Contribution of arterial excess pressure and arterial stiffness to central augmentation pressure in healthy subjects

2013 ◽  
Vol 168 (3) ◽  
pp. 2899-2900 ◽  
Author(s):  
J. Piskorski ◽  
T. Krauze ◽  
K. Katulska ◽  
M. Wykrętowicz ◽  
A. Milewska ◽  
...  
2015 ◽  
Vol 27 (03) ◽  
pp. 1550021
Author(s):  
S. Mohanalakshmi ◽  
A. Sivasubramanian

Arterial stiffness, resulting in loss of the elastic properties of arteries walls, is an indicator of cardiovascular risk, though the presence of disease is not clinically evident. Augmentation index is an important biomarker of arterial stiffness by which the cardiac risk of the patient can be diagnosed. The current paper outlines the non-invasive assessment of arterial stiffness by analyzing the morphology or contour of PhotoPlethysmoGraph (PPG) signal. PPG pulse was optically acquired with the developed photometric measurement device and the desired features were extracted to determine PPG augmentation Index (PAI) through advanced signal processing implemented in MATLAB. PAI was quantified by the fourth derivative of the signal by enhancing the location of inflection point (augmentation point) after conditioning the signal by efficient pre-processing and filtering techniques. The results reveal that the statistical distribution of PAI for healthy subjects presents a very low value and a very tight distribution. On the contrary, patients have a higher value of PAI and a wide asymmetrical shape of distribution. This work also establishes the usefulness of PPG contour analysis in the investigation of changes in the elastic properties of the vascular system. In conclusion, PAI has revealed to be a non-invasive indicator for arterial stiffness assessments.


Author(s):  
Daniel W. Riggs ◽  
Ray Yeager ◽  
Daniel J. Conklin ◽  
Natasha DeJarnett ◽  
Rachel J Keith ◽  
...  

Background: Residential proximity to greenness is associated with a lower risk of cardiovascular disease (CVD) and all-cause mortality. However, it is unclear whether the beneficial effects of greenness are linked to a reduction in the effects of ambient air pollutants. Methods and Results: We measured arterial stiffness in 73 participants with moderate to high CVD risk. Average levels of ambient PM2.5 and ozone were calculated from local monitoring stations. Residential greenness was estimated using satellite-derived normalized difference vegetation index (NDVI) for a 200m and 1km radius around each participant's home. Participants were 51% female; average age of 52 years; and, 79% had diagnosed hypertension. In multiple linear regression models, residential NDVI was negatively associated with augmentation index (-3.8% per 0.1 NDVI). Ambient levels of PM2.5 (per interquartile range (IQR) of 6.9 μg/m3) were positively associated with augmentation pressure (3.1 mmHg), pulse pressure (5.9 mmHg), and aortic systolic pressure (8.1 mmHg). Ozone (per IQR of 0.03 ppm) was positively associated with augmentation index (5.5%), augmentation pressure (3.1 mmHg), and aortic systolic pressure (10 mmHg). In areas of low greenness, both PM2.5 and ozone were positively associated with pulse pressure. Additionally, ozone was positively associated with augmentation pressure and systolic blood pressure. However, in areas of high greenness, there was no significant association between indices of arterial stiffness with either PM2.5 or ozone.Conclusions: Residential proximity to greenness is associated with lower values of arterial stiffness. Residential greenness may mitigate the adverse effects of PM2.5 and ozone on arterial stiffness.


2020 ◽  
Vol 25 (Supplement 1) ◽  
pp. S52
Author(s):  
Smriti Badhwar ◽  
Dinu Chandran ◽  
Ashok Jaryal ◽  
Rajiv Narang ◽  
Chetan Patel ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Stella Brilli ◽  
Dimitris Tousoulis ◽  
Charalambos Antoniades ◽  
George Hatzis ◽  
Nikos Ioakeimidis ◽  
...  

Background: Marfan syndrome is characterised by high risk of aortic dissections and increased cardiovascular risk. However, the impact of Marfan syndrome on endothelial function and arterial stiffness is unclear, while the role of matrix metalloproteinases is unknown. We examined the impact of Marfan syndrome on the elastic properties of the arterial tree, and vascular endothelial function, and we evaluated the potential role of matrix metalloproteinases in these effects. Methods: The study population consisted of 17 subjects with Marfan syndrome, aged 26.6±2.3 years old, with BMI 20.5±1.03Kg/m2 and 22 healthy individuals matched for gender, age (26.4±0.78 years old, p=NS) and BMI (22.4±0.86 Kg/m2). Arterial stiffness was evaluated by measuring carotid-femoral pulse wave velocity (PWV), while augmentation pressure and augmentation index (AIx) were also determined, as measures of arterial wave reflections. Endothelial function was evaluated by determining flow mediated dilation (FMD) in the brachial artery while matrix metalloproteinase 9 (MMP-9) levels were determined by ELISA. Results: Patients with Marfan syndrome had significantly lower pulse pressure in the radial artery (41.0±1.07mmHg) compared to controls (51.3±4.4mmHg). In addition, patients had higher AIx (17.6±2.4%) and augmentation pressure (5.44±0.65mmHg) compared to controls (7.72±3.43% and 2.41±1.14mmHg respectively, p<0.05 for both). However, the difference in PWV between patients and controls did not reach statistical significance (6.33±0.33 vs 5.96±0.23m/s respectively, p=NS). Patients with Marfan syndrome had lower FMD (2.05±1.13%) and higher plasma MMP-9 (827±70ng/ml) compared to controls (6.8±2.3% p<0.05 and 326±50ng/ml, p<0.01). Conclusions: Marfan syndrome is associated with increased MMP-9 levels, as well as with elevated augmentation index and augmentation pressure compared to healthy individuals, matched for age, gender and body mass index. Moreover, flow-mediated dilation is also impaired in these subjects. These findings suggest that Marfan syndrome directly affects the elastic properties and endothelial function of the arterial tree, with matrix metalloproteinases being important mediators in the pathophysiology of this syndrome.


2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e106
Author(s):  
Dong Hyeon Lee ◽  
Sang Hyun Ihm ◽  
Ho Joong Youn

2005 ◽  
Vol 6 (1) ◽  
pp. 130
Author(s):  
T. Shoji ◽  
S. Hatsuda ◽  
K. Shinohara ◽  
E. Kimoto ◽  
T. Araki ◽  
...  

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