Search

Background: Wave separation analysis enables individualized evaluation of the aortic pulse wave components. Previous studies focused on the pressure height with overall positive but differing results. In the present analysis, we assessed the associations of the pressure of forward and backward (P for and P ref ) pulse waves with prospective cardiovascular end points, with extended analysis for time to pressure peak (T for and T ref )., Methods: Participants in 3 IDCARS (International Database of Central Arterial Properties for Risk Stratification) cohorts (Argentina, Belgium, and Finland) aged ≥20 years with valid pulse wave analysis and follow-up data were included. Pulse wave analysis was done using the SphygmoCor device, and pulse wave separation was done using the triangular method. The primary end points consisted of cardiovascular mortality and nonfatal cardiovascular and cerebrovascular events. Multivariable-adjusted Cox regression was used to calculate hazard ratios., Results: A total of 2206 participants (mean age, 57.0 years; 55.0% women) were analyzed. Mean±SDs for P for , P ref , T for , and T for /T ref were 31.0±9.1 mm Hg, 20.8±8.4 mm Hg, 130.8±35.5, and 0.51±0.11, respectively. Over a median follow-up of 4.4 years, 146 (6.6%) participants experienced a primary end point. Every 1 SD increment in P for , T for , and T for /T ref was associated with 27% (95% CI, 1.07-1.49), 25% (95% CI, 1.07-1.45), and 32% (95% CI, 1.12-1.56) higher risk, respectively. Adding T for and T for /T ref to existing risk models improved model prediction (∆Uno's C, 0.020; P <0.01)., Conclusions: Pulse wave components were predictive of composite cardiovascular end points, with T for /T ref showing significant improvement in risk prediction. Pending further confirmation, the ratio of time to forward and backward pressure peak may be useful to evaluate increased afterload and signify increased cardiovascular risk., Competing Interests: Disclosures None.

Background: Aortic pulse wave velocity (PWV) predicts cardiovascular events (CVEs) and total mortality (TM), but previous studies proposing actionable PWV thresholds have limited generalizability. This individual-participant meta-analysis is aimed at defining, testing calibration, and validating an outcome-driven threshold for PWV, using 2 populations studies, respectively, for derivation IDCARS (International Database of Central Arterial Properties for Risk Stratification) and replication MONICA (Monitoring of Trends and Determinants in Cardiovascular Disease Health Survey - Copenhagen)., Methods: A risk-carrying PWV threshold for CVE and TM was defined by multivariable Cox regression, using stepwise increasing PWV thresholds and by determining the threshold yielding a 5-year risk equivalent with systolic blood pressure of 140 mm Hg. The predictive performance of the PWV threshold was assessed by computing the integrated discrimination improvement and the net reclassification improvement., Results: In well-calibrated models in IDCARS, the risk-carrying PWV thresholds converged at 9 m/s (10 m/s considering the anatomic pulse wave travel distance). With full adjustments applied, the threshold predicted CVE (hazard ratio [CI]: 1.68 [1.15-2.45]) and TM (1.61 [1.01-2.55]) in IDCARS and in MONICA (1.40 [1.09-1.79] and 1.55 [1.23-1.95]). In IDCARS and MONICA, the predictive accuracy of the threshold for both end points was ≈0.75. Integrated discrimination improvement was significant for TM in IDCARS and for both TM and CVE in MONICA, whereas net reclassification improvement was not for any outcome., Conclusions: PWV integrates multiple risk factors into a single variable and might replace a large panel of traditional risk factors. Exceeding the outcome-driven PWV threshold should motivate clinicians to stringent management of risk factors, in particular hypertension, which over a person's lifetime causes stiffening of the elastic arteries as waypoint to CVE and death., Competing Interests: Disclosures None.

In a cross-sectional analysis of a case-control study in 2015, we revealed the association between increased arterial stiffness (pulse wave velocity) and aircraft noise exposure. In June 2020, we evaluated the long-term effects, and the impact of a sudden decline in noise exposure during the coronavirus disease 2019 (COVID-19) lockdown, on blood pressure and pulse wave velocity, comparing 74 participants exposed to long-term day-evening-night aircraft noise level > 60 dB and 75 unexposed individuals. During the 5-year follow-up, the prevalence of hypertension increased in the exposed (42% versus 59%, P =0.048) but not in the unexposed group. The decline in noise exposure since April 2020 was accompanied with a significant decrease of noise annoyance, 24-hour systolic (121.2 versus 117.9 mm Hg; P =0.034) and diastolic (75.1 versus 72.0 mm Hg; P =0.003) blood pressure, and pulse wave velocity (10.2 versus 8.8 m/s; P =0.001) in the exposed group. Less profound decreases of these parameters were noticed in the unexposed group. Significant between group differences were observed for declines in office and night-time diastolic blood pressure and pulse wave velocity. Importantly, the difference in the reduction of pulse wave velocity between exposed and unexposed participants remained significant after adjustment for covariates (-1.49 versus -0.35 m/s; P =0.017). The observed difference in insomnia prevalence between exposed and unexposed individuals at baseline was no more significant at follow-up. Thus, long-term aircraft noise exposure may increase the prevalence of hypertension and accelerate arterial stiffening. However, even short-term noise reduction, as experienced during the COVID-19 lockdown, may reverse those unfavorable effects.

Background: Atherosclerosis is as a systemic inflammatory disease associated with the activationof many mediators, including matrix metalloproteinases (MMPs), and may be amplified by abnormal high serum uric acid (UA) concentration (hyperuricemia, HU). The aim of the study was to determine the relationship between serum UA concentration and activity of MMPs and their correlation with the hypertension-mediated organ damage (HMOD) intensity., Methods: One hundred and nine patients untreated with antihypertensive, hypolipemic or uratelowering drugs with diagnosed stage 1-2 essential hypertension were included in this study. In all participants blood pressure (BP) was measured, carotid-femoral pulse wave velocity (PWV), intima-media thickness (IMT), echocardiography and blood tests including UA, lipids and serum concentrations of MMPs (1, 2, 3, 9) were observed. The participants were divided into hyper- and normuricemic groups., Results: Uric acid concentration in the whole study group positively correlated with some HMOD parameters (IMT, PWV, left ventricular mass index, left atrial dimension). Among the studied metalloproteinases only MMP-3 activity positively correlated with serum UA concentration independently of age, body mass index and serum lipids (R2 = 0.11, p = 0.048). Multivariate regression analysis showed positive association between IMT and BP, UA concentration and MMP-3 activity, independently of waist circumference and serum lipids (R2 = 0.328, p < 0.002). Patients with HU were characterized by higher activity of MMP-3 than those without (19.41 [14.45; 21.74] vs. 13.98 [9.52; 18.97] ng/mL, p = 0.016)., Conclusions: The present results may support the thesis that UA and the increased by UA activity of MMPs may take part in the development of HMOD, especially IMT.

Objective: To assess the impact of long-term exposure to aircraft noise on blood pressure (BP), prevalence of arterial hypertension, and indices of asymptomatic organ damage., Methods: Using acoustic maps, we selected and further compared people living (average 35 years) in areas exposed to high, more than 60 dB (n = 101), and low aircraft noise, less than 55 dB (n = 100). Medical history taking, office BP measurement, ambulatory BP monitoring, and echocardiographic and arterial stiffness measurements were performed., Results: Exposure to aircraft noise did not increase the prevalence of arterial hypertension (50%, both groups) but was associated with higher office (88.3 ± 11.4 vs. 79.8 ± 8.6 mmHg, P < 0.001) and night-time DBP (66.6 ± 9.5 vs. 63.6 ± 7.3 mmHg, P < 0.01). Participants exposed to a high aircraft noise level had a higher carotid-femoral pulse wave velocity (PWV) (10.3 ± 1.8 vs. 9.4 ± 1.4 m/s, P < 0.01) and lower early mitral annulus velocity (e') (8.4 ± 2.9 vs. 9.2 ± 3.4 cm/s, P = 0.047). These differences were independent of age, sex, BMI, education, time spent at home, smoking status, alcohol consumption, and antihypertensive treatment. Higher office and night-time DBP, PWV, and e' values were explicitly observed in exposed normotensive participants. PWV in aircraft noise-exposed normotensive participants was equal to that of two decades older unexposed normotensive participants and was significantly associated with noise annoyance., Conclusion: Long-term aircraft noise exposure is related to higher office and night-time DBP, more advanced arterial stiffness, and unfavourable left ventricle diastolic function changes. Accelerated arterial stiffening was observed in those exposed to aircraft noise, even normotensive participants, to a degree depending on noise annoyance.

Background: Late-systolic loading of the left ventricular (LV) is determined by arterial wave reflections and central vascular stiffening. We, therefore, investigated the relationship between various Doppler indexes reflecting LV systolic and diastolic function and arterial stiffness in the framework of a large population study of randomly recruited study participants., Methods: In 1233 study participants (51.7% women; mean age, 48 years; 41.5% hypertensive), using conventional and tissue Doppler imaging, we measured: the transmitral early (E) and late (A) diastolic velocities; tissue Doppler imaging systolic and early (e') and late diastolic mitral annular velocities; and end-systolic longitudinal and radial strain. Using applanation tonometry, we assessed central pulse pressure (cPP), augmentation pressure and carotid-femoral pulse wave velocity., Results: After full adjustment, transmitral E and A peaks increased with augmentation pressure and cPP (P less than 0.0001) and e' was positively associated with cPP (P = 0.013). The E/e' ratio increased significantly with augmentation pressure (P less than 0.0001), cPP (P less than 0.0001) and pulse wave velocity (P = 0.048). Although accounting for covariables, all arterial indexes were on average significantly higher in the diastolic dysfunction group with elevated filling pressure (n = 171) when compared to participants with normal diastolic function (n = 961; P ≤ 0.0004) or with impaired relaxation (n = 101; P ≤ 0.008). Longitudinal strain decreased independently with mean arterial pressure (P = 0.03). The correlation between radial strain and the arterial indexes shifted from positive at middle age (50-60 years) to negative at older (P less than 0.0001 for interaction)., Conclusion: Our study underscored the importance of arterial characteristics as a mediator of LV systolic and diastolic dysfunction. We demonstrated an age-dependent relationship between radial strain and indexes of arterial stiffness.

Unlabelled: The aim of the study was to compare therapeutic effects of chosen antihypertensive drugs on arterial stiffness, shear stress in carotid arteries and metalloproteinases activity, moreover analysis of relationship of these variables in the course of treatment., Methods: 95 patients with essential arterial hypertension stage 1 or 2 were randomized to 6 months monotherapy with: quinapril, amlodipine, hydrochlorothiazide, losartan or bisoprolol. Each therapeutic group consisted of 19 patients (N=19). Before and then after 1, 3 and 6 months of treatment carotid-femoral pulse wave velocity (PWV) by using a Complior device, ultrasound of carotid arteries were performed. Blood samples for the measurement of whole blood viscosity were taken during each visit. Shear stress (SS) was calculated using measured variables: blood viscosity and velocity of blood flow. Serum concentration of metalloproteinase 3 (MMP-3) and plasma concentration of tissue inhibitor of metalloproteinase I (TIMP-1) were measured at the initial visit and after 6 months of treatment., Results: ANOVA for repeated measurements revealed for all groups significant decrease of PWV (ΔPWV) and MMP-3 (ΔMMP-3) concentration and increase of shear stress in carotid artery and TIMP-1 (ΔTIMP-1) concentration (p<0.05). No between groups differences appeared in above effects (p>0.05). The multiple regression analysis for the change of PWV (ΔPWV) in the study group considering all investigated variables at R2 = 0,27 revealed its significant relation to PWV at first visit, ΔTIMP-1, ΔMMP-3 and Δ shear stress counted for the maximum flow velocity in common carotid artery. Conclusion: Irrespectively of chosen drug we observed similar effect for PWV drop. Reduction of arterial stiffness as a result of antihypertensive therapy is strongly connected with shear stress increase that is secondary to blood flow velocity growth and changes in connective tissue metabolism.

Background: The relationship between hypertension and oxidative stress remains unexplained. Nevertheless, it is well established that reactive oxygen species have an influence on the arterial wall, endothelial function and therefore determine blood pressure., Aim: The evaluation of selected oxidative stress markers in hypertensive patients and an assessment of the relationship between oxidative stress markers and the arterial structure and function. We also aimed to investigate whether the influence of oxidative stress on remodelling of arteries, their structural and functional changes is independent of hypertension or is related to hypertension., Methods: Altogether 217 subjects (114 female, 103 male) were enrolled from hypertensive families. The mean age was 45.5 ± 16 years, and the group included 155 hypertensives. In every subject, the pulse wave velocity and intima-media thickness (IMT) in carotid arteries were measured as well as selected oxidative stress markers such as asymmetric dimethylarginin (ADMA), symmetric dimethylarginin (SDMA), advanced oxidation protein products (AOPP) and oxidised low density lipoproteins (ox-LDL)., Results: The results of multivariate analysis show that in hypertensive patients: the ADMA level increased with increasing peripheral pulse pressure (b = 0.003; p < 0.001), and AOPP was related to higher carotid IMT (b = 0.91; p = 0.036). In normotensive subjects, the following associations were found: between ADMA and central pulse pressure (b = 0.006; p = 0.008), between SDMA and the peripheral augmentation index (b = -0.03; p = 0.014), between AOPP and the peripheral augmentation index (b = 0.011; p = 0.04), and between ox-LDL/LDL ratio and the peripheral augmentation index (b = -0.025; p = 0.004). The SDMA/ADMA ratio was associated with estimated glomerular filtration rate in both groups (b = -0.0061; p < 0.0001 and b = -0.005; p < 0.017, respectively). In hypertensives, we observed a relation with peripheral pulse pressure (b = -0.0067; p = 0.0143). Moreover, in normotensives there was an association between the SDMA/ADMA ratio and uric acid (b = 1.3629; p = 0.046)., Conclusions: We found that the influence of oxidative stress on the structure and function of large arteries was independent of hypertension. Therefore oxidative stress may play a significant role in the development of arterial stiffness. Higher oxidative stress is associated with more advanced arterial remodelling in hypertension.

This review summarizes several scientific contributions at the recent Satellite Symposium of the European Society of Hypertension, held in Milan, Italy. Arterial stiffening and its hemodynamic consequences can be easily and reliably measured using a range of noninvasive techniques. However, like blood pressure (BP) measurements, arterial stiffness should be measured carefully under standardized patient conditions. Carotid-femoral pulse wave velocity has been proposed as the gold standard for arterial stiffness measurement and is a well recognized predictor of adverse cardiovascular outcome. Systolic BP and pulse pressure in the ascending aorta may be lower than pressures measured in the upper limb, especially in young individuals. A number of studies suggest closer correlation of end-organ damage with central BP than with peripheral BP, and central BP may provide additional prognostic information regarding cardiovascular risk. Moreover, BP-lowering drugs can have differential effects on central aortic pressures and hemodynamics compared with brachial BP. This may explain the greater beneficial effect provided by newer antihypertensive drugs beyond peripheral BP reduction. Although many methodological problems still hinder the wide clinical application of parameters of arterial stiffness, these will likely contribute to cardiovascular assessment and management in future clinical practice. Each of the abovementioned parameters reflects a different characteristic of the atherosclerotic process, involving functional and/or morphological changes in the vessel wall. Therefore, acquiring simultaneous measurements of different parameters of vascular function and structure could theoretically enhance the power to improve risk stratification. Continuous technological effort is necessary to refine our methods of investigation in order to detect early arterial abnormalities. Arterial stiffness and its consequences represent the great challenge of the twenty-first century for affluent countries, and "de-stiffening" will be the goal of the next decades.