Primary prevention of CVD (cardiovascular disease) is mainly based on the assessment of individual cardiovascular risk factors. However, often, only the most important (conventional) cardiovascular risk factors are determined, and every level of risk factor exposure is associated with a substantial variation in the amount of atherosclerosis. Measuring the effect of risk factor exposure over time directly in the vessel might (partially) overcome these shortcomings. Several non-invasive imaging techniques have the potential to accomplish this, each of these techniques focusing on a different stage of the atherosclerotic process. In this review, we aim to define the current role of various of these non-invasive measurements of atherosclerosis in individual cardiovascular risk prediction, taking into account the most recent insights about validity and reproducibility of these techniques and the results of recent prospective outcome trials. We conclude that, although the clinical application of FMD (flow-mediated dilation) and PWA (pulse wave analysis) in individual cardiovascular risk prediction seems far away, there may be a role for PWV (pulse wave velocity) and IMT (intima-media thickness) measurements in the near future.

The effects of exercise on the distensibility of large and medium-sized arteries are poorly understood, but can be attributed to a combination of local vasodilator effects of exercise opposed by sympathetic vasoconstrictor tone. We sought to examine this relationship at the conduit artery level, with particular reference to the role of the sympatho-excitatory muscle metaboreflex. The effect of maintained muscle metaboreflex activation on a previously passive or exercised limb femoral artery was investigated. A total of ten healthy volunteers performed 2 min of isometric ankle plantar-flexion at 40% MVC (maximal voluntary force), in conjunction with 2 min of either non-ischaemic isometric HG (handgrip; control condition) or IHG (ischaemic HG) at 40% MVC. IHG was followed by 2 min of PECO (post-exercise circulatory occlusion) to maintain muscle metaboreflex activation. FTPWV [femoral–tibial PWV (pulse wave velocity)] was measured in the exercised or contralateral limb at baseline and immediately following calf exercise. BP (blood pressure) and HR (heart rate) were measured continuously throughout. In the HG condition, BP and HR returned promptly to baseline post-exercise, whereas exercised leg FTPWV was decreased (less stiff) by 0.6 m/s ( P <0.05) and the non-exercised leg PWV was not changed from baseline. PECO caused a sustained increase in BP, but not HR, in the IHG condition. Contralateral leg PWV increased (stiffened) during PECO by 0.9 m/s ( P <0.05), whereas exercised limb FTPWV was not changed from baseline. In conclusion, muscle metaboreflex activation causes a systemic stiffening of the arterial tree, which can overcome local exercise-induced decreases in arterial PWV.

The aim of the present study was to assess the association between invasive PWV (pulse wave velocity), serum levels of MMPs (matrix metalloproteinases) and the echocardiographic severity and calcification score of degenerative AS (aortic stenosis). We enrolled 30 patients (16 males; age, 61.3±8.2 years) diagnosed with degenerative AS and an additional 30 age- and sex-matched control patients. Invasive PWV methods with a pigtail catheter and double-channel recording were performed in both groups in our catheterization laboratory. We scored the severity of calcification at the AV (aortic valve) during two-dimensional echocardiography. The association between the trans-valvular pressure gradient, the severity of calcification of the AV and the value of PWV were analysed. We also analysed the serum levels of MMP-9, MMP-3 and TIMP-1 (tissue inhibitor of metalloproteinases-1) in these patients. In the group with degenerative AS, mean AV pressure gradients (56.0 compared with 9.5 mmHg; P <0.001) and calcified AV scoring (3.3±1.2 compared with 2.1±0.9; P <0.001) were higher than in the control group. In addition, PWV was faster in the group with degenerative AS (15.5±3.8 compared with 8.0±2.7 m/s; P =0.001). After being adjusted for age, sex, mean blood pressure and left ventricular function, both the AV pressure gradient and the severity of calcification were strongly correlated with PWV ( R =0.706, P <0.0001, and R =0.561, P =0.03 respectively). In addition, the serum levels of MMP-9, MMP-3 and TIMP-1 were all significantly higher and correlated with PWV in the group with AS (all P <0.05). With higher serum levels of MMPs and their inhibitors, we found that this invasive measurement of PWV was associated strongly with the pressure gradient and calcification of AV. More advanced degenerative changes in AV was probably associated with more severe aortic arteriosclerosis.