In recent years, great emphasis has been placed on the role of arterial stiffness in the development of cardiovascular diseases. Indeed, the assessment of arterial stiffness is increasingly used in the clinical assessment of patients. Although several papers have previously addressed the methodological issues concerning the various indices of arterial stiffness currently available, and their clinical applications, clinicians and researchers still report difficulties in selecting the most appropriate methodology for their specific use. This paper summarizes the proceedings of several meetings of the European Network for Non-invasive Investigation of Large Arteries and is aimed at providing an updated and practical overview of the most relevant methodological aspects and clinical applications in this area.

In vivo arterial stiffness is a dynamic property based on vascular function and structure. It is influenced by confounding factors like blood pressure (BP), age, gender, body mass index, heart rate, and treatment. As a consequence, standardization of the measurement conditions is imperative. General and method/device-specific user procedures are discussed. The subject's conditions should be standardized before starting measurements. These conditions include a minimal resting period of 10 min in a quiet room. It also includes prohibitions on smoking, meals, alcohol, and beverages containing caffeine before measurements. The position of the subject and time of measurements should be standardized. In comparative studies, corrections should be made for confounding factors. Repeated measurements are done preferably by the same investigator, and if available validated with user-independent automated procedures. As it is not feasible to discuss all methods or devices measuring arterial stiffness in one article, more attention is given to user procedures of commercially available devices, because these devices are of interest for a wider group of investigators. User procedures of methods/devices are discussed according to the nature of arterial stiffness measured: systemic, regional, or local arterial stiffness. Each section discusses general or method/device-specific user procedures and is followed by recommendations. Each recommendation discussed during the First International Consensus Conference on the Clinical Applications of Arterial Stiffness is quoted with the level of agreement reached during the conference. Also proposals for future research are made.

HIV subjects showed a higher prevalence and a different pattern of metabolic syndrome components. HAART, more than HIV infection per se, appeared to be responsible for the increased prevalence of metabolic syndrome and arterial function derangement.

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptorheart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n=16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 ±2.4 hours (mean± SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 ±0.5 vs. 5.9±0.6 msec/mm Hg, p<0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2±0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p<0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later. (Circulation 1990;81:939-948) E xperimental coronary occlusion or acutely induced damage of the myocardium is followed by an abrupt impairment of the baroreceptor control of the sinus node,1-4 which is still evident several weeks later.3 This is potentially harmful because baroreceptors increase and reduce vagal and sympathetic influences on the heart, respectively, thereby opposing the adverse effects of ischemia on the electrical stability of the myocardium.5-8 In patients with a previous myocardial infarction (MI), the Valsalva maneuver and the administration of vasoactive drugs cause small changes in heart rate.9-12 Furthermore, a recent study from our institution has shown that in some patients, injection of phenylephrine induced somewhat greater bradycardias months as compared with weeks after the occurrence of an MI.13 This suggests that MI impairs the baroreceptor control of heart rate in humans as well as experimentally, but that some recovery later appears.In all human studies, the baroreceptor-heart ra...