118 research outputs found

    Comment on 'Numerical assessment and comparison of pulse wave velocity methods aiming at measuring aortic stiffness'

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    A recent numerical study investigated the potential utility of peripheral PWV measurements for assessing aortic stiffness by simulating pulse wave propagation through the arterial tree. In this Comment we provide additional analysis of the simulations in which arterial compliances were changed. The analysis indicates that relationships between aortic and peripheral pulse transit times (PTTs) may not be constant when compliances change. Consequently, peripheral PWV measurements may have greatest utility in particular clinical settings in which either: an assumption can be made about possible changes in compliance, allowing aortic PTT to be estimated from peripheral PTT; or, one wishes to assess changes in peripheral PWV over time

    RELATION OF PULSE WAVE VELOCITY TO CONTEMPORANEOUS AND HISTORICAL BLOOD PRESSURE IN FEMALE TWINS:Arterial Stiffness and Blood Pressure

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    An association between blood pressure and aortic stiffness is well known, but ambiguity remains as to whether one precedes the other. This study aimed to investigate the association of aortic stiffness with contemporaneous versus historic blood pressure and direction of causality between aortic stiffening and hypertension in female twins. METHODS: Aortic stiffness, measured by carotid-femoral pulse wave velocity (PWV), and mean arterial pressure (MAP) was recorded in 2037 female TwinsUK participants (mean age: 62.4±9.7 years) at a single time point. A subset of 947 participants had repeat PWV and MAP measures (mean interval 5.5±1.7 years) with additional historic MAP (mean interval 6.6±3.3 years before baseline). RESULTS: Cross-sectional multivariable linear regression analysis confirmed PWV significantly associated with age and MAP. In longitudinal analysis, annual progression of PWV was not associated with historic MAP (standardized beta coefficient [β]=-0.02, P=0.698), weakly associated with baseline MAP (β=0.09, P=0.049) but strongly associated with progression (from baseline to most recent measurement) of MAP (β= 0.26, P<0.001). Progression of MAP associated with both baseline and progression of PWV (β=0.13, P=0.003 and β=0.24, P<0.001, respectively). CONCLUSIONS: Progression of aortic stiffness associates more strongly with contemporaneous MAP compared with historic MAP. In contrast, progression of MAP is associated with prior arterial stiffness. These findings suggest a bidirectional relationship between arterial stiffness and blood pressure, and that lowering blood pressure may prevent a cycle of arterial stiffening and hypertension

    Cardiac contractility is a key factor in determining pulse pressure and its peripheral amplification

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    Background: Arterial stiffening and peripheral wave reflections have been considered the major determinants of raised pulse pressure (PP) and isolated systolic hypertension, but the importance of cardiac contractility and ventricular ejection dynamics is also recognised.Methods: We examined the contributions of arterial compliance and ventricular contractility to variations in aortic flow and increased central (cPP) and peripheral (pPP) pulse pressure, and PP amplification (PPa) in normotensive subjects during pharmacological modulation of physiology, in hypertensive subjects, and in silico using a cardiovascular model accounting for ventricular-aortic coupling. Reflections at the aortic root and from downstream vessels were quantified using emission and reflection coefficients, respectively.Results: cPP was strongly associated with contractility and compliance, whereas pPP and PPa were strongly associated with contractility. Increased contractility by inotropic stimulation increased peak aortic flow (323.9 +/- 52.8 vs. 389.1 +/- 65.1 ml/s), and the rate of increase (3193.6 +/- 793.0 vs. 4848.3 +/- 450.4 ml/s(2)) in aortic flow, leading to larger cPP (36.1 +/- 8.8 vs. 59.0 +/- 10.8 mmHg), pPP (56.9 +/- 13.1 vs. 93.0 +/- 17.0 mmHg) and PPa (20.8 +/- 4.8 vs. 34.0 +/- 7.3 mmHg). Increased compliance by vasodilation decreased cPP (62.2 +/- 20.2 vs. 45.2 +/- 17.8 mmHg) without altering dP/dt, pPP or PPa. The emission coefficient changed with increasing cPP, but the reflection coefficient did not. These results agreed with in silico data obtained by independently changing contractility/compliance over the range observed in vivo.Conclusions: Ventricular contractility plays a key role in raising and amplifying PP, by altering aortic flow wave morphology

    Increased potassium intake from fruit and vegetables or supplements does not lower blood pressure or improve vascular function in UK men and women with early hypertension: a randomised controlled trial

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    K-rich fruit and vegetables may lower blood pressure (BP) and improve vascular function. A randomised controlled trial (ISRCTN50011192) with a cross-over design was conducted in free-living participants with early stages of hypertension (diastolic BP . 80 and , 100 mmHg, not receiving BP-lowering medication) to test this hypothesis. Following a 3-week run-in period on a control diet, each subject completed four dietary 6-week dietary interventions (control þ placebo capsules, an additional 20 or 40 mmol K þ /d from fruit and vegetables or 40 mmol potassium citrate capsules/d) using a Latin square design with a washout period $ 5 weeks between the treatment periods. Out of fifty-seven subjects who were randomised, twenty-three male and twenty-five female participants completed the study; compliance to the intervention was corroborated by food intake records and increased urinary K þ excretion; plasma lipids, vitamin C, folate and homocysteine concentrations, urinary Na excretion, and body weight remained were unchanged. On the control diet, mean ambulatory 24 h systolic/diastolic BP were 132·3 (SD 12·0)/81·9 (SD 7·9) mmHg, and changes (Bonferroni&apos;s adjusted 95 % CI) compared with the control on the diets providing 20 and 40 mmol K þ /d as fruit and vegetables were 0·8 (23·5, 5·3)/0·8 (21·9, 3·5) and 1·7 (2 3·0, 5·3)/1·5 (2 1·5, 4·4), respectively, and were 1·8 (2 2·1, 5·8)/1·4 (2 1·6, 4·4) mmHg on the 40 mmol potassium citrate supplement, and were not statistically significant. Arterial stiffness, endothelial function, and urinary and plasma isoprostane and C-reactive protein (CRP) concentrations did not differ significantly between the diets. The present study provides no evidence to support dietary advice to increase K intake above usual UK intakes in the subjects with early stages of hypertension
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