Promotion Of Cardiovascular Disease Research Articles

Exploring the role of uterine fibroids in promotion of cardiovascular diseases by diabetes exposure: Findings from national health and nutrition examination survey 1999-2006.

ObjectiveThe relationship between uterine fibroids (UF) and cardiovascular diseases (CVDs) in the diabetes population seemed to remain undetermined in previous studies. This study aims to explore the association between UF and CVDs by using the database from the National Health and Nutrition Examination Survey (NHANES). To further evaluate the connection between UF and CVDs we also tested the potential differences due to diabetes exposure.Materials and methodsNational Health and Nutrition Examination Survey data (1999–2006) were collected and used in this study. A total of 5,509 individuals were included and analyzed. The student’s t-test and the chi-squared test were used to explore the demographic characteristic between UF and non-UF groups. Logistic regression analysis was performed to determine the odds ratios of UF and covariates.ResultsFemale participants were divided into UF (n = 694, 12.60%) and non-UF (n = 4,815, 87.40%) groups. The incidence of CVDs in UF patients (n = 245, 35.30%) were higher than non-UF individuals (n = 776, 16.12%) (p < 0.001). In addition, each subtype of CVDs were also different, which contains hypertension (33.29 vs. 15.31%, p < 0.001), heart failure (1.59 vs. 0.52%, p < 0.01), angina (2.59 vs. 0.62%, p < 0.001), heart attack (1.73 vs. 0.58%, p < 0.01) and coronary heart disease (1.44 vs. 0.54%, p < 0.01). The odds ratios of CVDs according to logistic regression were 2.840 (95% CI: 2.387–3.379) for UF patients (p < 0.001), while the odds ratios (ORs) were 1.438 (95% CI: 1.175–1.760) after taking account for the age, body mass index (BMI), diabetes, race, education, and annual family income (p < 0.001). In addition, secondary analysis indicated more adverse effects in by UF exposure on CVDs risk among non-diabetes individuals (OR = 1.389, 95% CI = 1.124–1.718, p < 0.01) than diabetes patients (p = 0.063).ConclusionOverall, UFs were positively associated with CVDs, and this effect seems blunted by diabetes exposure.

Trans-10 18:1 in ruminant meats: A review.

Trans (t) fatty acids (TFA) from partially hydrogenated vegetable oils (i.e., industrial trans) have been phased out of foods in many countries due to their promotion of cardiovascular disease. This leaves ruminant-derived foods as the main source of TFA. Unlike industrial TFA where catalytic hydrogenation yields a broad distribution of isomers, ruminant TFA are enzymatically derived and can result in enrichment of specific isomers. Comparisons between industrial and ruminant TFA have often exonerated ruminant TFA due to their lack or at times positive effects on health. At extremes, however, ruminant-sourced foods can have either high levels of t10- or t11-18:1, and when considering enriched sources, t10-18:1 has properties similar to industrial TFA, whereas t11-18:1 can be converted to an isomer of conjugated linoleic acid (cis(c)9,t11-conjugated linoleic acid), both of which have potential positive health effects. Increased t10-18:1 in meat-producing ruminants has not been associated with negative effects on live animal production or meat quality. As such, reducing t10-18:1 has not been of immediate concern to ruminant meat producers, as there have been no economic consequences for its enrichment; nevertheless at high levels, it can compromise the nutritional quality of beef and lamb. In anticipation that regulations regarding TFA may focus more on t10-18:1 in beef and lamb, the present review will cover its production, analysis, biological effects, strategies for manipulation, and regulatory policy.

Selected Aspects of Tobacco-Induced Prothrombotic State, Inflammation and Oxidative Stress: Modeled and Analyzed Using Petri Nets

Many factors, such as endothelial dysfunction, inflammation and hemostatic disturbances, affect formation and progression of atherosclerotic plaque. In our study, we have focused on hemostatic disturbances with particular emphasis on the extrinsic pathways of coagulation. Thrombin is a main enzyme of coagulation and it is engaged in many different subprocesses. It leads to activation of factors of the coagulation cascade, transition of fibrinogen to fibrin monomer, endothelial damage, inflammation, activation of platelets and proliferation. In our study, selected aspects of disorders in prothrombotic states influenced by cigarette smoke have been modeled and analyzed. Tobacco-induced increased tissue factor, which is associated with less plasminogen activator and increased plasminogen activator-1 inhibitor, has been included in the presented model. These disorders together with accompanying inflammatory state are closely related to thrombus formation and cardiovascular disease promotion. The proposed model has been built using Petri nets and the analysis has been based mainly on t-invariants. Using the Petri net theory to model and analyze the investigated phenomena allows to better understand them by revealing some interesting dependencies in the studied biological system. It explains how tobacco smoke affects the analyzed processes and how harmful these effects are.

Uric acid is associated with long-term adverse cardiovascular outcomes in patients with acute coronary syndrome undergoing percutaneous coronary intervention

Background and aimsEvidence links uric acid (UA) with the promotion of cardiovascular disease. We assessed the prognostic value of UA on long-term major adverse outcomes (MACE) in patients with acute coronary syndrome (ACS), undergoing percutaneous coronary intervention (PCI). MethodsAs primary endpoint, we assessed the association of UA (continuous and dichotomized) with MACE, including cardiovascular death, myocardial infarction (MI) and stroke, using Cox regression and propensity matching. As secondary endpoints, the influence of hyperuricemia (defined as UA levels > 6.0 mg/dl in women, and >7.0 mg/dl in men) was analysed separately for cardiovascular death, MI, and stroke. The incremental prognostic value of UA was tested using the net reclassification improvement (NRI), and the integrated discrimination improvement (IDI). ResultsWe included 1215 patients. Hyperuricemia was present in 356 (29.3%) patients. Mean follow-up was 5.5 years.UA (HR 1.091 [1.035–1.150]; p = 0.001) and hyperuricemia (HR 1.750 [1.388–2.207]; p < 0.001) were significantly associated with MACE. Results were consistent between Cox regression and propensity matched analysis. Patients with hyperuricemia had a 1.6-fold increased relative risk for cardiovascular death (p = 0.005) and a 1.5-fold increased risk for MI (p = 0.032). For stroke, hyperuricemia only constituted a confounder (HR 1.104; p = 0.970). The prognostic accuracy of an established risk prediction model was significantly increased by adding UA (continuous NRI p = 0.004; categorical NRI p = 0.029; IDI p = 0.002). ConclusionsOur data suggest an independent association of elevated UA with long-term MACE in ACS patients undergoing PCI. Whether lowering UA might be beneficial remains to be elucidated in large clinical trials.

Uric acid promotes vascular stiffness, maladaptive inflammatory responses and proteinuria in western diet fed mice

ObjectiveAortic vascular stiffness has been implicated in the development of cardiovascular disease (CVD) and chronic kidney disease (CKD) in obese individuals. However, the mechanism promoting these adverse effects are unclear. In this context, promotion of obesity through consumption of a western diet (WD) high in fat and fructose leads to excess circulating uric acid. There is accumulating data implicating elevated uric acid in the promotion of CVD and CKD. Accordingly, we hypothesized that xanthine oxidase(XO) inhibition with allopurinol would prevent a rise in vascular stiffness and proteinuria in a translationally relevant model of WD-induced obesity. Materials/MethodsFour-week-old C57BL6/J male mice were fed a WD with excess fat (46%) and fructose (17.5%) with or without allopurinol (125mg/L in drinking water) for 16weeks. Aortic endothelial and extracellular matrix/vascular smooth muscle stiffness was evaluated by atomic force microscopy. Aortic XO activity, 3-nitrotyrosine (3-NT) and aortic endothelial sodium channel (EnNaC) expression were evaluated along with aortic expression of inflammatory markers. In the kidney, expression of toll like receptor 4 (TLR4) and fibronectin were assessed along with evaluation of proteinuria. ResultsXO inhibition significantly attenuated WD-induced increases in plasma uric acid, vascular XO activity and oxidative stress, in concert with reductions in proteinuria. Further, XO inhibition prevented WD-induced increases in aortic EnNaC expression and associated endothelial and subendothelial stiffness. XO inhibition also reduced vascular pro-inflammatory and maladaptive immune responses induced by consumption of a WD. XO inhibition also decreased WD-induced increases in renal TLR4 and fibronectin that associated proteinuria. ConclusionsConsumption of a WD leads to elevations in plasma uric acid, increased vascular XO activity, oxidative stress, vascular stiffness, and proteinuria all of which are attenuated with allopurinol administration.

Augmentation du risque cardiovasculaire et accélération de l’athérosclérose au cours de la polyarthrite rhumatoïde

Patients with rheumatoid arthritis (RA) are at increased risk of mortality compared with the general population. Evidence suggests that this increased mortality can largely be attributed to increased cardiovascular (CV) death. In a prospective study, 34 patients with RA were compared with age- and sex-matched controls. ResultsWe found a lower C-HDL, apolipoprotein A1 and B in patients with RA. However, CT/C-HDL and C-LDL/C-HDL were significantly higher than control patients. The intima-media thickness was significantly higher in patients with RA (0.759mm vs 0.558mm; P<0.001). ConclusionIncreased attention to cardiovascular risk in RA will be necessary to reduce the excess CV mortality and morbidity in RA patients. It appears that the excess risk that is observed in the RA population can be explained, in part, by promotion of CV disease through increased systemic inflammation associated with RA.

Promotion of cardiovascular disease by exposure to the air pollutant ozone

in the decades following the discovery of the chemical nature of environmental air pollutants and the biochemical reactions they could undergo, it was viewed that the primary tissue target of air pollution would be our lungs. This made sense, as the principal constituents of photochemical air

Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation

There is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways. The development of translational models of intermittent hypoxia has allowed investigation of its role in the activation of inflammatory mechanisms and promotion of cardiovascular disease in OSAS. There are noticeable differences in the response to intermittent hypoxia between body tissues but the hypoxia-sensitive transcription factors hypoxia-inducible factor-1 and nuclear factor-kappaB appear to play a key role in mediating the inflammatory and cardiovascular consequences of OSAS. Expanding our understanding of these pathways, the cross-talk between them and the activation of inflammatory mechanisms by intermittent hypoxia in OSAS will provide new avenues of therapeutic opportunity for the disease.

Partial substitution of sodium with potassium in white bread: feasibility and bioavailability

A high sodium intake, to which bread makes a major contribution, and a low potassium intake are believed to be important factors in the promotion of cardiovascular disease. Our aims was to determine to what extent salts of potassium could substitute sodium chloride and potassium-rich soya flour could replace wheat flour without detrimental effect on acceptability, and to measure the bioavailability of a potassium salt added to bread. A single-blind organoleptic evaluation was carried out on eight different potassium-enriched breads by 41 panellists. Thereafter, six volunteers consumed standard or potassium-chloride-fortified bread in an 11-day single-blind cross-over feeding trial to determine the bioavailability of the supplemental potassium. Two breads in which 30% of the sodium was replaced by potassium salts, and bread in which 10% of wheat flour was replaced with soy flour, had acceptability scores similar to the standard bread. In the metabolic study a supplement of 22 mmol/day potassium chloride incorporated into the bread was found to be wholly bioavailable. A substantial reduction in sodium and an increase in potassium intake could be achieved by substituting potassium salts for sodium chloride in bread.

Establishing A New Option for Target-organ Protection: Rationale for ARB Plus ACE Inhibitor Combination Therapy

Activation of the renin-angiotensin system (RAS) plays an important role in the promotion of cardiovascular disease and target-organ damage, mediated in part by hypertension. Combination therapy targeting RAS activation may reduce target-organ damage and provide superior blood pressure (BP) control; combining angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) represents one possible approach. In monotherapy studies, both ACE inhibitors and ARBs have demonstrated similar positive effects on BP and on RAS-related target-organ damage, including nephropathy and congestive heart failure. Studies of combination therapy, most of which involved addition of an ARB to existing ACE inhibitor therapy, have demonstrated benefits among patients with congestive heart failure and renal disease. However, variances in study design and populations, dosing and titration methods, and clinical end points, in addition to inherent differences between agents, limit the ability to reach clinically meaningful conclusions about the value of dual RAS inhibition. Trials designed to document such efficacy are currently underway.

Measuring nuclear factor-KB—who cares?

A convincing body of evidence now exists that obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular morbidity and mortality [1–3]. OSAS has been specifically associated with hypertension [4], myocardial infarctions [2], stroke [5], and congestive heart failure [6]. Apneic episodes and arousals cause surges in sympathetic tone with the release of vasoactive mediators including catecholamines [7]. Intermittent hypoxia leads to hypoxic vasoconstriction and hypoxia reperfusion oxidative stresses [8]. These metabolic stresses result in a systemic inflammatory response and vascular remodeling. Because treatment of sleep apnea is believed to prevent these complications, it is important that providers of sleep medicine verify effectiveness of treatment, including the ability of patients to comply with prescribed therapy. Commonly employed measures of adherence to therapy include the patient's self-reported history and selfreported change in Epworth Sleepiness Scale or other subjective symptom scales. Such historical self-reports are frequently unreliable. Recent experience has shown that continuous positive airway pressure (CPAP) devices capable of recording the duration and frequency of use provide the best available objective data regarding adherence to CPAP therapy. These data are helpful in explaining symptomatic response to therapy, an important outcome of treatment. However, they are in reality surrogate markers for the long-term outcomes we are interested in knowing. The clinician and patient need to know the impact that the prescribed treatment has had on reducing risk for adverse events such as heart disease and stroke. In their article on nuclear factor-KB (NF-KB) in this journal, Htoo et al. [9] may have provided us a first step toward a new measure of the effectiveness of OSAS therapy in reducing cardiovascular risk. Htoo et al. [9] report their investigation of a potential new surrogate marker that is closely related to systemic inflammation, a probable causative link to cardiovascular disease promotion. There are two very interesting findings in the paper by Htoo et al. [9]. The first is a direct correlation between neutrophil NF-KB activity with indices of apnea severity. The second finding was demonstrated in a subgroup of patients with severe apnea who received CPAP therapy for 1 month. Plasma levels of NF-KB-controlled gene products were reduced in 4 out of 5 of these CPAP-treated subjects. These novel findings suggest that measuring NF-KB activity may be useful for assessing clinical impact of therapy with CPAP, just as measuring cholesterol fractions has become utilized to assess impact of drug therapy for hyperlipidemias. The routine measurement of NFKB is far from ready for prime time. This first report was small, and while A. H. Eliasson . C. J. Lettieri Sleep Disorders Center, Walter Reed Army Medical Center, Washington, DC 20307-5001, USA

Benefits and risks of transfer from oral agents to insulin in type 2 diabetes mellitus.

The treatment of type 2 diabetes mellitus remains controversial. Since most patients are overweight or obese, regimens based on dietary modification and increased physical exercise are logical and safe treatment approaches. However, the long term impact of these interventions is frequently disappointing and pharmacotherapy is therefore required in the majority of patients. Oral antidiabetic agents, principally the sulphonylureas and biguanides, are often only partially effective, even in combination. Insulin is the treatment of choice for certain clinical situations, for example, pregnancy. Often insulin will be a temporary measure. Safety considerations will also point to the preferential use of insulin in other circumstances, for example, in patients with pronounced renal impairment. In addition, a significant proportion of patients with type 2 diabetes mellitus will ultimately require insulin therapy in the long term because of failure of oral agents to provide adequate glycaemic control (i.e. secondary failure). Reservations about insulin therapy in patients with type 2 diabetes mellitus, particularly elderly patients with cardiovascular complications, include hypoglycaemia and bodyweight gain. However, severe hypoglycaemia occurs with considerably lower frequency than in patients with type 1 diabetes mellitus. To date, no clear evidence has emerged implicating exogenous insulin therapy in the promotion of cardiovascular disease. On the contrary, recent clinical and experimental studies suggest anti-atherogenic effects. Insulin therapy can be successful in type 2 diabetes mellitus if patients are carefully selected. Twice daily isophane (neutral protamine Hagedom; NPH) or pre-mixed insulin is used routinely in many centres. The role of combinations of insulin and oral agents remains an area of controversy. Combined therapy with sulphonylureas may be more expensive and clear clinical advantages have not been consistently demonstrated. Bodyweight gain may be lessened by the concomitant use of metformin and troglitazone may improve glycaemic control in obese patients. Procrastination about transfer to insulin is not uncommon. Patient acceptance may be facilitated by a positive attitude from the diabetes care team and discussion of the possibility at a relatively early stage. Adequate support from a multidisciplinary team is important for safe and effective insulin therapy. Even so, in the long term, attainment of glycaemic targets may prove difficult to sustain with present therapeutic strategies.

Mechanisms by Which Dietary Antioxidants May Prevent Cardiovascular Diseases

Cardiovascular disease is the number one cause of death in the United States. Cholesterollowering drugs and dietary and behavioral modifications have been the traditional choice of treatment for the disease. Recently, there has been an increased advocacy for the use of antioxidants to retard the progression of the disease. In this review, the role of oxidants in the promotion of cardiovascular disease and the means by which antioxidants may prevent the disease are outlined. Specifically, multiple pathways by which antioxidants may retard the progression of cardiovascular disease are described.