Fructose May Be Driving Increase in CV Disease

2010 ◽  
Vol 43 (1) ◽  
pp. 39
Author(s):  
SHERRY BOSCHERT
Keyword(s):  
2012 ◽  
Vol 42 (15) ◽  
pp. 13
Author(s):  
DIANA MAHONEY
Keyword(s):  

2020 ◽  
Vol 19 (2) ◽  
pp. 210-232 ◽  
Author(s):  
Theodora A. Manolis ◽  
Antonis A. Manolis ◽  
Evdoxia J. Apostolopoulos ◽  
Helen Melita ◽  
Antonis S. Manolis

: Sleep is essential to and an integral part of life and when lacking or disrupted, a multitude of mental and physical pathologies ensue, including cardiovascular (CV) disease, which increases health care costs. Several prospective studies and meta-analyses show that insomnia, short (<7h) or long (>9h) sleep and other sleep disorders are associated with an increased risk of hypertension, metabolic syndrome, myocardial infarction, heart failure, arrhythmias, CV disease risk and/or mortality. The mechanisms by which insomnia and other sleep disorders lead to increased CV risk may encompass inflammatory, immunological, neuro-autonomic, endocrinological, genetic and microbiome perturbations. Guidelines are emerging that recommend a target of >7 h of sleep for all adults >18 years for optimal CV health. Treatment of sleep disorders includes cognitive-behavioral therapy considered the mainstay of non-pharmacologic management of chronic insomnia, and drug treatment with benzodiazepine receptor agonists binding to gamma aminobutyric acid type A (benzodiazepine and non-benzodiazepine agents) and some antidepressants. However, observational studies and meta-analyses indicate an increased mortality risk of anxiolytics and hypnotics, although bias may be involved due to confounding and high heterogeneity in these studies. Nevertheless, it seems that the risk incurred by the non-benzodiazepine hypnotic agents (Z drugs) may be relatively less than the risk of anxiolytics, with evidence indicating that at least one of these agents, zolpidem, may even confer a lower risk of mortality in adjusted models. All these issues are herein reviewed.


2019 ◽  
Vol 17 (3) ◽  
pp. 270-277 ◽  
Author(s):  
Thomas F. Whayne

The non-traditional cardiovascular (CV) risk factors that appear to be of most clinical interest include: apolipoprotein A (ApoA), apolipoprotein B (ApoB), high-sensitivity C-Reactive protein (hsCRP), homocysteine, interleukin 1 (IL1), lipoprotein (a) [Lp(a)], the density of low-density lipoprotein (LDL) particles, the LDL particle number, tissue/tumor necrosis factor-α (TNF-α) and uric acid. These non-traditional risk factors may be of value in adding further confirmation and attention to suspected significant CV risk. They can also provide a better understanding of current concepts of atherogenesis (e.g. various potential mechanisms associated with inflammation) as an etiology and in guiding current plus future therapies. In the mid-20th century, atherosclerosis and CV disease were considered mechanistic occurrences with essentially no attention to possible metabolic and molecular etiologies. Therefore, the only treatments then centered around mainly surgical procedures to try to improve blood flow, first with peripheral arterial disease (PAD) and later coronary artery disease (CAD). Now, failure to treat CV risk factors, especially where there is good evidence-based medicine, as in the case of statins for high CV risk patients, is considered medical negligence. Nevertheless, many problems remain to be solved regarding atherosclerosis prevention and treatment.


2020 ◽  
Vol 18 (5) ◽  
pp. 431-446 ◽  
Author(s):  
George E. Fragoulis ◽  
Ismini Panayotidis ◽  
Elena Nikiphorou

Rheumatoid arthritis (RA) is an autoimmune inflammatory arthritis. Inflammation, however, can spread beyond the joints to involve other organs. During the past few years, it has been well recognized that RA associates with increased risk for cardiovascular (CV) disease (CVD) compared with the general population. This seems to be due not only to the increased occurrence in RA of classical CVD risk factors and comorbidities like smoking, obesity, hypertension, diabetes, metabolic syndrome, and others but also to the inflammatory burden that RA itself carries. This is not unexpected given the strong links between inflammation and atherosclerosis and CVD. It has been shown that inflammatory cytokines which are present in abundance in RA play a significant role in every step of plaque formation and rupture. Most of the therapeutic regimes used in RA treatment seem to offer significant benefits to that end. However, more studies are needed to clarify the effect of these drugs on various parameters, including the lipid profile. Of note, although pharmacological intervention significantly helps reduce the inflammatory burden and therefore the CVD risk, control of the so-called classical risk factors is equally important. Herein, we review the current evidence for the underlying pathogenic mechanisms linking inflammation with CVD in the context of RA and reflect on the possible impact of treatments used in RA.


2020 ◽  
Vol 18 (3) ◽  
pp. 254-261
Author(s):  
Thomas F. Whayne

Supplementary estrogen plays important roles for female patients as convenient birth control, relief of postmenopausal symptoms, and in the management of other selected problems. However, as is the case for essentially all medications, there are side effects. Short of a major pulmonary embolus, the most severe side effect of estrogen would appear to be sporadic, rare, and severe hypertriglyceridemia associated with acute pancreatitis. The occurrence of this fortunately rare problem usually happens in the presence of some preexisting and usually mild increase in triglycerides (TG). A case of chronic and severe recurrent acute pancreatitis is described in the introduction and the management was complete estrogen avoidance. Started close to menopause and continued for a relatively short period, estrogens may have some cardiovascular (CV) benefit but the general recommendation is not to prescribe them for CV disease prevention. Estrogens may contribute to decreased diabetes mellitus (DM) risk and control. Administration of estrogens by the transdermal route may decrease some problems such as venous thromboembolism (VTE) and elevation of TG. Administration of estrogen in the right situation brings significant benefit to the female patient but skillful, careful, and knowledgeable use is essential.


Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 789
Author(s):  
Agata Winiarska ◽  
Iwona Filipska ◽  
Monika Knysak ◽  
Tomasz Stompór

Phosphorus is an essential nutrient that is critically important in the control of cell and tissue function and body homeostasis. Phosphorus excess may result in severe adverse medical consequences. The most apparent is an impact on cardiovascular (CV) disease, mainly through the ability of phosphate to change the phenotype of vascular smooth muscle cells and its contribution to pathologic vascular, valvular and other soft tissue calcification. Chronic kidney disease (CKD) is the most prevalent chronic disease manifesting with the persistent derangement of phosphate homeostasis. Diabetes and resulting diabetic kidney disease (DKD) remain the leading causes of CKD and end-stage kidney disease (ESRD) worldwide. Mineral and bone disorders of CKD (CKD-MBD), profound derangement of mineral metabolism, develop in the course of the disease and adversely impact on bone health and the CV system. In this review we aimed to discuss the data concerning CKD-MBD in patients with diabetes and to analyze the possible link between hyperphosphatemia, certain biomarkers of CKD-MBD and high dietary phosphate intake on prognosis in patients with diabetes and DKD. We also attempted to clarify if hyperphosphatemia and high phosphorus intake may impact the onset and progression of DKD. Careful analysis of the available literature brings us to the conclusion that, as for today, no clear recommendations based on the firm clinical data can be provided in terms of phosphorus intake aiming to prevent the incidence or progression of diabetic kidney disease.


Author(s):  
Emir M. Muzurović ◽  
Snežana Vujošević ◽  
Dimitri P. Mikhailidis

Diabetes mellitus (DM) is a chronic and complex metabolic disorder and also an important cause of cardiovascular (CV) disease (CVD). Patients with type 2 DM (T2DM) and obesity show a greater propensity for visceral fat deposition (and excessive fat deposits elsewhere) and the link between adiposity and CVD risk is greater for visceral than for subcutaneous (SC) adipose tissue (AT). There is growing evidence that epicardial AT (EAT) and pericardial AT (PAT) play a role in the development of DM-related atherosclerosis, atrial fibrillation (AF), myocardial dysfunction, and heart failure (HF). In this review, we will highlight the importance of PAT and EAT in patients with DM. We also consider therapeutic interventions that could have a beneficial effect in terms of reducing the amount of AT and thus CV risk. EAT is biologically active and a likely determinant of CV morbidity and mortality in patients with DM, given its anatomical characteristics and proinflammatory secretory pattern. Consequently, modification of EAT/PAT may become a therapeutic target to reduce the CV burden. In patients with DM, a low calorie diet, exercise, antidiabetics and statins may change the quantity of EAT, PAT or both, alter the secretory pattern of EAT, improve the metabolic profile, and reduce inflammation. However, well-designed studies are needed to clearly define CV benefits and a therapeutic approach to EAT/PAT in patients with DM.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Malik ◽  
H Chen ◽  
A Cooper ◽  
M Gomes ◽  
V Hejjaji ◽  
...  

Abstract Background In patients with type 2 diabetes (T2D), optimal management of cardiovascular (CV) risk factors is critical for primary prevention of CV disease. Purpose To describe the association of country income and patient socioeconomic factors with risk factor control in patients with T2D. Methods DISCOVER is a 37-country, prospective, observational study of 15,983 patients with T2D enrolled between January 2016 and December 2018 at initiation of 2nd-line glucose-lowering therapy and followed for 3 years. In patients without known CV disease with sub-optimally controlled risk factors at baseline, we examined achievement of risk factor control (HbA1c &lt;7%, BP &lt;140/90 mmHg, appropriate statin) at the 3 year follow-up. Countries were stratified by gross national income (GNI)/capita, per World Bank report. We explored variability across countries in risk factor control achievement using hierarchical logistic regression models and examined the association of country- and patient-level economic factors with risk factor control. Results Among 9,613 patients with T2D but without CV disease (mean age 57.2 years, 47.9% women), 83.1%, 37.5%, and 66.3% did not have optimal control of glucose, BP, and statins, respectively, at baseline. Of these, 40.8%, 55.5%, and 28.6% achieved optimal control at 3 years of follow-up. There was substantial variability in achievement of risk factor control across countries (Figure) but no association of country GNI/capita on achievement of risk factor control (Table). Insurance status, which differed substantially by GNI group, was strongly associated with glycemic control, with no insurance and public insurance associated with lower odds of patients achieving HbA1c &lt;7%. Conclusions In a global cohort of patients with T2D, a substantial proportion do not achieve risk factor control even after 3 years of follow-up. The variability across countries in risk factor control is not explained by the GNI/capita of the country. Proportion of patients at goal Funding Acknowledgement Type of funding source: Private company. Main funding source(s): The DISCOVER study is funded by AstraZeneca


2013 ◽  
Vol 33 (4) ◽  
pp. 411-418 ◽  
Author(s):  
Yun Li ◽  
Lihua Zhang ◽  
Yong Gu ◽  
Chuanming Hao ◽  
Tongying Zhu

BackgroundInsulin resistance is associated with multiple risk factors for cardiovascular (CV) disease in the general population. Patients on peritoneal dialysis (PD) are more likely to develop insulin resistance. However, no evaluation of the impact of insulin resistance on CV disease morbidity or mortality in patients on PD has been performed.MethodsOur prospective cohort study included all non-diabetic patients on PD at our center ( n = 66). Insulin resistance was evaluated at baseline by the homeostasis model assessment method (HOMA-IR) using fasting glucose and insulin levels. The cohort was followed for up to 58 months (median: 41.3 months; interquartile range: 34.3 months). A multivariate Cox model was used to analyze the impact of insulin resistance on CV disease mortality.ResultsFourteen CV events occurred in the higher HOMA-IR group [IR-H (HOMA-IR values in the range 2.85 – 19.5), n = 33], but only one event occurred in the lower HOMA-IR group (IR-L (HOMA-IR values in the range 0.83 – 2.71), n = 33) during the follow-up period. Level of HOMA-IR was a significant predictor of CV events [risk ratio: 17.7; 95% confidence interval (CI): 2.10 to 149.5; p = 0.008]. In the IR-H group, 10 patients died (8 CV events), but in the IR-L group, only 4 patients died (1 CV event). Patients in the IR-H group experienced significantly higher CV mortality (hazard ratio: 9.02; 95% CI: 1.13 to 72.2; p = 0.04). Even after adjustments for age, systolic blood pressure, body mass index, C-reactive protein, triglycerides, resistin, and leptin, HOMA-IR remained an independent predictor of CV mortality (hazard ratio: 14.8; 95% CI: 1.22 to 179.1; p = 0.03).ConclusionsInsulin resistance assessed using HOMA-IR was an independent predictor of CV morbidity and mortality in a cohort of nondiabetic patients on PD. Insulin resistance is a modifiable risk factor; the reduction of insulin resistance may reduce CV risk and improve survival in this group of patients.


2011 ◽  
Vol 9 (3) ◽  
pp. 238-240 ◽  
Author(s):  
Inayat ur Rahman ◽  
Muhammad Idrees ◽  
Mohammad Salman ◽  
Rooh Ullah Khan ◽  
MI Khan ◽  
...  

Although management of hyperglycaemia represents one of the principal treatment goals of diabetes therapy, the high incidence of cardiovascular (CV) complications in diabetes also needs effective management. Therefore, the present study was designed to determine and compare the effect of glitazones on serum sialic acid (SSA), a known risk marker for CV disease, along with fasting plasma glucose (FPG), glycohaemoglobin (HbA1-c) and blood lipids, in overweight, previously only diet-treated patients with type 2 diabetes ( n=60). The study was conducted for a period of 12 months. Significant improvement in FPG and HbA1-c were shown by both rosiglitazone ( p<0.003 and p<0.001, respectively) and pioglitazone ( p<0.005 and p<0.001, respectively), compared with baseline, and pioglitazone showed greater beneficial effects on other parameters monitored, significantly reducing total cholesterol (TC) ( p≤0.05). Both the drugs showed a decrease in SSA and no significant differences were observed between the groups. However, the decrease was significant only in the pioglitazone-treated group at month 12 ( p≤0.05), compared with baseline. A significant decrease in SSA by pioglitazone indicates its greater cardioprotective effect compared with rosiglitazone.


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