Metabolic syndrome and prediabetes identify overlapping but not identical populations.

OBJECTIVE: The metabolic syndrome (MetS) is a cluster of risk factors related to cardiovascular disease. Prediabetes, identified by impaired fasting glucose and/or impaired glucose tolerance, may predict future development of diabetes mellitus. However, it is not clear whether MetS and prediabetes represent the same or different clinical entities. This study compares MetS and prediabetes in terms of cardiovascular risk factors and target organ damage. RESEARCH DESIGN AND METHODS: A total of 524 overweight and obese (body mass index, BMI >or= 27 kg/m (2)) adults, mean age 53.6 +/- 10.3 years, 264 men and 260 women, were studied. All participants underwent a thorough clinical and laboratory evaluation, including an oral glucose tolerance test and insulin measurements. Echocardiography, carotid ultrasonography, and pulse wave analysis were also performed for the detection of target organ damage. NCEP-ATP III and ADA criteria were used for the diagnosis of MetS and prediabetes. RESULTS: The prevalence of MetS and prediabetes was 38.7 and 25.4 %, respectively. Overall, 129 individuals (24.6 %) had MetS without prediabetes (group M) and another 59 (11.3 %) prediabetes without MetS (group P). Group P had decreased albumin excretion (p = 0.033) and more thickened common carotid intima-media in comparison to group M (p = 0.032). Furthermore, group M was associated with higher C-reactive protein levels. Multiple logistic regression analysis revealed that advanced age (p < 0.0001, OR 1.11, 95 % CI 1.06 - 1.16), low insulin secretion (p < 0.0001, OR 0.05, 95 % CI 0.02 - 0.18 for insulinogenic index), and increased insulin resistance (p = 0.0003, OR 3.22, 95 % CI 1.71 - 6.07 for HOMA-IR) were associated with group P. CONCLUSIONS: Our data demonstrate that MetS and prediabetes have an overlapping pattern. MetS appears to have a more pronounced effect on early renal dysfunction and increased inflammatory activation, while prediabetes tends to be associated with early carotid structural changes. These findings may be due to a different pathophysiologic substrate of these clinical phenotypes in terms of insulin resistance and secretion, as well as to the varying prevalence of cardiovascular risk factors.

Early vascular lesions in subjects with metabolic syndrome and prediabetes.

AIM: The metabolic syndrome (MetS) is a cluster of cardiovascular risk factors, while prediabetes, identified by impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT), predicts future development of diabetes mellitus. Although MetS and prediabetes have a strong interrelation, it is unclear whether they denote the same risk for cardiovascular complications. The aim of the study was to compare overweight and obese individuals with MetS and prediabetes in terms of early carotid artery atheromatosis and renal dysfunction. METHODS: A total of 524 overweight and obese (body mass index, BMI = or >27 kg/m2) adults, mean age 56.7+/-11.8 years, 264 men and 260 women, were studied. All participants underwent a thorough clinical and laboratory evaluation, including an oral glucose tolerance test. Carotid artery ultrasonography was performed and 24 h urine albumin excretion was measured. NCEP-ATP III and ADA criteria were used for the diagnosis of MetS and prediabetes. RESULTS: Overall, 129 individuals (24.6%) had MetS without prediabetes and another 59 (11.3%) prediabetes without MetS. Individuals with prediabetes had lower albumin excretion (P=0.033) and more thickened common carotid intima-media in comparison to those with MetS (P=0.032). Furthermore, MetS was associated with higher C-reactive protein levels in comparison to prediabetes (P=0.05). CONCLUSIONS: The MetS seems to have a more pronounced impact on early renal dysfunction than prediabetes, while the latter to early carotid artery structural changes.

High-dose monotherapy vs low-dose combination therapy of calcium channel blockers and angiotensin receptor blockers in mild to moderate hypertension.

The objectives of the study were to compare long-acting dihydropyridine calcium channel blockers (CCBs) with angiotensin II receptor blockers (ARBs) according to the ambulatory blood pressure monitoring (ABPM) profile in stage 1 and 2 newly diagnosed hypertensives and also to evaluate the efficacy of high-dose monotherapy vs low-dose combination therapy of the two drug categories among the subjects with inadequate blood pressure (BP) control after conventional low-dose monotherapy. We obtained 24-h ABPM readings from 302 subjects with newly diagnosed stage 1 or 2 essential hypertension. The study protocol consisted of initial drug treatment with a low dose of either CCBs or ARBs. Hypertensives who did not achieve BP control were randomized to high-dose monotherapy of either category of drug or low-dose combination therapy. CCBs and ARBs in low-dose monotherapy achieved BP control in 53.8 and 55.3% of the cases, respectively. However, subjects under treatment with CCBs experienced side effects more often and required that treatment be discontinued. Hypertensives who failed to control their BP with low-dose monotherapy did significantly better with low-dose combination treatment (61.6%) than with high-dose CCBs (42.8%) or ARBs (40.5%) monotherapy (P<0.05). In terms of ABPM, low-dose combination therapy exhibited better 24-h BP profile according to trough-to-peak ratio, hypertensive burden and BP variability. In conclusion, low-dose ARBs and CCBs have a comparable effect in subjects with grade 1 and 2 arterial hypertension. In hypertensives who are not controlled by low-dose monotherapy, low-dose combination therapy proves be more efficacious than high-dose monotherapy.

HLA phenotypes as promoters of cardiovascular remodelling in subjects with arterial hypertension.

The objective of this study was to investigate the association between human leukocyte antigens (HLA) phenotypes and cardiovascular remodelling, as expressed by left ventricular mass (LVM) and carotid intima-media thickness (IMT), in hypertensives. We examined 153 subjects with arterial hypertension and 61 normotensive controls living in the greater Athens area. The population was classified into three groups and specifically group I (normotensives), group II with Grade 1 hypertension and group III with Grade 2 or 3 hypertension. HLA class I and class II antigens were studied by microlymphocytotoxic technique. Carotid IMT and LVM were determined by ultrasonography. The prevalence of HLA DQ7 in the hypertensive cohort was 27.4% that was significantly smaller than the 52.5% among the controls (P = 0.002). The HLA DR11 was found in 24.0% of the hypertensives and in 52.5% of the controls (P < 0.001). Group III hypertensives with HLA DR11 exhibited significantly higher LVM/h in comparison to the hypertensives without this HLA (199.0 +/- 28.8 vs 171.2+44.1g/m, P = 0.009). This association was not present in groups I and II. Similarly, group III hypertensives with HLA DQ7 were characterized by higher IMT in comparison to those without this HLA (0.94 +/- 0.19 vs 0.83 +/- 0.23 mm, P = 0.048). HLA DR17 was associated with higher IMT in both groups II and III (1.00 +/- 0.19 vs 0.82 +/- 0.19 mm, P = 0.046 and 1.01 +/- 0.23 vs 0.84 +/- 0.22 mm, P = 0.049, respectively) but not in group I. In conclusion, certain HLA phenotypes may be related to the levels of arterial blood pressure. Moreover, it seems that these HLA phenotypes may identify subjects with arterial hypertension that are more prone to develop cardiovascular hypertrophy.

Differential impact of angiotensin receptor blockers and calcium channel blockers on arterial stiffness.

AIM: Arterial stiffness, assessed by ambulatory arterial stiffness index (AASI), is an independent predictor of cardiovascular disease (CVD) mortality in hypertensives. However, it is unclear whether certain antihypertensive drugs are conducive to the reduction in CVD morbidity and mortality through their beneficial effect on arterial stiffness. Therefore, we compared the effect of angiotensin receptor blockers (ARBs) and calcium channel blockers (CCBs) on AASI in a hypertensive population. METHODS: We studied 188 individuals with newly-diagnosed essential hypertension without organ damage or CVD. AASI was calculated from twenty-four-hour ambulatory blood pressure monitoring (ABPM) readings at baseline and after twelve weeks of antihypertensive treatment. Therapy was initiated with a low-dose of CCB (group A) or ARB (group B). After six weeks, subjects with poor office blood pressure (BP) control were further randomized to high-dose monotherapy (CCB in group C or ARB in group D) or low-dose combination therapy (CCB plus ARB, group E). RESULTS: Groups A and B showed similar reductions in systolic and diastolic BP (r=-0.12, P=0.92 and r=-0.07, P=0.58 in group A and r=-0.06, P=0.67 and r=-0.04, P=0.73 in group B, respectively). However, only subjects in group B achieved significant AASI decrease (P<0.001). Similarly, subjects in groups C, D and E also displayed a comparable BP reduction, but only those in group E attained significant AASI decrease (P=0.001). CONCLUSION: ARB treatment, either as low-dose monotherapy or in combination with a CCB in hypertensives who do not achieve BP control with monotherapy, has a beneficial effect on arterial stiffness. As arterial stiffness is an important modifiable risk factor, our findings highlight the value of ARBs beyond their BP lowering properties.

The effect of metformin on the incidence of type 2 diabetes mellitus and cardiovascular disease risk factors in overweight and obese subjects--the Carmos study.

UNLABELLED: We investigated whether the addition of metformin to the treatment of overweight and obese individuals further reduces the incidence of type 2 diabetes mellitus (T (2)DM), prediabetes and metabolic syndrome (MetS) and improves cardiovascular disease (CVD) risk factors (RFs). DESIGN AND METHODS: We studied 366 adults (mean age 53.0+/-0.5 SE years, and mean BMI 32.3+/-0.2 SE Kg/m (2)) without CVD. All subjects received lifestyle recommendations and drug management of CVD-RFs, whilst 95 of them were additionally given metformin. The follow-up period lasted 12 months. RESULTS: At the end of the study the frequency of T (2)DM in the metformin and non-metformin group was 1.1 and 8.1%, respectively (risk difference=-7% with 95% CI from -12.7% to -1.4%, p=0.012). Participants with prediabetes displayed a greater reduction in the incidence of T (2)DM after taking metformin compared to those who had not received this drug (risk difference=-18.5% with 95%CI from -33.1% to -3.9%, p=0.010). Metformin had a similar beneficial impact on subjects with MetS (risk difference=-12.9% with 95% from -25% to -0.7%, p=0.040) and this was attributed to the greater increase in HDL-C (p=0.046) and decrease in fasting plasma glucose levels (p=0.024). Metformin also achieved a greater reduction in total cholesterol and LDL-C levels (metformin vs. non-metformin treated subjects: -31.9 vs. -17.3 mg/dl, p=0.001, and -26.2 vs. -15.9 mg/dl, p=0.006, respectively). CONCLUSIONS: Metformin reduces the occurrence of T (2)DM in overweight and obese non-diabetic adults and decreases the rate of MetS by improving the CVD risk factor profile.