Abstract P057: Arterial Stiffness And Pressure Wave Reflection In The Development Of Isolated Diastolic Hypertension

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Hirofumi Tomiyama ◽  
Kazuki N Shiina ◽  
Taishiro Chikamori ◽  
Akira Yamashina

Importance: While increased arterial stiffness and augmented pressure wave reflection are thought to be key factors in the development of systolic/diastolic hypertension (SDHT) or isolated systolic hypertension (ISHT) via the elevation of systolic blood pressure, their associations with the development of isolated diastolic hypertension (IDHT) have not been clarified. Objective: To examine the significance of augmented pressure wave reflection in the absence of accompanying increase of the arterial stiffness in the development of IDHT. Design and Setting: The prospective observational study conducted in the employees of a Japanese construction company at its health care center from year 2007 through year 2015 with a mean follow-up of 6.4 years, respectively. Participants: A total of 3022 Japanese male employees without hypertension at the start of this study. Main Outcomes and Measures: The annual assessment of prevalence of any phenotypes of hypertension. The blood pressure, brachial-ankle pulse wave velocity (baPWV), and radial augmentation index (rAI) were measured annually during the study period. Results: At the end of the study period, 129 subjects were diagnosed as having SDHT, 112 as having ISHT, and 74 as having IDHT. Both the baPWV and rAI showed significant individual odds ratios for new onset of SDHT and new onset of ISHT. However, only rAI, but not the brachial-ankle PWV, showed a significant odds ratio (1.44, P<0.01) for new onset of IDHT. This association was significant in subjects without elevated baPWV values at the start of the study (i.e., baPWV < 1224 cm/sec), but not in those with elevated brachial-ankle PWV at the start of the study. Generalized estimating equation analyses demonstrated a significant longitudinal association of the rAI, but not baPWV, with the prevalence of IDHT (estimate = 0.02, P=0.02). Conclusions: While increased arterial stiffness and augmented pressure wave reflection present concomitantly may be associated with the development of SDHT and ISHT, augmented pressure wave reflection alone, which may be related to isolated peripheral vascular damage, in the absence of accompanying increase of the arterial stiffness, may be a significant factor in the development of IDHT.

2007 ◽  
Vol 232 (9) ◽  
pp. 1228-1235 ◽  
Author(s):  
Darren P. Casey ◽  
Darren T. Beck ◽  
Randy W. Braith

Endurance exercise is efficacious in reducing arterial stiffness. However, the effect of resistance training (RT) on arterial stiffening is controversial. High-intensity, high-volume RT has been shown to increase arterial stiffness in young adults. We tested the hypothesis that an RT protocol consisting of progressively higher intensity without concurrent increases in training volume would not elicit increases in either central or peripheral arterial stiffness or alter aortic pressure wave reflection in young men and women. The RT group ( n = 24; 21 ± 1 years) performed two sets of 8–12 repetitions to volitional fatigue on seven exercise machines on 3 days/week for 12 weeks, whereas the control group ( n = 18; 22 ± 1 years) did not perform RT. Central and peripheral arterial pulse wave velocity (PWV), aortic pressure wave reflection (augmentation index; AIx), brachial flow–mediated dilation (FMD), and plasma levels of nitrate/nitrite (NOx) and norepinephrine (NE) were measured before and after RT. RT increased the one-repetition maximum for the chest press and the leg extension ( P < 0.001). RT also increased lean body mass ( P < 0.01) and reduced body fat (%; P < 0.01). However, RT did not affect carotid-radial, carotid-femoral, and femoral-distal PWV (8.4 ± 0.2 vs. 8.0 ± 0.2 m/sec; 6.5 ± 0.1 vs. 6.3 ± 0.2 m/sec; 9.5 ± 0.3 vs. 9.5 ± 0.3 m/sec, respectively) or AIx (2.5% ± 2.3% vs. 4.8% ± 1.8 %, respectively). Additionally, no changes were observed in brachial FMD, NOx, NE, or blood pressures. These results suggest that an RT protocol consisting of progressively higher intensity without concurrent increases in training volume does not increase central or peripheral arterial stiffness or alter aortic pressure wave characteristics in young subjects.


2021 ◽  
Author(s):  
William B Horton ◽  
Linda A Jahn ◽  
Lee M Hartline ◽  
Kevin W Aylor ◽  
James T Patrie ◽  
...  

Abstract Introduction: Increasing arterial stiffness is a feature of vascular aging that is accelerated by conditions that enhance cardiovascular risk, including diabetes mellitus. Multiple studies demonstrate divergence of carotid-femoral pulse wave velocity and augmentation index in persons with diabetes mellitus, though mechanisms responsible for this are unclear.Materials and Methods: We tested the effect of acutely and independently increasing plasma glucose, plasma insulin, or both on hemodynamic function and markers of arterial stiffness (including carotid-femoral pulse wave velocity, augmentation index, forward and backward wave reflection amplitude, and wave reflection magnitude) in a four-arm, randomized study of healthy young adults.Results: Carotid-femoral pulse wave velocity increased only during hyperglycemic-hyperinsulinemia (+0.36 m/s; p=0.032), while other markers of arterial stiffness did not change (all p>0.05). Heart rate (+3.62 bpm; p=0.009), mean arterial pressure (+4.14 mmHg; p=0.033), central diastolic blood pressure (+4.16 mmHg; p=0.038), and peripheral diastolic blood pressure (+4.09 mmHg; p=0.044) also significantly increased during hyperglycemic-hyperinsulinemia.Conclusions: We conclude that the acute combination of moderate hyperglycemia and hyperinsulinemia preferentially stiffens central elastic arteries. This effect may be due to increased sympathetic activity. (ClinicalTrials.gov number NCT03520569; registered 9 May 2018).


2021 ◽  
Author(s):  
William B Horton ◽  
Linda A Jahn ◽  
Lee M Hartline ◽  
Kevin W Aylor ◽  
James T Patrie ◽  
...  

Abstract Introduction: Increasing arterial stiffness is a feature of vascular aging that is accelerated by conditions that enhance cardiovascular risk, including diabetes mellitus. Multiple studies demonstrate divergence of carotid-femoral pulse wave velocity and augmentation index in persons with diabetes mellitus, though mechanisms responsible for this are unclear.Materials and Methods: We tested the effect of acutely and independently increasing plasma glucose, plasma insulin, or both on hemodynamic function and markers of arterial stiffness (including carotid-femoral pulse wave velocity, augmentation index, forward and backward wave reflection amplitude, and wave reflection magnitude) in a four-arm, randomized study of healthy young adults.Results: Carotid-femoral pulse wave velocity increased only during hyperglycemic-hyperinsulinemia (+0.36 m/s; p=0.032), while other markers of arterial stiffness did not change (all p>0.05). Heart rate (+3.62 bpm; p=0.009), mean arterial pressure (+4.14 mmHg; p=0.033), central diastolic blood pressure (+4.16 mmHg; p=0.038), and peripheral diastolic blood pressure (+4.09 mmHg; p=0.044) also significantly increased during hyperglycemic-hyperinsulinemia.Conclusions: Hyperglycemic-hyperinsulinemia acutely increased cfPWV, heart rate, mean arterial pressure, and diastolic blood pressure in healthy humans, perhaps reflecting enhanced sympathetic tone. Whether repeated bouts of hyperglycemia with hyperinsulinemia contribute to chronically-enhanced arterial stiffness remains unknown. (ClinicalTrials.gov number NCT03520569; registered 9 May 2018).Clinical Trial Information: ClinicalTrials.gov identifier NCT03520569 (registered 9 May 2018).


2021 ◽  
Vol 18 (2) ◽  
pp. 147916412110110
Author(s):  
William B Horton ◽  
Linda A Jahn ◽  
Lee M Hartline ◽  
Kevin W Aylor ◽  
James T Patrie ◽  
...  

Introduction: Increasing arterial stiffness is a feature of vascular aging that is accelerated by conditions that enhance cardiovascular risk, including diabetes mellitus. Multiple studies demonstrate divergence of carotid-femoral pulse wave velocity and augmentation index in persons with diabetes mellitus, though mechanisms responsible for this are unclear. Materials and methods: We tested the effect of acutely and independently increasing plasma glucose, plasma insulin, or both on hemodynamic function and markers of arterial stiffness (including carotid-femoral pulse wave velocity, augmentation index, forward and backward wave reflection amplitude, and wave reflection magnitude) in a four-arm, randomized study of healthy young adults. Results: Carotid-femoral pulse wave velocity increased only during hyperglycemic-hyperinsulinemia (+0.36 m/s; p = 0.032), while other markers of arterial stiffness did not change (all p > 0.05). Heart rate (+3.62 bpm; p = 0.009), mean arterial pressure (+4.14 mmHg; p = 0.033), central diastolic blood pressure (+4.16 mmHg; p = 0.038), and peripheral diastolic blood pressure (+4.09 mmHg; p = 0.044) also significantly increased during hyperglycemic-hyperinsulinemia. Conclusions: Hyperglycemic-hyperinsulinemia acutely increased cfPWV, heart rate, mean arterial pressure, and diastolic blood pressure in healthy humans, perhaps reflecting enhanced sympathetic tone. Whether repeated bouts of hyperglycemia with hyperinsulinemia contribute to chronically-enhanced arterial stiffness remains unknown.


2020 ◽  
Vol 38 (10) ◽  
pp. 2000-2007 ◽  
Author(s):  
Hirofumi Tomiyama ◽  
Kazuki Shiina ◽  
Hiroki Nakano ◽  
Yoichi Iwasaki ◽  
Chisa Matsumoto ◽  
...  

2021 ◽  
Author(s):  
William B Horton ◽  
Linda A Jahn ◽  
Lee M Hartline ◽  
Kevin W Aylor ◽  
Eugene J Barrett

Abstract Introduction: Increasing arterial stiffness is a feature of vascular aging that is accelerated by conditions that enhance cardiovascular risk, including diabetes mellitus. Multiple studies demonstrate divergence of carotid-femoral pulse wave velocity and augmentation index in persons with diabetes mellitus, though mechanisms responsible for this are unclear.Materials and Methods: We tested the effect of acutely and independently increasing plasma glucose, plasma insulin, or both on hemodynamic function and markers of arterial stiffness (including carotid-femoral pulse wave velocity, augmentation index, forward and backward wave reflection amplitude, and wave reflection magnitude) in a four-arm, randomized study of healthy young adults.Results: Carotid-femoral pulse wave velocity increased only during hyperglycemic-hyperinsulinemia (+0.36 m/s; p=0.032), while other markers of arterial stiffness did not change (all p>0.05). Heart rate (+3.62 bpm; p=0.009), mean arterial pressure (+4.14 mmHg; p=0.033), central diastolic blood pressure (+4.16 mmHg; p=0.038), and peripheral diastolic blood pressure (+4.09 mmHg; p=0.044) also significantly increased during hyperglycemic-hyperinsulinemia.Conclusions: We conclude that the acute combination of moderate hyperglycemia and hyperinsulinemia preferentially stiffens central elastic arteries. This effect may be due to increased sympathetic activity. (ClinicalTrials.gov number NCT03520569; registered 9 May 2018).


2016 ◽  
Vol 116 (2) ◽  
pp. 279-285 ◽  
Author(s):  
Arturo Figueroa ◽  
Stacey Alvarez-Alvarado ◽  
Salvador J. Jaime ◽  
Roy Kalfon

AbstractCombined isometric exercise or metaboreflex activation (post-exercise muscle ischaemia (PEMI)) and cold pressor test (CPT) increase cardiac afterload, which may lead to adverse cardiovascular events. l-Citrulline supplementation (l-CIT) reduces systemic arterial stiffness (brachial-ankle pulse wave velocity (baPWV)) at rest and aortic haemodynamic responses to CPT. The aim of this study was to determine the effect of l-CIT on aortic haemodynamic and baPWV responses to PEMI+CPT. In all, sixteen healthy, overweight/obese males (age 24 (sem 6) years; BMI 29·3 (sem 4·0) kg/m2) were randomly assigned to placebo or l-CIT (6 g/d) for 14 d in a cross-over design. Brachial and aortic systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP), aortic augmented pressure (AP), augmentation index (AIx), baPWV, reflection timing (Tr) and heart rate (HR) were evaluated at rest and during isometric handgrip exercise (IHG), PEMI and PEMI+CPT at baseline and after 14 d. No significant effects were evident after l-CIT at rest. l-CIT attenuated the increases in aortic SBP and wave reflection (AP and AIx) during IHG, aortic DBP, MAP and AIx during PEMI, and aortic SBP, DBP, MAP, AP, AIx and baPWV during PEMI+CPT compared with placebo. HR and Tr were unaffected by l-CIT in all conditions. Our findings demonstrate that l-CIT attenuates aortic blood pressure and wave reflection responses to exercise-related metabolites. Moreover, l-CIT attenuates the exaggerated arterial stiffness response to combined metaboreflex activation and cold exposure, suggesting a protective effect against increased cardiac afterload during physical stress.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paulo Farinatti ◽  
Alex da Silva Itaborahy ◽  
Tainah de Paula ◽  
Walace David Monteiro ◽  
Mário F. Neves

AbstractThe acute effects of exercise modes on pulse wave reflection (PWR) and their relationship with autonomic control remain undefined, particularly in individuals with elevated blood pressure (BP). We compared PWR and autonomic modulation after acute aerobic (AE), resistance (RE), and concurrent exercise (CE) in 15 men with stage-1 hypertension (mean ± SE: 34.7 ± 2.5 years, 28.4 ± 0.6 kg/m2, 133 ± 1/82 ± 2 mmHg). Participants underwent AE, RE, and CE on different days in counterbalanced order. Applanation tonometry and heart rate variability assessments were performed before and 30-min postexercise. Aortic pressure decreased after AE (− 2.4 ± 0.7 mmHg; P = 0.01), RE (− 2.2 ± 0.6 mmHg; P = 0.03), and CE (− 3.1 ± 0.5 mmHg; P = 0.003). Augmentation index remained stable after RE, but lowered after AE (− 5.1 ± 1.7%; P = 0.03) and CE (− 7.6 ± 2.4% P = 0.002). Systolic BP reduction occurred after CE (− 5.3 ± 1.9 mmHg). RR-intervals and parasympathetic modulation lowered after all conditions (~ 30–40%; P < 0.05), while the sympathovagal balance increased after RE (1.2 ± 0.3–1.3 ± 0.3 n.u., P < 0.05). Changes in PWR correlated inversely with sympathetic and directly with vagal modulation in CE. In conclusion, AE, RE, and CE lowered central aortic pressure, but only AE and CE reduced PWR. Overall, those reductions related to decreased parasympathetic and increased sympathetic outflows. Autonomic fluctuations seemed to represent more a consequence than a cause of reduced PWR.


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