Neuroadrenergic and reflex abnormalities in patients with metabolic syndrome.

AIMS/HYPOTHESIS: Previous studies have shown that alterations in vascular, metabolic, inflammatory and haemocoagulative functions characterise the metabolic syndrome. Whether this is also the case for sympathetic function is not clear. We therefore aimed to clarify this issue and to determine whether metabolic or reflex mechanisms might be responsible for the possible adrenergic dysfunction. METHODS: In 43 healthy control subjects (age 48.2+/-1.0 years, mean+/-SEM) and in 48 untreated age-matched subjects with metabolic syndrome (National Cholesterol Education Program's Adult Treatment Panel III Report criteria) we measured, along with anthropometric and metabolic variables, blood pressure (Finapres), heart rate (ECG) and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor manipulation (vasoactive drug infusion technique). RESULTS: Compared with control subjects, subjects with metabolic syndrome had higher BMI, waist circumference, blood pressure, cholesterol, triglycerides, insulin and homeostasis model assessment (HOMA) index values but lower HDL cholesterol values. Sympathetic nerve traffic was significantly greater in subjects with metabolic syndrome than in control subjects (61.1+/-2.6 vs 43.8+/-2.8 bursts/100 heartbeats, p<0.01), the presence of sympathetic activation also being detectable when the metabolic syndrome did not include hypertension as a component. Muscle sympathetic nerve traffic correlated directly and significantly with waist circumference (r=0.46, p<0.001) and HOMA index (r=0.49, p<0.001) and was inversely related to baroreflex sensitivity (r=-0.44, p<0.001), which was impaired in the metabolic syndrome. CONCLUSIONS/INTERPRETATION: These data provide evidence that the metabolic syndrome is characterised by sympathetic activation and that this abnormality (1) is also detectable when blood pressure is normal and (2) depends on insulin resistance as well as on reflex alterations.

Progression of large artery structural and functional alterations in Type I diabetes.

AIMS/HYPOTHESIS: Type I (insulin-dependent) diabetes mellitus is accompanied by reduced arterial distensibility and increased arterial wall thickness even in normotensive subjects with no micro-macrovascular complications. It is not known whether, and how fast, these subclinical markers of vascular damage develop over time. METHODS: We measured arterial wall distensibility in radial, common carotid artery and abdominal aorta in 60 normotensive patients (aged 35.0 +/- 1.2 years, means +/- SE) with Type I diabetes with no microvascular or macrovascular complications and in 20 healthy control subjects matched for age. Arterial distensibility was determined by continuous measurements of arterial diameter through echotracking techniques and by using either the Langewouters (radial artery) or the Reneman formula (carotid artery and aorta). The same echotracking techniques allowed us to ascertain the radial and carotid artery wall thickness. Data were collected before and after 23 +/- 1 months. RESULTS: In the first study, carotid artery distensibility was similar but radial artey and aortic distensibility was less (p < 0.01) in patients with diabetes than in control subjects (-39 % and 25 % respectively). This was accompanied by an increase (p < 0.01) in both radial (42 %) and carotid artery wall thickness (46 %). After 23 +/- 1 months diabetic subjects showed a further reduction in arterial distensibility (radial-12 %, p < 0.05; carotid-8 %, NS; aorta-20% p < 0.05) and an increase in arterial wall thickness (radial + 15 %; carotid 14%, p < 0,05). No change in distensibility and wall thickness values occurred in control subjects. CONCLUSION/INTERPRETATION: The early reduction in arterial distensibility and increase in arterial wall thickness characterizing uncomplicated normotensive Type I diabetes patients shows a measurable worsening over the short term.

Ambulatory blood pressure monitoring.

PREDICTIVE VALUE OF 24-H AMBULATORY BLOOD PRESSURE MONITORING: Average 24-h blood pressure values are more closely related to the target-organ damage of hypertension than are clinic blood pressure readings. Preliminary evidence from longitudinal studies suggests that ambulatory blood pressure is also superior to isolated clinic readings in the prognostic evaluation of hypertensive patients. This is supported by the demonstration that in hypertensive patients with left ventricular hypertrophy, regression of cardiac hypertrophy following treatment was better predicted by the drug-induced reduction in 24-h average blood pressure than clinic blood pressure. BLOOD PRESSURE VARIABILITY: Also, 24-h blood pressure variability seems to be involved in the genesis of hypertension target-organ damage, while the clinical value of specific components of the 24-h blood pressure profile, such the nocturnal blood pressure fall, is still a matter of debate. Similar caution is needed in approaching the clinical significance of white coat hypertension, the definition of which is still affected by important methodological problems.