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Greater very short- to mid-term blood pressure variability (BPV) has been associated with an increased CVD risk, especially stroke. However, this link remains incompletely understood. We hypothesized that increased arterial stiffness and maladaptive carotid arterial remodeling may underlie this association. We therefore investigated the association between very short- to mid-term systolic BPV, aortic and carotid stiffness and carotid arterial remodeling using cross-sectional data from The Maastricht Study (aged 60 ± 8 years; 53% men). Aortic (carotid-femoral pulse wave velocity, n = 1671) and carotid stiffness (ultrasonography, n = 1690) were assessed. A composite index of systolic BPV was derived by standardizing and averaging systolic within-visit, 24-hour, and 7-day BPV. We performed linear regression analyses with adjustment for age, sex, glucose metabolism status, mean arterial pressure and cardiovascular risk factors. A 1-SD greater systolic BPV was statistically significantly associated with 0.10 m/s (95%CI: 0.01 – 0.20) greater cfPWV, but not with carotid distensibility (−0.033·10-3/kPa [−0.255 – 0.190]). In addition, a 1-SD greater systolic BPV was statistically significantly associated with greater carotid circumferential wall tension (0.84 dyne/cm [0.51 – 1.17]), circumferential wall stress (0.79 kPa [0.031 – 1.27]) and intima-media thickness (8.6 μm [1.0 – 16.3]). These results are indicative of maladaptive carotid remodeling, as circumferential wall tension and stress were not normalized despite greater intima-media thickness. In conclusion, greater very short- to mid-term BPV is associated with greater aortic stiffness and maladaptive carotid arterial remodeling, but not with carotid stiffness. These findings may explain, at least partially, the increased BPV-associated CVD risk, in particular stroke.

Background: Vascular research demonstrated that pulse wave velocity (PWV), a measure of arterial stiffness, is inherently blood pressure-dependent. Considering the hypothesised pathophysiological chain of increased arterial stiffness leading to increased blood pressure load with consequent left ventricle hypertrophy (LVH) development, we conducted a systematic review of antihypertensive and lifestyle intervention studies to determine the association between on the one hand changes in arterial stiffness and blood pressure, and on the other hand changes in LV mass (LVM). Methods: Using PubMed, EMBASE, Cochrane and Web of Science, we identified 23 studies, containing 2573 patients. Studies reported changes in arterial stiffness (assessed by means of PWV), systolic- and diastolic blood pressure (SBP, DBP), and LVM index (LVMI), respectively. Results: Statistically significant reductions in SBP, PWV and LVMI were reported in 16, 14, and 20 studies, respectively. Pooled analysis of studies showed that the proportion in SBP reduction did not correlate significantly to the proportion in reductions of the other two variables. On the other hand, we found a significant positive correlation (r = 0.58, p = 0.007) between arterial stiffness and LVM regression, expressed as a relevant reduction in LVMI of 6.5 g/m2 per 1.0 m/s reduction in PWV. Conclusions: Our findings provide evidence that a decrease in arterial stiffness is associated with regression of LVH. To investigate whether there exists a causal relation between LVH due to arterial stiffness increases and in turn blood pressure load increases, future studies should strive for a multiple followup design and use of blood pressure-independent or -corrected stiffness indices.

Background: We recently found in patients that the pressure dependency of arterial stiffness is age-dependent, explaining clinically observed changes in stiffness with blood pressure (BP) lowering. Pulse wave velocity, BP and age found in the Reference Values for Arterial Stiffness Collaboration show a corresponding pattern. We hypothesised that the impact of age on the pressure-dependency of arterial stiffness actually reflects changes in wall constituent properties and adaptation to mechanical stress Methods and results: We applied a constitutive model of arterial wall biomechanics (Zulliger, AJP-Heart 2004) to simulate ageing, based on detailed pressure-area curves obtained in our younger (mean age 40 yrs, n=6) and older (65 yrs, n=7) hypertensive patients. Ageing was simulated by adapting the model (initially fitted to the "young" pressure-area curve) to fit the "old" curve (Figure); allowing for elastin degradation, collagen rearrangement and wall thickness adaptation, but not for changes in fractional volumes. The simulation showed a physiologically significant transfer of pressure-load bearing from elastin to collagen, caused by a 40% loss in elastin stiffness and a 5-fold increase in collagen recruitment (Table). Presuming normalisation and homogeneous distribution of wall stress with ageing, the predicted increase in wall thickness was in accordance with intima-media thickness Reference Values (2010 data; 25-yr increment, corresponding risk category). Conclusion: Ageing influences observed arterial stiffness values at given blood pressures through underlying changes in the properties and mechanical loading of arterial wall constituents.

Background: Arterial calcification is commonly observed in cardiovascular disease and is associated with increased arterial stiffness, systolic hypertension and adverse cardiovascular outcome. Arterial calcification is an actively regulated process with several stimulating and inhibiting factors. An important inhibitor of arterial calcification is the Vitamin K-dependent Matrix Gla Protein (MGP). In animal studies, inhibition of Vitamin K by warfarin-treatment was associated with increased arterial calcification. We investigated in this pilot-study whether this effect of Vitamin-K antagonists could also be observed in humans. Methods: From five different thrombosis services in the Netherlands, we recruited 19 patients that have used oral vitamin-K antagonists for more than 10 years due to an history of cardiac valve replacement or venous thrombo-embolic event. We also recruited 17 control-subjects. We excluded subjects older than 55 years or subjects with a history of diabetes, hyperhomocysteinemia, hyperlipidemia and previous cardiovascular events. To detect arterial calcification, anterior soft-tissue radiographs from the femoral arteries were obtained in all subjects. In addition, the carotid Intima Media Thickness (cIMT) and carotid-femoral Pulse-wave Velocity (PWV) were measured. Results and conclusion: Femoral radiographs of sufficient quality were obtained for 18 patients and 16 controls. Fourteen (77.8%) patients on vitamin-K antagonists versus 4 (25%) control subjects had femoral artery calcifications (Odds-ratio 10.5; 95%–CI 2.15 – 51.28). Patients had a slightly higher mean cIMT (0.61±0.09mm) than control subjects (0.56±0.07mm; p=0.04).There was no difference in carotid-femoral PWV between the groups. Chronic use of Vitamin-K antagonists is associated with increased arterial calcification.