Our data support the value of the AASI as an indirect estimate of AS and as an element in the evaluation of CV risk in hypertensive patients. However, the reproducibility of this index is less, and its predictive value for complications is poorer, than that of QKD100-60, a parameter that we believe is more closely linked to AS.

We lack non-invasive tools for evaluating the coronary and renal microcirculations. Since cutaneous Doppler laser exploration has evidenced impaired cutaneous microvascular responses in coronary artery disease and in impaired renal function, we wanted to find out if there was a link between the impairments in the cutaneous and renal microcirculations. To specify the significance of the rise in the renal resistive index (RI), which is still unclear, we also sought relations between RI and arterial stiffness. We conducted a cross-sectional controlled study in a heterogeneous population including hypertensive patients of various ages with or without a history of cardiovascular disease along with a healthy control group. The cutaneous microcirculation was evaluated by laser Doppler flowmetry of the post-occlusive reactive hyperhemy (PORH) and of the hyperhemy to heat. The renal microcirculation was evaluated by measurement of the RI. Arterial stiffness was evaluated from an ambulatory measurement of the corrected QKD 100-60 interval. We included 22 hypertensives and 11 controls of mean age 60.6 vs 40.8 years. In this population, there was a correlation between RI and basal zero to peak flow variation (BZ-PF) (r ¼ À0.42; P ¼ 0.02) and a correlation between RI and rest flow to peak flow variation (RF-PF) (r ¼ À0.44; P ¼ 0.01). There was also a significant correlation between RI and the corrected QKD 100-60 (r ¼ À0.47; P ¼ 0.01). The significant correlation between PORH parameters and RI indicates that the functional modifications of the renal and cutaneous microcirculations tend to evolve in parallel during ageing or hypertension. The relation between RI and arterial stiffness shows that RI is a compound index of both renal microvascular impairment and the deterioration of macrovascular mechanics.

We confirm LVMI as a powerful risk factor in hypertension with a cutoff of 51 g/m(2.7), which offers the same sensitivity and specificity whether the LVM was determined before or during treatment. The progression of LVM, on average 5 years after the initial measurement had a prognostic value independent of the initial determination.

In the interpretation of an ECG in the hypertensive patient, the single measurement of the R wave in aVL gives results at least as good as those of more complicated indices, which do not appear to contribute further to the diagnosis of LVH and the prediction of cardiovascular risk.