Abstract 2994: Gender-Related Differences in the Central Arterial Pressure Waveform Begin in Childhood and are Independent of Height

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Julian G Ayer ◽  
Albert Avolio ◽  
Guy Marks ◽  
Jason A Harmer ◽  
David S Celermajer

Introduction Women develop age-related LV hypertrophy and symptomatic heart failure to a greater extent than men. Contributing to this may be a higher pulsatile afterload in women, with a higher central arterial systolic augmentation pressure (AP, peak pressure minus pressure at systolic shoulder) and augmentation index (AIx, ratio of AP to pulse pressure). It is unclear if these differences are due to gender per se or shorter female stature. We studied 8-year old children to determine if gender-related differences in carotid pressure augmentation are present in early life and if so, whether they are independent of height (Ht). Methods 406 children (age 8.0 ± 0.1, 49% girls) had anthropometry, brachial systolic and diastolic BP (SBP, DBP), heart rate (HR) and carotid and radial pressure waveforms (by applanation tonometry, calibrated to mean BP and DBP) assessed. Carotid ultrasound evaluated arterial elasticity [Carotid Artery Compliance (CAC), Stiffness Index (SI) and Young’s Elastic Modulus (YEM)]. Results Boys and girls had a similar Ht (129 ± 6 v 128 ± 6 cm), BMI (17.6 ± 3.1 v 17.5 ± 3.0), SBP (100 ± 7 v 101 ± 5 mmHg), DBP (59 ± 6 v 60 ± 5 mmHg) and HR (80 ± 10 v 82 ± 10 bpm). The carotid AP and AIx were significantly higher in girls (−4 ± 3 v −6 ± 4 mmHg and −12 ± 8 v −16 ± 9 respectively, p < 0.001), indicating greater systolic pressure augmentation. Time to onset of the reflected wave ( Tr ) and time to peak of the reflected wave were shorter in girls (154 ± 19 v 163 ± 18 msec, p < 0.001 and 206 ± 23 v 212 ± 22 msec, p = 0.03 respectively), indicating earlier wave reflection. Girls had a higher velocity index (Vr) estimated from Ht ( Vr = Ht /Tr , 8.4 ± 1.0 v 8.0 ± 0.9 m/sec, p = 0.001). Ejection duration, maximum rate of pressure rise and time to systolic peak (indicating effect of ventricular ejection on the carotid waveform) were not significantly different between genders. Boys, however, had stiffer carotid arteries than girls [lower CAC (5.8 ± 1.5 v 6.2 ± 1.8 %/10 mmHg, p = 0.016), higher SI (2.7 ± 0.7 v 2.5 ± 0.7, p = 0.012) and YEM (735 ± 217 v 681 ± 237, p = 0.021)]. Conclusion Even in the first decade of life, girls demonstrate greater central arterial pressure augmentation than boys, with earlier wave reflection. This is independent of height and may contribute to cardiovascular morbidity in females, later in life.

2008 ◽  
Vol 294 (6) ◽  
pp. H2535-H2539 ◽  
Author(s):  
David G. Edwards ◽  
Matthew S. Roy ◽  
Raju Y. Prasad

Cardiovascular events are more common in the winter months, possibly because of hemodynamic alterations in response to cold exposure. The purpose of this study was to determine the effect of acute facial cooling on central aortic pressure, arterial stiffness, and wave reflection. Twelve healthy subjects (age 23 ± 3 yr; 6 men, 6 women) underwent supine measurements of carotid-femoral pulse wave velocity (PWV), brachial artery blood pressure, and central aortic pressure (via the synthesis of a central aortic pressure waveform by radial artery applanation tonometry and generalized transfer function) during a control trial (supine rest) and a facial cooling trial (0°C gel pack). Aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform. Measurements were made at baseline, 2 min, and 7 min during each trial. Facial cooling increased ( P < 0.05) peripheral and central diastolic and systolic pressures. Central systolic pressure increased more than peripheral systolic pressure (22 ± 3 vs. 15 ± 2 mmHg; P < 0.05), resulting in decreased pulse pressure amplification ratio. Facial cooling resulted in a robust increase in AI and a modest increase in PWV (AI: −1.4 ± 3.8 vs. 21.2 ± 3.0 and 19.9 ± 3.6%; PWV: 5.6 ± 0.2 vs. 6.5 ± 0.3 and 6.2 ± 0.2 m/s; P < 0.05). Change in mean arterial pressure but not PWV predicted the change in AI, suggesting that facial cooling may increase AI independent of aortic PWV. Facial cooling and the resulting peripheral vasoconstriction are associated with an increase in wave reflection and augmentation of central systolic pressure, potentially explaining ischemia and cardiovascular events in the cold.


2014 ◽  
Vol 34 (6) ◽  
pp. 971-978 ◽  
Author(s):  
Takashi Tarumi ◽  
Muhammad Ayaz Khan ◽  
Jie Liu ◽  
Benjamin M Tseng ◽  
Rosemary Parker ◽  
...  

Blood ejected from the left ventricle perfuses the brain via central elastic arteries, which stiffen with advancing age and may elevate the risk of end-organ damage. The purpose of this study was to determine the impact of central arterial aging on cerebral hemodynamics. Eighty-three healthy participants aged 22 to 80 years underwent the measurements of cerebral blood flow (CBF) and CBF velocity (CBFV) using magnetic resonance imaging (MRI) and transcranial Doppler, respectively. The CBF pulsatility was determined by the relative amplitude of CBFV to the mean value (CBFV%). Central arterial stiffness (carotid-femoral pulse wave velocity), wave reflection (carotid augmentation index), and pressure were measured using applanation tonometry. Total volume of white-matter hyperintensity (WMH) was quantified from MR images. Total CBF decreased with age while systolic and pulsatile CBFV% increased and diastolic CBFV% decreased. Women showed greater total CBF and lower cerebrovascular resistance than men. Diastolic CBFV% was lower in women than in men. Age- and sex-related differences in CBF pulsatility were independently associated with carotid pulse pressure and arterial wave reflection. In older participants, higher pulsatility of CBF was associated with the greater total volume of WMH. These findings indicate that central arterial aging has an important role in age-related differences in cerebral hemodynamics.


2006 ◽  
Vol 100 (4) ◽  
pp. 1210-1214 ◽  
Author(s):  
David G. Edwards ◽  
Amie L. Gauthier ◽  
Melissa A. Hayman ◽  
Jesse T. Lang ◽  
Robert W. Kenefick

The purpose of this study was to determine the effects of acute cold exposure on the timing and amplitude of central aortic wave reflection and central pressure. We hypothesized that cold exposure would result in an early return of reflected pressure waves from the periphery and an increase in central aortic systolic pressure as a result of cold-induced vasoconstriction. Twelve apparently healthy men (age 27.8 ± 2.0 yr) were studied at random, in either temperate (24°C) or cold (4°C) conditions. Measurements of brachial artery blood pressure and the synthesis of a central aortic pressure waveform (by noninvasive radial artery applanation tonometry and use of a generalized transfer) were conducted at baseline and after 30 min in each condition. Central aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform. Cold induced an increase ( P < 0.05) in AI from 3.4 ± 1.9 to 19.4 ± 1.8%. Cold increased ( P < 0.05) both brachial and central systolic pressure; however, the magnitude of change in central systolic pressure was greater ( P < 0.05) than brachial (13 vs. 2.5%). These results demonstrate that cold exposure and the resulting peripheral vasoconstriction increase wave reflection and central systolic pressure. Additionally, alterations in central pressure during cold exposure were not evident from measures of brachial blood pressure.


2019 ◽  
Vol 12 (2) ◽  
pp. 94-99
Author(s):  
Rene D. Mileva-Popova ◽  
Nina Y. Belova

Summary Vascular-ventricular coupling is a major determinant of left ventricular load. The aim of our study was to assess non- invasively left ventricular load and its dependency on central hemodynamics. Sixty-five healthy and gender-matched individuals were divided in two groups according to their age: 20y/o and 50y/o. Applanation tonometry was performed using the Sphygmocor device. Central pressures and pulse wave analysis indices were computed. Central systolic (120±3 vs. 98±2 mm Hg) and pulse pressures (43±3 vs. 29±1 mm Hg) as well as the augmentation index (AIx75) (23±3 vs. 6±2%) were significantly higher in the 50y/o group (p<0.01). These parameters are relevant markers of arterial stiffness and evidenced the development of central arterial morphological and functional alterations in the older subjects. The time-tension index (TTI) computed from the systolic pressure area was significantly higher in the 50y/o subjects as compared to the 20y/o group (2378±66 vs. 1954±73 mmHg×s, p<0.01). Moreover, we have shown the presence of significant correlation between TTI and AIx75 (p<0.01) in both age groups. This finding confirmed the contribution of arterial stiffness for the impaired vascular-ventricular coupling. In conclusion, applanation tonometry might be utilized for non-invasive evaluation of the left ventricular load, which is an important parameter of cardiovascular risk.


2006 ◽  
Vol 84 (10) ◽  
pp. 985-991 ◽  
Author(s):  
T.V. Kondratiev ◽  
T. Tveita

This experimental study was performed to explore hemodynamic effects of a moderate dose epinephrine (Epi) during hypothermia and to test the hypothesis whether sympathetic stimulation during cooling affects myocardial function following rewarming. Two groups of male Wistar rats (each, n = 7) were cooled to 15 °C, maintained at this temperature for 1 h, and then rewarmed. Group 1 received 1 μg/min Epi, i.v., for 1 h during cooling to 28 °C, a dose known to elevate cardiac output (CO) by approximately 25% at 37 °C. Group 2 served a saline solution control. At 37 °C, Epi infusion elevated CO, left ventricular systolic pressure, maximum rate of left ventricle pressure rise, and mean arterial pressure. During cooling to 28 °C, these variables, with the exception of mean arterial pressure, decreased in parallel to those in the saline solution group. In contrast, in the Epi group, mean arterial pressure remained increased and total peripheral resistance was significantly elevated at 28 °C. Compared with corresponding prehypothermic values, most hemodynamic variables were lowered after 1 h at 15 °C in both groups (except for stroke volume). After rewarming, alterations in hemodynamic variables in the Epi-treated group were more prominent than in saline solution controls. Thus, before cooling, continuous Epi infusion predominantly stimulates myocardial mechanical function, materialized as elevation of CO, left ventricular systolic pressure, and maximum rate of left ventricle pressure rise. Cooling, on the other hand, apparently eradicates central hemodynamic effects of Epi and during stable hypothermia, elevation of peripheral vascular vasopressor effects seem to take over. In contrast to temperature-matched, non-Epi stimulated control rats, a significant depression of myocardial mechanical function occurs during rewarming following a moderate sympathetic stimulus during initial cooling.


2010 ◽  
Vol 298 (2) ◽  
pp. H580-H586 ◽  
Author(s):  
Justin E. Davies ◽  
John Baksi ◽  
Darrel P. Francis ◽  
Nearchos Hadjiloizou ◽  
Zachary I. Whinnett ◽  
...  

The augmentation index predicts cardiovascular mortality and is usually explained as a distally reflected wave adding to the forward wave generated by systole. We propose that the capacitative properties of the aorta (the arterial reservoir) also contribute significantly to the augmentation index and have calculated the contribution of the arterial reservoir, independently of wave reflection, and assessed how these contributions change with aging. In 15 subjects (aged 53 ± 10 yr), we measured pressure and Doppler velocity simultaneously in the proximal aorta using intra-arterial wires. We calculated the components of augmentation pressure in two ways: 1) into forward and backward (reflected) components by established separation methods, and 2) using an approach that accounts for an additional reservoir component. When the reservoir was ignored, augmentation pressure (22.7 ± 13.9 mmHg) comprised a small forward wave (peak pressure = 6.5 ± 9.4 mmHg) and a larger backward wave (peak pressure = 16.2 ± 7.6 mmHg). After we took account of the reservoir, the contribution to augmentation pressure of the backward wave was reduced by 64% to 5.8 ± 4.4 mmHg ( P < 0.001), forward pressure was negligible, and reservoir pressure was the largest component (peak pressure = 19.8 ± 9.3 mmHg). With age, reservoir pressure increased progressively (9.9 mmHg/decade, r = 0.69, P < 0.001). In conclusion, the augmentation index is principally determined by aortic reservoir function and other elastic arteries and only to a minor extent by reflected waves. Reservoir function rather than wave reflection changes markedly with aging, which accounts for the age-related changes in the aortic pressure waveform.


2002 ◽  
Vol 103 (5) ◽  
pp. 493-499 ◽  
Author(s):  
Alison J. DEARY ◽  
Anne L. SCHUMANN ◽  
Helen MURFET ◽  
Stephen HAYDOCK ◽  
Roger S. FOO ◽  
...  

Recent studies have suggested a differential influence of mean pressure and pulse pressure on myocardial infarction and stroke, and differences among the major drugs in their efficacy at preventing these individual endpoints. We hypothesized that antihypertensive drugs have differing influences upon the pulse wave even when their effects on blood pressure are the same. We studied 30 untreated hypertensive patients, aged 28—55 years, who were rotated through six 6-week periods of daily treatment with amlodipine 5mg, doxazosin 4mg, lisinopril 10mg, bisoprolol 5mg, bendrofluazide 2.5mg or placebo. The best drug was repeated at the end of the rotation. Blood pressure readings and radial pulse tonometry (by Sphygmocor®) were performed at each visit, and blood was taken for measurement of levels of atrial natriuretic peptide and brain natriuretic peptide (BNP). The Sphygmocor derivation of the central aortic pulse wave was used to measure time for transmission of the reflected wave (TR) and the augmentation index (AI), which is the proportional increase in systolic pressure due to the reflected wave. There was a dissociation between the effects of the drugs on blood pressure and pulse wave analysis. Bisoprolol caused the greatest falls in blood pressure and TR, but was the only drug to increase AI. This paradoxical response to bisoprolol was associated with a 3-fold increase in plasma BNP levels. There was a smaller elevation of BNP in women compared with men, as described previously, and this elevation also was associated with significantly higher values of AI. Other drugs reduced AI, and this was associated with a significant decrease in BNP by amlodipine. In conclusion, antihypertensive drugs differ in their short-term effects on augmentation of the systolic pulse wave and secretion of BNP from the heart, regarded as a sensitive measure of strain on cardiomyocytes. These differences may help to explain cause-specific differences in outcome in recent trials.


2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Haroon Kamran ◽  
Jason M. Lazar ◽  
Rinkesh Patel ◽  
IIir Maraj ◽  
Heather Berman ◽  
...  

Aging is associated with increased central aortic systolic pressure (CSP) and pulse pressure which are predictive of cardiovascular events. Mechanisms implicated for higher central pressures include a higher forward incident pressure wave (P1), higher augmented pressure (AP), and shorter reflected wave round trip travel time (Tr). African-Americans (AA) have more frequent and deleterious blood pressure elevation. Using applanation tonometry, we studied the association of age and CSP with P1 and AP in 900 AA subjects. Data showed that in subjects ≤50 years old, CSP was mediated by AP but not P1 or Tr, whereas in those >50, CSP was mediated by both AP and P1 and to a lesser extent by Tr. Predictive models were significant () for both age groups. In conclusion, wave reflection is the primary determinant of CSP in younger AA, while in older subjects, CSP is mediated by both the magnitude and timing of wave reflection as well as aortic impedance.


2006 ◽  
Vol 290 (3) ◽  
pp. H1059-H1063 ◽  
Author(s):  
Maria Cristina O. Salgado ◽  
Soraia V. S. Justo ◽  
Luis F. Joaquim ◽  
Rubens Fazan ◽  
Helio C. Salgado

Because the regulation of vascular function involves complex mutual interactions between nitric oxide (NO) synthase (NOS) and cyclooxygenase (COX) products, we examined the contribution of NO and prostanoids derived from the COX pathway in modulating aortic baroreceptor resetting during an acute (30 min) increase in arterial pressure in anesthetized rats. Increase in pressure was induced either by administration of the nonselective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME) or aortic coarctation (COA) with or without treatment with the COX inhibitor indomethacin (INDO) or the selective neuronal NOS inhibitor 1-(2-trifluoromethylphenyl)imidazole (TRIM). The activity of the aortic depressor nerve and arterial pressure were simultaneously recorded, and the degree of resetting was determined by the shift of the pressure-nerve activity curve using the ratio [Δ systolic pressure at 50% of maximum baroreceptor activity/Δ systolic pressure] × 100. The magnitude of pressure rise was similar in the different groups (59 ± 6, 53 ± 5, 53 ± 5, 45 ± 5, 49 ± 3, and 41 ± 3 mmHg for COA, l-NAME, INDO+COA, INDO+l-NAME, TRIM+COA, and TRIM+INDO+COA, respectively, P = 0.27). The degree of resetting that occurred with l-NAME or COA combined with treatment with TRIM was attenuated compared with COA alone (7 ± 4, 5 ± 2, and 31 ± 6%, respectively, P = 0.04). INDO failed to influence baroreceptor resetting to higher pressure but prevented l-NAME- and TRIM-induced effects (20 ± 7, 21 ± 8, and 32 ± 6% for INDO+COA, INDO+l-NAME, and INDO+TRIM+COA, respectively; P = 0.38). Baroreceptor gain was affected only by l-NAME. These findings indicate that NO, probably from neuronal origin, may exert stimulatory influence on the degree of rapid baroreceptor resetting to hypertension that involves COX-derived prostanoids.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Priit Pauklin ◽  
Jaan Eha ◽  
Kaspar Tootsi ◽  
Rein Kolk ◽  
Rain Paju ◽  
...  

Background: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in clinical practice, yet there is a lack of information about the hemodynamic profile and arterial stiffness of these patients. Purpose: The purpose of this study is to describe the differences in arterial stiffness and central blood pressures in patients with paroxysmal/persistent AF compared to a healthy control group. Methods: We included 76 patients with paroxysmal and persistent AF who underwent electrical cardioversion or pulmonary vein isolation (PVI) for AF. Carotid-femoral pulse wave velocity (cfPWV), augmentation index (AIx) and central blood pressure (cBP) were measured by applanation tonometry. All measurements were done in sinus rhythm (SR). We compared the results with 75 healthy age matched individuals. Results: Patients with a history of AF had higher cfPWV compared to the control group (8,0 m/s vs 7,2 m/s, p<0,001). AF patients also had higher central systolic blood pressure (cSBP) (118 mmHg vs 114 mmHg, p=0,03) and central pulse pressure (cPP) (39 mmHg vs 37 mmHg, p=0,03), without differences in peripheral systolic pressure (pSBP) (127 mmHg vs 123 mmHg, p=0,13), peripheral diastolic blood pressure (pDPB) (78 mmHg vs 76 mmHg, p=0,14) and peripheral pulse pressure (pPP) (48 mmHg vs 47 mmHg, p=0,37). There was no difference in heart rate (HR) (58 vs 61 bpm, p=0,08) (Table 1). In a multiple regression analysis (adjusted R 2 = 0,37) where cfPWV was set as the dependent variable and adjusting for age, sex, HR, weight, mean central arterial pressure (cMAP), estimated glomerular filtration rate (eGFR), the AF group remained to be an independent predictor for cfPWV (p=0,016). Conclusions: Patients with atrial fibrillation have a higher cSBP, cPP and cfPWV compared to healthy subjects without differences in peripheral blood pressure and HR. These findings support the hypothesis that arterial stiffness may play an important role in the development of atrial fibrillation.


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