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Table 2 Factors influencing prognosis Risk factors Subclinical Organ Damage Systolic and diastolic BP levels Electrocardiographic LVH (Sokolow-Lyon > 38 mm; Cornell > 2440 mm M ms) or: Levels of pulse pressure (in the elderly) Echocardiographic LVH8 (LVMI M ! 125 g/m 2 , W ! 110 g/m 2 ) Age (M > 55 years; W > 65 years) Carotid wall thickening (IMT > 0.9 mm) or plaque Smoking Carotid-femoral pulse wave velocity >12 m/s Dyslipidaemia Ankle/brachial BP index < 0.9 -TC > 5.0 mmol/l (190 mg/dl) or:Slight increase in plasma creatinine:-LDL-C > 3.0 mmol/l (115 mg/dl) or: M: 115-133 mmol/l (1.3-1.5 mg/dl); -HDL-C: M < 1.0 mmol/l (40 mg/dl), W < 1.2 mmol/l (46 mg/dl) or:Low estimated glomerular filtration rate y (< 60 ml/min/1.73 m 2 ) or creatinine clearance^(< 60 ml/min) -TG > 1.7 mmol/l (150 mg/dl) Fasting plasma glucose 5.6-6.9 mmol/L (102-125 mg/dl) Microalbuminuria 30-300 mg/24 h or albumin-creatinine ratio: ! 22 (M); or ! 31(W) mg/g creatinine Abnormal glucose tolerance test Abdominal obesity (Waist circumference > 102 cm (M), > 88 cm (W)) Family history of premature CV disease (M at age < 55 years; W at age < 65 years) Diabetes Mellitus Established CV or renal disease Fasting plasma glucose ! 7.0 mmol/l (126 mg/dl) on repeated measurements, or Cerebrovascular disease: ischaemic stroke; cerebral haemorrhage; transient ischaemic attack Postload plasma glucose > 11.0 mmol/l (198 mg/dl) Heart disease: myocardial infarction; angina; coronary revascularization; heart failure Renal disease: diabetic nephropathy; renal impairment (serum creatinine M > 133, W > 124 mmol/l); proteinuria (> 300 mg/24 h) Peripheral artery disease Advanced retinopathy: haemorrhages or exudates, papilloedema Note: the cluster of three out of 5 risk factors among abdominal obesity, altered fasting plasma glucose, BP > --130/85 mmHg, low HDL-cholesterol and high TG (as defined above) indicates the presence of metabolic syndrome M: men; W: women; CV: cardiovascular disease; IMT: intima-media thickness; BP: blood pressure; TG: triglycerides; C: cholesterol;^Cockroft Gault formula; y MDRD formula; 8Risk maximal for concentric LVH (left ventricular hypertrophy): increased LVMI (left ventricular mass index) with a wall thickness/radius ratio ! 0.42.

Background-Inflammation in adipose tissue has been implicated in vascular dysfunction, but the local mechanisms by which this occurs are unknown. Methods and Results-Small arteries with and without perivascular adipose tissue were taken from subcutaneous gluteal fat biopsy samples and studied with wire myography and immunohistochemistry. We established that healthy adipose tissue around human small arteries secretes factors that influence vasodilation by increasing nitric oxide bioavailability. However, in perivascular fat from obese subjects with metabolic syndrome (waist circumference 111Ϯ2.8 versus 91.1Ϯ3.5 cm in control subjects, PϽ0.001; insulin sensitivity 41Ϯ5.9% versus 121Ϯ18.6% in control subjects, PϽ0.001), the loss of this dilator effect was accompanied by an increase in adipocyte area (1786Ϯ346 versus 673Ϯ60 m 2 , PϽ0.01) and immunohistochemical evidence of inflammation (tumor necrosis factor receptor 1 12.4Ϯ1.1% versus 6.7Ϯ1%, PϽ0.001). Application of the cytokines tumor necrosis factor receptor-␣ and interleukin-6 to perivascular fat around healthy blood vessels reduced dilator activity, resulting in the obese phenotype. These effects could be reversed with free radical scavengers or cytokine antagonists. Similarly, induction of hypoxia stimulated inflammation and resulted in loss of anticontractile capacity, which could be rescued by catalase and superoxide dismutase or cytokine antagonists. Incubation with a soluble fragment of adiponectin type 1 receptor or inhibition of nitric oxide synthase blocked the vasodilator effect of healthy perivascular adipose tissue. Conclusions-We conclude that adipocytes secrete adiponectin and provide the first functional evidence that it is a physiological modulator of local vascular tone by increasing nitric oxide bioavailability. This capacity is lost in obesity by the development of adipocyte hypertrophy, leading to hypoxia, inflammation, and oxidative stress. Key Words: hypoxia Ⅲ inflammation Ⅲ obesity Ⅲ microcirculation Ⅲ nitric oxide synthase M etabolic syndrome is a precursor to type 2 diabetes mellitus and cardiovascular disease, with a prevalence of almost 40% in the adult population. 1 Central obesity is believed to be the main cause of metabolic syndrome, and this is reflected in newer definitions of the condition with large waist circumference as a prerequisite. 2 Although associations of obesity with hypertension, 3 insulin resistance, 4 and cardiovascular disease 5 are well described, the underlying mechanisms are poorly understood. Two areas of research that may provide insight into these are the vasoactive properties of perivascular adipose tissue (PVAT) and the inflammatory changes that occur in fat as obesity develops. Demonstrated in 1991, 6 it is now accepted that healthy PVAT has an anticontractile effect. [7][8][9][10] The mechanism appears to be both endothelium dependent via release of nitric oxide 8,10 and endothelium-independent via generation of hydrogen peroxide. 8 In obesity and metabolic syndrome, there is also a conformational chang...

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These practice guidelines on the management of arterial hypertension are a concise summary of the more extensive ones prepared by a Task Force jointly appointed by the European Society of Hypertension and the European Society of Cardiology.Stratification of CV risk in four categories of added risk. SBP = systolic blood pressure; DBP = diastolic blood pressure; CV = cardiovascular; HT = hypertension; OD = subclinical organ damage; MS = metabolic syndrome.Normal values for 24 hour average BP are lower than for office BP, i.e. < 125-130 mmHg systolic and < 80 mmHg diastolic. Normal values of daytime BP are < 130-135 mmHg systolic and < 85 mmHg diastolic.

The functional and morphologic characteristics of isolated subcutaneous resistance vessels (about 170 fitn i.d.) from 15 untreated subjects with essential hypertension and 15 matched controls were examined. The vessels from the hypertensives had a 29% increase in the media-thickness-to-lumendiameter ratio. The maximal force development to noradrenaline (NA) expressed as active pressure (an estimate of the pressure the vessels could have contracted against in vivo) was 30 % higher in vessels from the hypertensives, while active media stress (force per square unit of smooth muscle) and sensitivity to NA was not significantly different. Increased active pressure, as well as unaltered active media stress and sensitivity, was seen for vasopressin, serotonin, angiotensin II, and K + . There was, however, an enhanced leftward shift of the NA sensitivity with cocaine (an inhibitor of the neuronal amine pump) in vessels from the hypertensives [pD 2 ( + cocaine) and pD 2 ( -cocaine) were 0.185 ± 0.053 and 0.040 ± 0.044, hypertensives and normotensives, respectively, p < 0.05] suggesting an abnormality of presynaptic function in essential hypertension. Furthermore, the calcium sensitivity was depressed (pD 2 was 4.197 ± 0.050 and 4.381 ± 0.068, hypertensives and normotensives, respectively, p < 0.05), and the rate of relaxation was faster (p < 0.05) in vessels from hypertensives, suggesting that excitation-contraction coupling might be depressed. The results suggest that the increased pressor response in essential hypertension can, to a large extent, be explained by altered vascular structure, while smooth muscle function is either unchanged or possibly depressed.