Noninvasive measures of cardiovascular changes in diabetes mellitus

Barbara Davis Center for Childhood Diabetes, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado 80045-6511, USA.
Current opinion in endocrinology, diabetes, and obesity (Impact Factor: 3.37). 09/2007; 14(4):263-8. DOI: 10.1097/MED.0b013e32825a674d
Source: PubMed


Advances in noninvasive medical technology have led to more aggressive pursuit of cardiovascular disease detection in patients with diabetes mellitus. Studies measuring carotid intima-media thickness, arterial stiffness and coronary artery calcification have documented early markers of cardiovascular disease. Such markers have gained popularity for research and clinical use. This paper reviews recent studies using noninvasive technology for detection and monitoring of cardiovascular disease as it pertains to diabetes patients.
Studies published in the review period have utilized noninvasive techniques to monitor subclinical cardiovascular disease in diabetes patients, including carotid intima-media thickness to evaluate carotid atherosclerosis, pulse wave velocity and pulse wave analysis to measure arterial stiffness, electron beam computed tomography to evaluate coronary artery calcification, and magnetic resonance imaging to study cardiovascular plaque. These techniques have shown promising results and will have useful application for diabetes patients in the future.
Noninvasive testing is being redefined to include new techniques for detection and monitoring of cardiovascular changes. In the appropriate clinical setting, these tests offer novel approaches to monitoring - each with its own benefits and caveats. Further refinement of techniques will lead to increased applicability and improved ability for early detection of subclinical cardiovascular disease.

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    • "CIMT as measured by B-mode ultrasound represents the combined thickness of the intimal and medial layers of the carotid artery and represents an important predictive factor which favorably correlates with the risk of myocardial infarction and stroke, even after excluding the impact of other cardiovascular disease risk factors [7]. "
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    ABSTRACT: Presence of Diabetes Mellitus increases the risk of subclinical atherosclerosis. In this study was aimed to determine the influence of hypertension (HTN) on surrogate markers of atherosclerosis in a population of patients with early type 2 diabetes. 125 diabetic subjects drawn from Dr. Shariati outpatient's clinic list and 153 non- diabetic subjects who were the relatives in law of diabetic participants were recruited. Participants with type 2 diabetes were free of clinical evidence of cardiovascular disease and renal involvement. Two groups of diabetic and control were further divided into two subgroups of hypertensive (known case of HTN or blood pressure >=140/90 mmHg) and normotensive, and anthropometric characteristics, metabolic biomarkers as well as markers of subclinical atherosclerosis including Carotid intima media thickness (CIMT), flow mediated dilation (FMD) and Ankle Brachial Index (ABI) were measured. Diabetic group with a mean age of 49.9 +/- 7.5 years had significantly higher CIMT (0.64 +/- 0.14 vs 0.76 +/- 0.19, p = 0.001) and lower FMD (16.5 +/- 8.1 vs 13.3 +/- 7.1, p = 0.003) and ABI (1.2 +/- 0.1 vs 1.1 +/- 0.1, p = 0.01) than control with mean age of 52.9 +/- 10.1 years. 34% of control and 59.2% of diabetic were hypertensive. Fasting blood sugar, insulin levels and calculated insulin resistance index of HOMA IR. of hypertensive subjects were higher than normotensive subjects in both groups of diabetic and non-diabetic. Similar pattern was presented for measured inflammatory mediators of hs-CRP and IL-6. Among subclinical atherosclerosis markers, only CIMT was significantly different between hypertensive and normotensive subjects in both groups. In adjusted linear regression analysis, a constant significant association existed between age and CIMT, ABI and FMD in non-diabetic, while in diabetic, age only correlated with CIMT and not the other two markers. In multiple regression model, HTN was recognized as a risk factor for increasing CIMT (OR = 2.93, 95% CI = 1.03-8.33, p = 0.04) but not attenuating FMD or ABI. Since FMD and CIMT may measure a different stage of subclinical atherosclerosis in diabetic patients, influence of HTN on these markers might be different.
    Journal of Diabetes and Metabolic Disorders 01/2014; 13(1):24. DOI:10.1186/2251-6581-13-24
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    • "On the other hands, subclinical atherosclerosis and increased arterial stiffness are early changes predicting the development of CVD. Various noninvasive measures of these changes, such as carotid intima-media thickness (IMT), pulse wave velocity (PWV), and coronary artery calcification have been developed and commonly used [7]. Of these methods, PWV is the most commonly used measure of arterial stiffness, and predicts the development of CVD and mortality in type 2 diabetes [8]. "
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    ABSTRACT: The phosphodiesterase inhibitor cilostazol has beneficial effects on atherosclerosis by virtue of vasodilatory and antiplatelet effects. However, less is known about the effect of cilostazol on arterial stiffness and biochemical markers related to vascular inflammation and endothelial dysfunction in type 2 diabetic patients with metabolic syndrome. In this randomized, double-blind, crossover trial, 45 diabetic patients with metabolic syndrome were randomly assigned to either the cilostazol group (50 mg for 2 weeks, 100 mg for 6 weeks) or placebo group for an 8-week treatment phase, and then crossed over. Brachial-ankle pulse wave velocity (baPWV) and serum levels of inflammatory cytokines and vascular cellular adhesion molecules were measured before and after each treatment phase. Compared with the placebo group, the mean baPWV did not improve in the cilostazol group (mean difference 31.42 cm/sec, 95% CI -55.67 to 118.5). Cilostazol treatment significantly reduced soluble vascular cellular adhesion molecule-1 (sVCAM-1) level (from 1288.7 +/- 285.6 to 1168.2 +/- 252.3 ng/dL, P = 0.0003), and there was also significant mean difference between groups (mean difference 105.18 ng/dL, 95% CI 10.65 to 199.71). However, other biochemical markers including lipid profiles, high sensitivity C-reactive protein, adiponectin, interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, and soluble intercellular adhesion molecule-1 did not improve with cilostazol treatment. Cilostazol treatment significantly reduced serum sVCAM-1 level, but this short term treatment was not associated with beneficial effect on arterial stiffness and other inflammatory markers.Trial registration(Clinical trial reg. no. NCT00573950,
    Diabetology and Metabolic Syndrome 07/2013; 5(1):41. DOI:10.1186/1758-5996-5-41 · 2.17 Impact Factor
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    ABSTRACT: Media calcification is a predictor of cardiovascular mortality in type 2 diabetes mellitus (T2DM). Undercarboxylation of some vitamin K-dependent proteins, due to genetic polymorphisms of VKORC1, can lead to calcification. We examined a potential association between VKORC1 -1639 G>A polymorphism and T2DM and, also, the association of this polymorphism with carotid intima-media thickness (cIMT). VKORC1 -1639 G>A polymorphism was determined in 299 T2DM patients and 328 controls of Caucasian origin using PCR-RFLP. cIMT was measured in a subgroup of 118 T2DM patients. The frequency of VKORC1 genotypes between diabetic and nondiabetic subjects differed significantly (p=0.01). VKORC1 genotype was associated with T2DM in an adjusted model (OR 1.36, p=0.009). A statistically significant difference was observed in the maximum value of cIMT among different genotypes. VKORC1 -1639 G>A polymorphism was an independent predictor of cIMT (p=0.029) after adjusting for established risk factors. The association between VKORC1 -1639 G>A polymorphism and risk of T2DM could be due to the higher prevalence of calcification in T2DM patients. This is supported by the independent association between VKORC1 -1639 G>A polymorphism and maximum cIMT in T2DM patients which is likely due to atherosclerosis characterized by increased calcification.
    Diabetes research and clinical practice 07/2011; 94(2):236-41. DOI:10.1016/j.diabres.2011.06.021 · 2.54 Impact Factor
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