scholarly journals Long-Term Effects of Renal Artery Denervation

Medicina ◽  
2021 ◽  
Vol 57 (7) ◽  
pp. 662
Author(s):  
Vytautas Juknevičius ◽  
Andrius Berūkštis ◽  
Renata Juknevičienė ◽  
Eugenijus Jasiūnas ◽  
Pranas Šerpytis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Renal Artery ◽  
Wave Velocity ◽  
Resistant Hypertension ◽  
Pulse Wave ◽  
Aortic Pulse Wave Velocity ◽  
Pill Group ◽  
Renal Artery Denervation

Background and Objectives: Renal artery denervation (RDN) procedure is a broadly discussed method in the treatment of resistant hypertension. Many studies report short-term (3–12 months) results for blood pressure and arterial stiffness. The primary endpoints were changes in 24 h mean systolic blood pressure (BP) and office systolic BP 48 months after RDN. The secondary endpoints were changes in aortic pulse wave velocity and impact of polypharmacy on these variables. Materials and Methods: Renal artery denervation was performed in 73 patients treated for resistant hypertension; 49 patients remained in final analysis. Patient examination was carried out before the procedure, and subsequently at 3, 6, 12, 24, and 48 months later. Patients’ antihypertensive and overall medication regimens were carefully analysed. Results: Mean 24 h arterial blood pressure lowered and was sustained at lower levels for up to 48 months; median (interequartile range—IQR) from 158(23.5)/100(14.2) to 140(26.5)/86(16.2) mmHg. Mean reduction in 24 h ambulatory systolic BP was −11 ± 25 mmHg (95% CI, −20 to −2; p < 0.001), while office systolic BP reduced by −7 ± 23 mmHg (95%CI, −24 to −1; p < 0.02). A significant reduction in median aortic pulse wave velocity 12 months after the procedure (drop from baseline 11.2 [3.15] m/s (95%CI 6.1 to 16.2) to 9.8 [2.1] m/s (95%CI 6.1 to 13.7; p = 0.002)). After 48 months, there was no worsening compared to the baseline level of 10.3 [4.0] m/s (95% CI 6.9 to 17.8) (p > 0.05). The total mean number of antihypertensive drugs remained unchanged: 5.97(±1.1) vs. 5.24 (±1.45). A higher number of pills after 48 months was associated with higher aortic pulse wave velocity (1–5 pill group: 8.1 ± 1.6 m/s; 6–10 pill group: 10.9 ± 1.8 m/s; >11 pill group: 15.1 ± 2.6 m/s) (p = 0.003). Conclusions: Antihypertensive effect after renal denervation lasts up to 48 months with no worsening of arterial stiffness compared to baseline. In our study, polypharmacy was associated with increased arterial stiffness 48 months after the procedure.

scholarly journals Arterial Destiffening Starts Early after Renal Artery Denervation

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Andrius Berukstis ◽  
Rokas Navickas ◽  
Gintarė Neverauskaite-Piliponiene ◽  
Ligita Ryliskyte ◽  
Jonas Misiura ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Risk ◽  
Arterial Stiffness ◽  
Renal Artery ◽  
Aortic Stiffness ◽  
Pulse Wave ◽  
Aortic Pulse Wave Velocity ◽  
Sustained Effects ◽  
Treatment Of Hypertension ◽  
Renal Artery Denervation

Introduction. Renal artery denervation (RDN) is a new widely discussed method in treatment of hypertension. Most of the RDN studies assessed BP and arterial changes 3 and 6 months after the procedure, but there is a lack of trials that investigated early changes after RDN. Aim. To investigate aortic stiffness 24-48 hours after the procedure and thus to examine whether RDN might have an early additive value for a cardiovascular risk decline beyond the lowering of blood pressure. Methods. RDN was performed for 73 patients with resistant hypertension. Arterial stiffness and central haemodynamics were measured before the procedure, the next day after the procedure, and subsequently after 1, 3, 6, and 12 months. Results. Within 48 hours, RDN significantly reduced aortic pulse wave velocity (AoPWV) from 11.3±2.7 to 10.3±2.6 m/s (p=0.001); reduction was sustained at months 1, 3, 6, and 12. Early changes in the AoPWV value did not correlate with changes in office systolic or diastolic BP (p=0.45; p=0.33). Furthermore, the higher the initial AoPWV value, the greater the reduction of AoPWV observed after 6 months: Q1 8.4±1, Δ0.05±1.6 / Q2 10.1±0.4, Δ1.1±1.4 / Q3 12.2±0.8, Δ1.8±1.7 / Q4 15.3±1.7, Δ2.8±2.1 (p=0.002). Conclusions. Early and sustained effects on AoPWV observed in our study suggest that RDN may have additional effects on reducing arterial stiffness and cardiovascular risk.

scholarly journals Prognostic Value of Aortic Pulse Wave Velocity as Index of Arterial Stiffness in the General Population

Circulation ◽  
2006 ◽  
Vol 113 (5) ◽  
pp. 664-670 ◽  
Author(s):  
Tine Willum Hansen ◽  
Jan A. Staessen ◽  
Christian Torp-Pedersen ◽  
Susanne Rasmussen ◽  
Lutgarde Thijs ◽  
...  
Keyword(s):  
General Population ◽  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Prognostic Value ◽  
Pulse Wave ◽  
Aortic Pulse Wave Velocity

Volume status and arterial blood pressures are associated with arterial stiffness in hemodialysis patients

2018 ◽  
Vol 41 (7) ◽  
pp. 378-384 ◽  
Author(s):  
Alper Erdan ◽  
Abdullah Ozkok ◽  
Nadir Alpay ◽  
Vakur Akkaya ◽  
Alaattin Yildiz
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Pressure ◽  
Pulse Wave ◽  
Augmentation Index ◽  
Mean Blood Pressure ◽  
Aortic Blood ◽  
Aortic Blood Pressure

Background: Arterial stiffness is a strong predictor of mortality in hemodialysis patients. In this study, we aimed to investigate possible relations of arterial stiffness with volume status determined by bioimpedance analysis and aortic blood pressure parameters. Also, effects of a single hemodialysis session on these parameters were studied. Methods: A total of 75 hemodialysis patients (M/F: 43/32; mean age: 53 ± 17) were enrolled. Carotid-femoral pulse wave velocity, augmentation index, and aortic pulse pressure were measured by applanation tonometry before and after hemodialysis. Extracellular fluid and total body fluid volumes were determined by bioimpedance analysis. Results: Carotid-femoral pulse wave velocity (9.30 ± 3.30 vs 7.59 ± 2.66 m/s, p < 0.001), augmentation index (24.52 ± 9.42 vs 20.28 ± 10.19, p < 0.001), and aortic pulse pressure (38 ± 14 vs 29 ± 8 mmHg, p < 0.001) significantly decreased after hemodialysis. Pre-dialysis carotid-femoral pulse wave velocity was associated with age (r2 = 0.15, p = 0.01), total cholesterol (r2 = 0.06, p = 0.02), peripheral mean blood pressure (r2 = 0.10, p = 0.005), aortic-mean blood pressure (r2 = 0.06, p = 0.02), aortic pulse pressure (r2 = 0.14, p = 0.001), and extracellular fluid/total body fluid (r2 = 0.30, p < 0.0001). Pre-dialysis augmentation index was associated with total cholesterol (r2 = 0.06, p = 0,02), aortic-mean blood pressure (r2 = 0.16, p < 0.001), and aortic pulse pressure (r2 = 0.22, p < 0.001). Δcarotid-femoral pulse wave velocity was associated with Δaortic-mean blood pressure (r2 = 0.06, p = 0.02) and inversely correlated with baseline carotid-femoral pulse wave velocity (r2 = 0.29, p < 0.001). Pre-dialysis Δaugmentation index was significantly associated with Δaortic-mean blood pressure (r2 = 0.09, p = 0.009) and Δaortic pulse pressure (r2 = 0.06, p = 0.03) and inversely associated with baseline augmentation index (r2 = 0.14, p = 0.001). In multiple linear regression analysis (adjusted R2 = 0.46, p < 0.001) to determine the factors predicting Log carotid-femoral pulse wave velocity, extracellular fluid/total body fluid and peripheral mean blood pressure significantly predicted Log carotid-femoral pulse wave velocity (p = 0.001 and p = 0.006, respectively). Conclusion: Carotid-femoral pulse wave velocity, augmentation index, and aortic pulse pressure significantly decreased after hemodialysis. Arterial stiffness was associated with both peripheral and aortic blood pressure. Furthermore, reduction in arterial stiffness parameters was related to reduction in aortic blood pressure. Pre-dialysis carotid-femoral pulse wave velocity was associated with volume status determined by bioimpedance analysis. Volume control may improve not only the aortic blood pressure measurements but also arterial stiffness in hemodialysis patients.

scholarly journals Spironolactone Reduces Aortic Stiffness in Patients With Resistant Hypertension Independent of Blood Pressure Change

2021 ◽  
Author(s):  
Sudeep R. Aryal ◽  
Mohammed Siddiqui ◽  
Oleg F. Sharifov ◽  
Megan D. Coffin ◽  
Bin Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Resistant Hypertension ◽  
Aortic Stiffness ◽  
Pulse Wave ◽  
Antihypertensive Medications ◽  
Mineralocorticoid Receptor Antagonist ◽  
Stiffness Reduction ◽  
Arterial Blood

Background Aortic stiffness is an independent predictor of cardiovascular events in patients with arterial hypertension. Resistant hypertension is often linked to hyperaldosteronism and associated with adverse outcomes. Spironolactone, a mineralocorticoid receptor antagonist, has been shown to reduce both the arterial blood pressure (BP) and aortic stiffness in resistant hypertension. However, the mechanism of aortic stiffness reduction by spironolactone is not well understood. We hypothesized that spironolactone reduces aortic stiffness in resistant hypertension independently of BP change. Methods and Results Patients with uncontrolled BP (≥140/90 mm Hg) despite use of ≥3 antihypertensive medications (including diuretics) were prospectively recruited. Participants were started on spironolactone at 25 mg/d, and increased to 50 mg/d at 4 weeks while other antihypertensive medications were withdrawn to maintain constant mean BP. Phase‐contrast cardiac magnetic resonance imaging of the ascending aorta was performed in 30 participants at baseline and after 6 months of spironolactone treatment to measure aortic pulsatility, distensibility, and pulse wave velocity. Pulse wave velocity decreased (6.3±2.3 m/s to 4.5±1.8 m/s, P <0.001) and pulsatility and distensibility increased (15.9%±5.3% to 22.1%±7.9%, P <0.001; and 0.28%±0.10%/mm Hg to 0.40%±0.14%/mm Hg, P <0.001, respectively) following 6 months of spironolactone. Conclusions Our results suggest that spironolactone improves aortic properties in resistant hypertension independently of BP, which may support the hypothesis of an effect of aldosterone on the arterial wall. A larger prospective study is needed to confirm our findings.

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