A18499 Evaluation of Central Aortic Blood Pressure and Pulse Wave Velocity in subjects with Ankylosing Spondylitis compared with healthy controls

2018 ◽  
Vol 36 ◽  
pp. e259 ◽  
Author(s):  
Ramos Becerra Carlos ◽  
David Cardona-Müller ◽  
Ernesto Cardona-Muñoz ◽  
Magid Hallab ◽  
Pierre Boutouyrie ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ankylosing Spondylitis ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Wave ◽  
Healthy Controls ◽  
Aortic Blood ◽  
Aortic Blood Pressure ◽  
Central Aortic Blood Pressure

scholarly journals Central Aortic Blood Pressure and Pulse Wave Velocity as Tools in the Hemodynamic Assessment of Hypertension

2020 ◽  
Vol 6 (3) ◽  
pp. 147-154
Author(s):  
Isabella Tan ◽  
Mark Butlin ◽  
Fatemeh Shirbani ◽  
James R. Cox ◽  
Karen Peebles ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Wave ◽  
Aortic Blood ◽  
Hemodynamic Assessment ◽  
Aortic Blood Pressure ◽  
Central Aortic Blood Pressure

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 THE EFFECT OF STATIN ADDED TO ANTIHYPERTENSIVE THERAPY ON ARTERIAL STIFFNESS IN HYPERTENSIVE PATIENTS AT HIGH CARDIOVASCULAR RISK

2018 ◽  
Vol 3 (5) ◽  
pp. 27-32
Author(s):  
O. V. Fedorishina ◽  
K. V. Protasov ◽  
A. M. Torunova
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Risk ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Antihypertensive Therapy ◽  
Pulse Wave ◽  
Augmentation Index ◽  
High Cardiovascular Risk ◽  
Hypertensive Patients ◽  
Aortic Blood Pressure

Background.Little is known about the effect of statins addition to standard antihypertensive therapy on blood pressure level and vascular stiffness in high-risk hypertensive patients.The aimof the study was to assess the dynamics of vascular stiffness in hypertensive patients of high or very high cardiovascular risk under the influence of rosuvastatin addition to combined two-component amlodipine and lisinopril antihypertensive therapy.Materials and methods.We investigated 60 hypertensive patients who were randomized into two groups: the 1st group received a fixed amlodipine/lisinopril combination, the 2nd one followed the same regimen of therapy with addition of 20 mg rosuvastatin. Mean office and ambulatory blood pressure as well as central aortic blood pressure and pulse wave velocity were evaluated in both groups before and after 24-week follow-up period.Results.At end of follow-up period the office and average daily blood pressure significantly decreased in both groups, with more prominent office diastolic blood pressure decline in the 2nd one. The central aortic blood pressure equally decreased in both groups. The augmentation index significantly reduced in both groups, mostly in the 2nd one. The carotid-femoral pulse wave velocity declined in both groups to the same extent. The carotid-radial pulse wave velocity decreased statistically only in the second group.Conclusions.Addition of rosuvastatin to a fixed amlodipine/lisinopril combination in high/very high cardiovascular risk hypertensive patients was accompanied by more pronounced decline of diastolic blood pressure and augmentation index, as well as significantly reduction of pulse wave velocity.

White matter hyperintensities in migraine: Clinical significance and central pulsatile hemodynamic correlates

Cephalalgia ◽  
2017 ◽  
Vol 38 (7) ◽  
pp. 1225-1236 ◽  
Author(s):  
Chun-Yu Cheng ◽  
Hao-Min Cheng ◽  
Shih-Pin Chen ◽  
Chih-Ping Chung ◽  
Yung-Yang Lin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
White Matter ◽  
Pulse Wave Velocity ◽  
Systolic Blood Pressure ◽  
Wave Velocity ◽  
Pulsatility Index ◽  
White Matter Hyperintensities ◽  
Pulse Wave ◽  
Healthy Controls ◽  
Central Systolic Blood Pressure

Background The role of central pulsatile hemodynamics in the pathogenesis of white matter hyperintensities in migraine patients has not been clarified. Methods Sixty patients with migraine (20–50 years old; women, 68%) without overt vascular risk factors and 30 demographically-matched healthy controls were recruited prospectively. Cerebral white matter hyperintensities volume was determined by T1-weighted magnetic resonance imaging with CUBE-fluid-attenuated-inversion-recovery sequences. Central systolic blood pressure, carotid-femoral pulse wave velocity, and carotid augmentation index were measured by applanation tonometry. Carotid pulsatility index was derived from Doppler ultrasound carotid artery flow analysis. Results Compared to the controls, the migraine patients had higher white matter hyperintensities frequency (odds ratio, 2.75; p = 0.04) and greater mean white matter hyperintensities volume (0.174 vs. 0.049, cm3, p = 0.04). Multivariable regression analysis showed that white matter hyperintensities volume in migraine patients was positively associated with central systolic blood pressure ( p = 0.04) and carotid-femoral pulse wave velocity ( p < 0.001), but negatively associated with carotid pulsatility index ( p = 0.04) after controlling for potential confounding factors. The interaction effects observed indicated that the influence of carotid-femoral pulse wave velocity ( p = 0.004) and central systolic blood pressure ( p = 0.03) on white matter hyperintensities formation was greater for the lower-carotid pulsatility index subgroup of migraine patients. White matter hyperintensities volume in migraine patients increased with decreasing carotid pulsatility index and with increasing central systolic blood pressure or carotid-femoral pulse wave velocity. Conclusions White matter hyperintensities are more common in patients with migraine than in healthy controls. Increased aortic stiffness or central systolic blood pressure in the presence of low intracranial artery resistance may predispose patients with migraine to white matter hyperintensities formation.

Zentraler aortaler Blutdruck: Bedeutender Parameter für Diagnostik und Therapie

2017 ◽  
Vol 142 (19) ◽  
pp. 1430-1436 ◽  
Author(s):  
Martin Middeke
Keyword(s):  
Blood Pressure ◽  
Pulse Wave ◽  
Antihypertensive Drugs ◽  
Clinical Aspects ◽  
Aortic Blood ◽  
Diagnostik Und Therapie ◽  
Aortic Blood Pressure ◽  
The Difference ◽  
Central Aortic Blood Pressure

AbstractIn recent years great emphasis has been placed on the role of central aortic blood pressure as measured non invasively using pulse wave analysis in pathophysiology of cardiovascular diseases and clinical aspects of hypertension. The difference of blood pressure between the central aorta and the brachial artery (amplification) is not constant but varies according to physiological, pathological and pharmacological mechanisms. Central aortic blood pressure is more strongly related to cardiovascular organ damages than does brachial pressure. Several antihypertensive drugs have different effects on aortic blood pressure as compared with brachial pressure. Central aortic blood pressure emerges superior to brachial pressure as target blood pressure in antihypertensive treatment.

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