Risk Of Cardiovascular Disease In Type Research Articles

Association between osteoprotegerin gene polymorphisms and cardiovascular disease in type 2 diabetic patients

Osteoprotegerin (OPG) gene polymorphisms (T245G, T950C and G1181C) have been associated with osteoporosis and early predictors of cardiovascular disease. The aim of this study was to evaluate whether these polymorphisms contribute to cardiovascular disease (CVD) in type 2 diabetic patients. We performed a case-control study with 178 CVD subjects with diabetes and 312 diabetic patients without CVD to assess the impact of variants of the OPG gene on the risk of CVD. The OPG gene polymorphisms were analyzed by using the polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). There was no significant association between the T245G and G1181C polymorphisms and CVD in the additive genetic model (OR = 0.96, 95% CI 0.64–1.45, p = 0.79; OR = 1.06, 95% CI 0.81–1.39, p = 0.65, respectively). However, the C allele of the T950C polymorphism was independently associated with a risk of CVD in type 2 diabetic patients in this genetic model (OR = 1.38, 95% CI 1.07–1.80, p = 0.01). This study provides evidence that the C allele of the T950C polymorphism is associated with increased risk of CVD in diabetic patients. However, well-designed prospective studies with a larger sample size are needed to validate these results.

Assessing Framingham cardiovascular risk scores in subjects with diabetes and their correlation with diabetic retinopathy

Sir, I read with interest the article entitled “Assessing Framingham cardiovascular risk scores in subjects with diabetes and their correlation with diabetic retinopathy” by Damkondwar, et al.[1] I want to raise certain issues concerning the validity of the results obtained in the said study. Sir, say, A (Framingham scores in type II diabetics), B [Cardiovascular Disease (CVD) risks in type II diabetics] and C (diabetic retinopathy) are three entities and if one wants to correlate B with C by measuring A, then A and B must have undoubted pre-existing correlation. But in the said study, it was admitted “There is no longitudinal study from India which can suggest whether the scores underestimate or overestimate the CVD risk among subjects with type II diabetes”. It was even not mentioned whether the cross-sectional data obtained in the study were in conformity with the Framingham study or not. Therefore when the standard (Framingham scores) was not standardized (validated) for CVD risks in Indian diabetic population, how can Framingham scores and/or CVD risks be correlated to diabetic retinopathy? Framingham cardiovascular risk score is notoriously known for its high interethnic variability.[2,3] In fact it is often said that Framingham cardiovascular risk score correlates well only in the race from where it is actually evolved. The authors themselves mentioned that in the United Kingdom Prospective Diabetic Study (UKPDS), the Framingham scores underestimated the 10-year risk of CVD in type II diabetics by 32%. Therefore, the said scores though being globally investigated are not globally accepted for application. Hence mentioning Framingham scoring as ‘global risk assessment tool’ and advocating interaction between treating physician/cardiologist and the ophthalmologist on its basis (in the ‘Abstract’ of the said article) is probably not warranted. The results of the study were not compared with other compatible Indian cross-sectional study, in which Framingham scoring was used. Authors’ estimation of 10-year CVD risks in Sankara Nethralaya – Diabetic Retinopathy Epidemiology and Molecular Genetic Study (SN – DREAMS 1) i.e., in the study in question was 33.5%, whereas that estimated by The Indian Atherosclerosis Research Study (IARS) group was only 5.32%.[3] Although the inclusion criteria of the two studies were different (type II diabetes in SN – DREAMS 1 and genetic predisposition in IARS), however, both the criteria were found to have similar CVD risk potentials in the Framingham's cohort and hence tend to be compatible.[4,5] Correlating CVD risks with risks of diabetic retinopathy lacks biological plausibility. While cardiovascular diseases in diabetes are macrovascular in origin, retinopathy is microvascular, and each has distinct and different set of major etiological factors. While cardiovascular diseases are predominantly due to atherosclerosis, retinopathy is predominantly due to glucose dysregulation. That diabetes increases the risk of atherosclerotic diseases by two to three folds is an established fact[5] but the reverse, that is, role of atherosclerotic factors like cholesterol, LDL etc., in the causation of retinopathy is not as clear. Neither any article showing such correlation was cited in the ‘discussion’ section. Therefore, while investigation to this effect is laudable, a hypothetical explanation of this association was expected, and in the absence of explanation, needless to say, the strength of association had been weakened further.

Reducing cardiovascular disease risk in type 2 diabetes: is the focus on glycaemia warranted?

Cardiovascular disease remains a major source of morbidity and mortality in type 2 diabetes mellitus. This article examines the recent evidence from trials and related meta-analyses on the effects of glycaemic control on cardiovascular disease (and, to a lesser extent, microvascular outcomes) in diabetes, and compares this with evidence accrued from blood pressure and statin trials. On the basis of such evidence, as well as pragmatic considerations, it is clear that clinicians should place stronger emphasis on lipid and blood pressure management to lessen cardiovascular risks. At the same time, cardiovascular disease benefits of glycaemia reduction appear less pronounced, with patient characteristics critically influencing risk to benefit ratio. Recent guidelines now reflect recent observations on glycaemic control (with relaxed targets in specific patient groups), whereas future guidelines should encourage physicians to prioritize lipid-lowering and blood pressure management in patients with diabetes.

Cardiovascular Risk in Children and Adolescents with Type 1 and Type 2 Diabetes Mellitus

Rising rates of both type 1 and type 2 diabetes mellitus in children have led to increased concern regarding cardiovascular disease (CVD) risk during childhood. Diabetic children face prolonged exposure to hyperglycemia, and have increased risk of both microvascular and macrovascular disease. These circumstances may result in a generation of young adults presenting with cardiovascular outcomes, a tremendous personal and public health toll. In this article, we review CVD risk in type 1 and type 2 diabetes, discuss aspects of pathophysiology, and review current methods of CVD risk assessment. We also identify crucial areas in need of future research in order to devise effective prevention and treatment of CVD risk in children.

Pulse wave analysis and prevalent cardiovascular disease in type 1 diabetes

Objective Type 1 diabetes (T1D) is associated with a high risk for and mortality from premature coronary artery disease (CAD), including coronary artery calcification (CAC), a subclinical marker, and lower extremity arterial disease (LEAD). Pulse wave analysis (PWA) arterial stiffness indices have been associated with cardiovascular disease (CVD) risk factors and outcomes in various populations, but little is known regarding these relationships in T1D. Methods PWA was performed using the SphygmoCor Px device on 144 participants in the Pittsburgh EDC Study of childhood-onset T1D. The cross-sectional associations between arterial stiffness indices, augmentation index (AIx) and augmentation pressure (AP), and subendocardial viability ratio (SEVR), an estimate of myocardial perfusion, with prevalent CAD, electron beam computed tomography-measured CAC and low (<0.90) ankle–brachial index (ABI) were examined. Results Higher AP (but not AIx) and lower SEVR were univariately associated with prevalent CAD, high CAC score, and low ABI. AP and SEVR's association with CAD and CAC did not, however, remain significant after adjustment for age. In individuals not using nitrates, which profoundly affect PWA measures, AP was significantly higher in those with CAD events and explained more of the variance than either age or brachial blood pressure measures. SEVR was associated with low ABI in multivariable models. Conclusions Greater augmentation pressure is independently associated with prevalent CAD and estimated myocardial perfusion with low ABI in type 1 diabetes. These measures may thus help to better characterize CVD risk in type 1 diabetes and need to be examined prospectively.

Differential effects of protein quality on postprandial lipemia in response to a fat-rich meal in type 2 diabetes: comparison of whey, casein, gluten, and cod protein

Background:Enhanced and prolonged postprandial triglyceride responses involve increased cardiovascular disease risk in type 2 diabetes. Dietary fat and carbohydrates profoundly influence postprandial hypertriglyceridemia, whereas little information exists on the effect of proteins. Objective:The objective was to compare the effects of the proteins casein, whey, cod, and gluten on postprandial lipid and incretin responses to a high-fat meal in persons with type 2 diabetes. Design:A crossover study was conducted in 12 patients with type 2 diabetes. Blood samples were collected over 8 h after ingestion of a test meal containing 100 g butter and 45 g carbohydrate in combination with 45 g casein (Cas-meal), whey (Whe-meal), cod (Cod-meal), or gluten (Glu-meal). We measured plasma concentrations of triglycerides, retinyl palmitate (RP), free fatty acids, insulin, glucose, glucagon, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide. Results:The incremental area under the curve for triglyceride was significantly lower after the Whe-meal than after the other meals. The RP response was lower after the Whe-meal than after the Cas-meal and Cod-meal in the chylomicron-rich fraction and higher after the Whe-meal than after Cod- and Glu-meals in the chylomicron-poor fraction. Free fatty acids were most pronouncedly suppressed after the Whe-meal. The glucose response was lower after the Whe-meal than after the other meals, whereas no significant differences were found in insulin, glucagon, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide responses. Conclusion:The data suggest that as a supplement to a fat-rich meal in patients with type 2 diabetes, whey protein seems to outperform other proteins in terms of postprandial lipemia improvement, possibly because of the formation of fewer chylomicrons or increased clearance of chylomicrons. The trial was registered at clinicaltrials.gov as NCT00817973.

C-Reactive Protein Inhibits Insulin Activation of Endothelial Nitric Oxide Synthase via the Immunoreceptor Tyrosine-Based Inhibition Motif of FcγRIIB and SHIP-1

Insulin promotes the cardiovascular protective functions of the endothelium including NO production by endothelial NO synthase (eNOS), which it stimulates via Akt kinase which phosphorylates eNOS Ser1179. C-reactive protein (CRP) is an acute-phase reactant that is positively correlated with cardiovascular disease risk in patients with type 2 diabetes. We previously showed that CRP inhibits eNOS activation by insulin by blunting Ser1179 phosphorylation. We now elucidate the underlying molecular mechanisms. We first show in mice that CRP inhibits insulin-induced eNOS phosphorylation, indicating that these processes are operative in vivo. In endothelial cells we find that CRP attenuates insulin-induced Akt phosphorylation, and CRP antagonism of eNOS is negated by expression of constitutively active Akt; the inhibitory effect of CRP on Akt is also observed in vivo. A requirement for the IgG receptor FcgammaRIIB was demonstrated in vitro using blocking antibody, and reconstitution experiments with wild-type and mutant FcgammaRIIB in NIH3T3IR cells revealed that these processes require the ITIM (immunoreceptor tyrosine-based inhibition motif) of the receptor. Furthermore, we find that endothelium express SHIP-1 (Src homology 2 domain-containing inositol 5'-phosphatase 1), that CRP induces SHIP-1 stimulatory phosphorylation in endothelium in culture and in vivo, and that SHIP-1 knockdown by small interfering RNA prevents CRP antagonism of insulin-induced eNOS activation. Thus, CRP inhibits eNOS stimulation by insulin via FcgammaRIIB and its ITIM, SHIP-1 activation, and resulting blunted activation of Akt. These findings provide mechanistic linkage among CRP, impaired insulin signaling in endothelium, and greater cardiovascular disease risk in type 2 diabetes.

294: The effect of a low glycemic index diet on markers of cardiovascular disease risk in type 2 diabetes

294: The effect of a low glycemic index diet on markers of cardiovascular disease risk in type 2 diabetes

Prevalence of Nonalcoholic Fatty Liver Disease and Its Association With Cardiovascular Disease Among Type 2 Diabetic Patients

We read with great interest the recent article by Targher et al. (1) reporting the prevalence of nonalcoholic fatty liver disease (NAFLD) and associated cardiovascular disease (CVD) risk factors in patients with type 2 diabetes. Proper identification of patients with NAFLD is of major importance for adequate treatment and reduction of CVD risk in type 2 diabetic patients. However, routine ultrasound examination of the abdomen for the screening of hepatic steatosis in combination with serologic …

Exercise, fitness, and cardiovascular disease risk in type 2 diabetes and the metabolic syndrome

This article highlights research supporting the concept that increased physical activity and cardiorespiratory fitness attenuate risk of cardiovascular disease, type 2 diabetes, and the metabolic syndrome. Increased activity and fitness also attenuate risk of developing cardiovascular disease in persons who have type 2 diabetes or the metabolic syndrome. Although controversial, relationships between physical activity/physical fitness and type 2 diabetes/metabolic syndrome are largely independent of body weight. Thus, physical inactivity and poor cardiorespiratory fitness are not only important determinants of cardiovascular and metabolic diseases, but they can also be considered common features of these conditions, much like traditional risk factors such as obesity and insulin resistance.

Diabetic dyslipidaemia: past, present and future

AbstractPrevention of cardiovascular disease (CVD) in diabetes remains a major challenge for both physicians and patients. Diabetic dyslipidaemia is a major risk factor for CVD and is open to therapeutic intervention. Information now available from randomised, controlled, clinical trials (principally with statins) confirms highly significant benefits in terms of CVD reduction for diabetic patients with and without symptomatic CVD. This evidence base has moved treatment of dyslipidaemia to centre stage in CVD prevention. Important European and American guidelines point to the high CVD risk in type 2 diabetes and type 1 diabetes with albuminuria and advocate aggressive lipid management for primary as well as secondary CVD prevention. Currently there is evidence of sub‐optimal uptake of appropriate lipid‐lowering therapy and guidelines need to be fully implemented in clinical practice for the benefit of individual patients. In the future it is likely that more combination therapy will be used to treat diabetic dyslipidaemia in order to achieve better overall lipid control. Copyright © 2004 John Wiley &amp; Sons, Ltd.

Stimulus-specific patterns of cardiovascular reactivity in type A and B subjects: evidence for enhanced vagal reactivity in type B.

ABSTRACTRecent evidence suggests that the differences in cardiovascular reactivity between individuals exhibiting the Type A behavior pattern and those that do not are not limited to excessive betaadrenergic reactivity in Type A's. Research also suggests the possibility of a tendency for enhanced alpha‐adrenergically and vagally mediated cardiovascular reactivity in Type B's. In the present study, Type A and Type B subjects were exposed to stressor stimuli known to elicit either betaadrenergic or alpha‐adrenergic and vagal responses in the cardiovascular system. Heart rate, blood pressure, and forearm blood flow and vascular resistance responses were measured. The two Types did not differ in response to the beta‐adrenergic stimulus (mental arithmetic). However, the alpha‐adrenergic/vagal stimulus (cold face stimulus) produced more prolonged heart rate and blood flow responses in Type B subjects. Results suggest that Type B's show hyperreactivity (compared to Type A) when alpha‐adrenergic or vagal cardiovascular responses are elicited. The nature of this hyperreactivity suggests possible mechanisms for reduced cardiovascular disease risk in Type B individuals.