Abstract 545: Modification Over Time of Pulse Wave Velocity Parallel to Changes in Both Office and 24h-ambulatory Peripheral BP as well as Aortic BP

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Anna Oliveras ◽  
Julián Segura ◽  
Carmen Suárez ◽  
Luis García-Ortiz ◽  
María Abad ◽  
...  

Aim: to assess the relationship of changes in pulse wave velocity (PWV), a marker of target organ damage, with the variation in BP over time, as assessed by three different methods of measurement: office and 24h-ambulatory peripheral BP as well as aortic BP. Methods: Observational prospective study in hypertensive subjects with impaired glucose metabolism consecutively recruited from Spanish Hypertension Units. Aortic BP and carotid-femoral PWV were evaluated by radial applanation tonometry (Sphygmocor®) at baseline ( b ) and after 12 months of follow-up ( fu ). Peripheral BP measurements were also recorded at baseline and at 12 months follow-up: office BP was obtained as the average of triplicate measurements taken at 1 min-intervals after 5 min of seated rest, using validated oscillometric devices; 24h-ambulatory BP recordings were taken with a validated device (Spacelabs®-90207) at 20-minute intervals throughout both the self-reported awake and asleep periods. Clinical and anthropometric features were also recorded. PWV variation (Δ) over time was calculated as follows: Δ PWV= [(PWV fu - PWV b ) / PWV b ] x 100. BP variation over time was calculated with the same formula applied to BP values obtained with the different measurement techniques. Correlations (Spearman “Rho”) of Δ PWV and Δ BP were calculated. Results: n=209 patients; mean age: 61.8 ± 11.2 y; 39% (81 of 209) were female; 80% (167 of 209) had type 2 diabetes. Other risk factors: hypertension: 100%; dyslipidemia: 69% (144 of 209); smokers: 13% (28 of 209); body mass index: 30.9 ± 4.4 Kg/m 2 . Baseline office systolic/diastolic BP (mmHg): oSBP = 143 ± 20; oDBP = 82 ± 12. Follow-up office systolic/diastolic BP (mmHg): oSBP = 136 ± 20; oDBP = 79 ± 12. Baseline PWV: 10.01 ± 3.5 m/s. Follow-up PWV: 10.19 ± 3.21 m/s. Δ PWV correlated with: Δ oSBP (Rho=0.212; p=0.002), Δ 24h-SBP (Rho=0.254; p<0.001), Δ daytime-BP (Rho=0.232; p=0.001), Δ nighttime-BP (Rho=0.320; p<0.001) and Δ aortic-SBP (Rho=0.320; p<0.001). Conclusion: Modification over time of PWV, a marker of target organ damage, parallel to changes in systolic BP, both office and 24h-ambulatory peripheral BP variation as well as aortic BP variation, at 12 months of follow-up. Among them, aortic SBP and nighttime peripheral SBP both showed the best correlation.

2017 ◽  
Vol 20 (C) ◽  
pp. 70
Author(s):  
Andrea Greco ◽  
Alessandro Maloberti ◽  
Marisa Varrenti ◽  
Ilaria Bassi ◽  
Enrico Piccinelli ◽  
...  

2003 ◽  
Vol 81 (3) ◽  
pp. 205-211 ◽  
Author(s):  
Karima Et-Taouil ◽  
Michel Safar ◽  
Gérard E Plante

In this review paper, the classical and more recently described mechanisms responsible for the structural and functional characteristics of large artery rigidity are described. Mostly important, these characteristics appear to be nonspecific to the primary disease process involved in arterial hypertension, diabetes mellitus, dyslipidemia, congestive heart failure, chronic uremia, and perhaps senescence, including vascular dementia. Nonspecific in terms of aetiology, the vasculopathy encountered in these diseases exhibits common structural and functional abnormalities. The identification of such abnormalities could well become the target of potent nonpharmacological and (or) pharmacological interventions capable of preventing or retarding morbidity and mortality. The structural characteristics responsible for large artery rigidity include smooth muscle cell hypertrophy, matrix collagen deposition, and recently described, dysfunction in proteoglycan metabolism. Functional abnormalities, such as bradykinin-dependent hyper-reactivity of smooth muscle cells and vasa vasorum microcirculation network disturbances, also appear to alter aortic wall rigidity. The physiopathology of target organ damage is then revisited, based on endothelial dysfunction, documented in large and resistance arteries, as well as in microcirculation networks, where altered permeability to macromolecules leads to interstitial matrix disorganization and cell damage. The clinical evaluation of large artery rigidity is described, and one of the noninvasive methods, evaluation of pulse-wave velocity, is validated in normal conditions and in disease processes. Finally, nonpharmacological and pharmacological therapeutic measures are presented, and includes physical exercise to reduce insulin resistance, and renin–angiotensin-II–aldosterone modulators.Key words: large artery compliance, aortic structure, collagen, elastin, proteoglycans, vascular smooth muscle cells, vasa vasorum, target organ damage, pulse wave velocity, vascular pharmacology.


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