically, based on the data presented in the Table, the NRI for ED was calculated as 3.1% (95% CI: -2.4%, 8.5%), which was not statistically significant (p = .27). CONCLUSIONS Independent of established CVD risk factors, ED is significantly associated with increased CVD incidence. Nonetheless, ED does not improve the prediction of who will and will not develop CVD beyond that offered by traditional risk factors. © 2010 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 183Issue 4SApril 2010Page: e23 Advertisement Copyright & Permissions© 2010 by American Urological Association Education and Research, Inc.MetricsAuthor Information Andre Araujo Watertown, MA More articles by this author Susan Hall Watertown, MA More articles by this author Peter Ganz San Francisco, CA More articles by this author Gretchen Chiu Watertown, MA More articles by this author Raymond Rosen Watertown, MA More articles by this author Varant Kupelian Watertown, MA More articles by this author John McKinlay Watertown, MA More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Does Erectile Dysfunction Contribute to Cardiovascular Disease Risk Prediction Beyond the Framingham Risk Score?

This study was designed to determine whether erectile dysfunction (ED) predicts cardiovascular disease (CVD) beyond traditional risk factors. Both ED and CVD share pathophysiological mechanisms and often co-occur. It is unknown whether ED improves the prediction of CVD beyond traditional risk factors. This was a prospective, population-based study of 1,709 men (of 3,258 eligible) age 40 to 70 years. The ED data were measured by self-report. Subjects were followed for CVD for an average follow-up of 11.7 years. The association between ED and CVD was examined using the Cox proportional hazards regression model. The discriminatory capability of ED was examined using C statistics. The reclassification of CVD risk associated with ED was assessed using a method that quantifies net reclassification improvement. Of the prospective population, 1,057 men with complete risk factor data who were free of CVD and diabetes at baseline were included. During follow-up, 261 new cases of CVD occurred. We found ED was associated with CVD incidence controlling for age (hazard ratio [HR]: 1.42, 95% confidence interval [CI]: 1.05 to 1.90), age and traditional CVD risk factors (HR: 1.41, 95% CI: 1.05 to 1.90), as well as age and Framingham risk score (HR: 1.40, 95% CI: 1.04 to 1.88). Despite these significant findings, ED did not significantly improve the prediction of CVD incidence beyond traditional risk factors. Independent of established CVD risk factors, ED is significantly associated with increased CVD incidence. Nonetheless, ED does not improve the prediction of who will and will not develop CVD beyond that offered by traditional risk factors.

Living Heart Valve and Small-Diameter Artery Substitutes - An Emerging Field for Intellectual Property Development

Cardiovascular diseases, such as heart valve dysfunction and coronary artery stenosis, are next to cancer the leading cause of death in the US. Treatments involve replacement of the heart valve or bypassing the obstructed coronary artery with a small-diameter vascular graft. The major limitation of currently used replacements is their inability to grow, adapt and repair in the patient. Considering the increasing age of the population and the subsequent increase in cardiovascular disease incidence, efforts to improve existing replacements and unraveling novel types of replacements are of paramount importance. Cardiovascular tissue engineering represents a rapid evolving field of research, providing living heart valve and small-diameter vascular substitutes with the ability to grow, adapt and repair after implantation. Various tissue engineering approaches are being employed, based on in vivo and/or in vitro tissue formation. This review provides an overview of the current heart valve and small-diameter vascular replacements and presents the status and future developments within the various tissue engineering approaches. The potential of tissue engineering for the development of living heart valve and small-diameter vascular substitutes is reflected in the numerous patents related to this emerging field of research.

Diabetic retinopathy is associated with an increased incidence of cardiovascular events in Type 2 diabetic patients

We investigated the association of diabetic retinopathy with the risk of incident cardiovascular disease (CVD) events in a large cohort of Type 2 diabetic adults. Our study cohort comprised 2103 Type 2 diabetic outpatients who were free of diagnosed CVD at baseline. Retinal findings were classified based on fundoscopy (by a single ophthalmologist) to categories of no retinopathy, non-proliferative retinopathy and proliferative/laser-treated retinopathy. Outcomes measures were incident CVD events (i.e. non-fatal myocardial infarction, non-fatal ischaemic stroke, coronary revascularization procedures or cardiovascular death). During approximately 7 years of follow-up, 406 participants subsequently developed incident CVD events, whereas 1697 participants remained free of diagnosed CVD. After adjustment for age, body mass index, waist circumference, smoking, lipids, glycated haemoglobin, diabetes duration and medications use, patients with non-proliferative or proliferative/laser-treated retinopathy had a greater risk (P < 0.001 for all) of incident CVD events than those without retinopathy [hazard ratio 1.61 (95% confidence interval 1.2-2.6) and 3.75 (2.0-7.4) for men, and 1.67 (1.3-2.8) and 3.81 (2.2-7.3) for women, respectively]. After additional adjustment for hypertension and advanced nephropathy (defined as overt proteinuria and/or estimated glomerular filtration rate < or = 60 ml/min/1.73 m(2)), the risk of incident CVD remained markedly increased in those with proliferative/laser-treated retinopathy [hazard ratio 2.08 (1.02-3.7) for men and 2.41 (1.05-3.9) for women], but not in those with non-proliferative retinopathy. Diabetic retinopathy (especially in its more advanced stages) is associated with an increased CVD incidence independent of other known cardiovascular risk factors.

Gender differences in cardiovascular disease and comorbid depression.

Although gender is increasingly perceived as a key determinant in health and illness, systematic gender studies in medicine are still lacking. For a long time, cardiovascular disease (CVD) has been seen as a "male" disease, due to men's higher absolute risk compared with women, but the relative risk in women of CVD morbidity and mortality is actually higher. Current knowledge points to important gender differences in age of onset, symptom presentation, management, and outcome, as well as traditional and psychosocial risk factors. Compared with men, CVD risk in women is increased to a greater extent by some traditional factors (e.g., diabetes, hypertension, hypercholesterolemia, obesity), and socioeconomic and psychosocial factors also seem to have a higher impact on CVD in women. With respect to differences in CVD management, a gender bias in favor of men has to be taken into account, in spite of greater age and higher comorbidity in women, possibly contributing to a poorer outcome. Depression has been shown to be an independent risk factor and consequence of CVD; however, concerning gender differences, the results have been inconsistent. Current evidence suggests that depression causes a greater increase in CVD incidence in women, and that female CVD 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 more effective.

Gamma Glutamyl Transferase and Metabolic Syndrome, Cardiovascular Disease, and Mortality Risk

To determine whether serum gamma-glutamyl transferase (GGT) predicts cardiovascular disease (CVD) morbidity and mortality, accounting for temporal changes in known CVD risk factors and C-reactive protein (CRP). In 3451 Framingham Study participants (mean age 44 years, 52% women) we examined the relations of GGT with CVD risk factors, and prospectively determined the risk of new-onset metabolic syndrome, incident CVD, and death. GGT was positively associated with body mass index, blood pressure, LDL cholesterol, triglycerides, and blood glucose in cross-sectional analysis (P<0.005). On follow-up (mean 19 years), 968 participants developed metabolic syndrome, 535 developed incident CVD, and 362 died. The risk of metabolic syndrome increased with higher GGT (multivariable-adjusted hazard ratio [HR] per SD increment log-GGT, 1.26 [95%CI; 1.18 to 1.35]). Adjusting for established CVD risk factors (as time-dependent covariates updated quadriennially) and baseline CRP, a 1-SD increase in log-GGT conferred a 13% increase in CVD risk (P=0.007) and 26% increased risk of death (P<0.001). Individuals in the highest GGT quartile experienced a 67% increase in CVD incidence (multivariable-adjusted HR 1.67, 95%CI; 1.25 to 2.22). An increase in serum GGT predicts onset of metabolic syndrome, incident CVD, and death suggesting that GGT is a marker of metabolic and cardiovascular risk.

Hormone Replacement Therapy and Cardiovascular Disease

In Canada, cardiovascular diseases (CVD) are the leading cause of mortality. In 1998, CVD were responsible for 39,447 deaths among Canadian women (almost 38% of all deaths in women), which is greater than the number of deaths for women due to all cancers combined. The proportion of deaths due to CVD in women increases significantly after menopause and continues to increase with advancing age. It remains unclear, however, whether this increase in incidence of CVD in middle-aged and elderly women is caused by lower estrogen levels or is an overall manifestation of advancing age. The use of hormone replacement therapy (HRT), especially estrogen, has been advocated as a means to reduce the risk of CVD. Menopause is associated with adverse effects on blood lipids including an increase in total cholesterol, LDL cholesterol, and triglycerides, and a decrease in HDL cholesterol. Reduced estrogen levels after menopause can also lead to adverse changes in blood pressure, obesity, body fat distribution, blood clotting factors, glucose metabolism and diabetes, all of which increase the risk of coronary heart disease. Laboratory studies have found evidence for both beneficial and adverse effects of estrogen. Oral estrogen has been shown to lower LDL cholesterol, lipoprotein (a), and increase HDL cholesterol. There is accumulating evidence that estrogen improves endothelial function, thus enhancing vasodilatation. In addition, estrogen replacement is associated with reduced blood levels of fibrinogen and plasminogen activator inhibitor-1, and may thus have anti-thrombotic and pro-fibrinolytic effects. However, other effects may be pro-inflammatory (increased C-reactive protein) and pro-coagulant and therefore detrimental to the overall cardiovascular risk profile. As estrogen is usually prescribed with progestin in those women with a uterus in order to protect against endometrial cancer, some of the beneficial cardiovascular effects may be attenuated by the addition of progestin (such as a lesser effect on HDL cholesterol). Other routes of administration of estrogen may have less favourable effects on plasma lipoproteins, but may be beneficial in other ways. Selective estrogen receptor modulators (SERMs) are also being studied because these may result in direct cardiovascular effects. The evidence for a protective effect of estrogen on coronary heart disease is based on over 30 observational epidemiologic studies conducted over the last two decades. These studies have shown a 40% reduction in the risk of coronary heart disease for current users of estrogen or estrogen and progestin compared to women who have never used these hormones. Recent updates have confirmed this conclusion, even with lower doses of estrogen, and have also found no effect of HRT on stroke. However, these types of studies are hampered by an inability to control completely for confounding factors, including the fact that women who are compliant with HRT