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Amsterdam, Netherlands

OBJECTIVE: The aim of this study was to validate the hyperbaric index (HBI) for first trimester prediction of preeclampsia and gestational hypertension. METHODS: Participants were low-risk and high-risk nulliparous women and high-risk multiparous women, and were recruited between April 2004 and June 2006. At a gestational age of 9 weeks (range 8-11 weeks), blood pressure (BP) was measured first by sphygmomanometry and thereafter by ambulatory BP measurement (ABPM) for 48 h. The first 90 low-risk women who had an uneventful pregnancy formed the reference group for calculation of a time-specified tolerance interval with 90% confidence limits. In the validation group, consisting of the remaining women, the HBI was calculated as the time-specified BP excess over this tolerance limit for SBP, DBP and mean arterial pressure. RESULTS: The validation group contained 101 women. Fifteen women developed preeclampsia and 13 developed gestational hypertension. For preeclampsia, the maximum HBI had the best predictive capacity with a sensitivity of 73% and a specificity of 86%. However, the difference with standard ABPM measurement or sphygmomanometry was small with a sensitivity between 75 and 73% and a specificity between 86 and 95%. The predictive efficacy for gestational hypertension was poor with all methods (sensitivity between 54 and 77%, specificity between 41 and 78%). CONCLUSION: Standardized sphygmomanometry, ABPM measurement and the HBI calculated from 48-h ABPM had a comparable, restricted predictive efficacy. The high predictive value of HBI as observed in earlier studies could not be reproduced. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source


Westerhof N.,VU University Amsterdam | Westerhof B.E.,BMEYE Inc | Westerhof B.E.,Heart Failure Research Center
Journal of Hypertension | Year: 2013

Objectives: In treatment of hypertension not only the pressure response is of interest, but also the effect on arterial parameters, for example, stiffness and resistance, is essential. We therefore reviewed what quantitative information on arterial stiffness can be obtained from pressure wave analysis. Methods: Using data from published large cohort studies, we derived relations between stiffness and the pressure-derived variables systolic pressure, pulse pressure, augmentation index (AIx), return time of reflected wave and reflection magnitude. Results: All pressure-derived variables give limited information on arterial function in terms of stiffness and resistance, except AIx (in low stiffness range only). Input impedance as a comprehensive description of the arterial system is too complex to derive and interpret in practice, but is accurately described by three parameters: systemic vascular resistance, total arterial stiffness, and aortic characteristic impedance (outflow tract size and proximal aortic stiffness). These parameters predict aortic pressure well in terms of magnitude and shape: with measured flow the predicted (p) and measured (m) systolic, Ps, and diastolic, Pd pressures relate as P sp = 0.997Psm- 1.63 and Pd, p = 1.03P dm-3.12mmHg (n=17). Therefore, methods should be developed to determine, preferably noninvasively, these three arterial parameters. Conclusion: Variables derived from pressure wave shape alone (e.g. inflection point, AIx among others), and wave separation (e.g. reflection magnitude), while predicting cardiovascular events, give little information on arterial function. We propose to develop new, and improve existing, noninvasive methods to determine systemic vascular resistance, total arterial stiffness, and aortic characteristic impedance. This will allow quantifying the response of arterial function to treatment. © 2013 Wolters Kluwer Health Lippincott Williams & Wilkins. Source


Bronzwaer A.-S.G.T.,University of Amsterdam | Bronzwaer A.-S.G.T.,Center for Heart Failure Research | Stok W.J.,Center for Heart Failure Research | Stok W.J.,University of Amsterdam | And 5 more authors.
Frontiers in Physiology | Year: 2014

Rationale: A critical reduction in central blood volume (CBV) is often characterized by hemodynamic instability. Restoration of a volume deficit may be established by goal-directed fluid therapy guided by respiration-related variation in systolic- and pulse pressure (SPV and PPV). Stroke volume index (SVI) serves as a surrogate end-point of a fluid challenge but tissue perfusion itself has not been addressed. Objective: To delineate the relationship between arterial pressure variations, SVI and regional brain perfusion during CBV depletion and repletion in spontaneously breathing volunteers. Methods: This study quantified in 14 healthy subjects (11 male) the effects of CBV depletion [by 30 and 70 degrees passive head-up tilt (HUT)] and a fluid challenge (by tilt back) on CBV (thoracic admittance), mean middle cerebral artery (MCA) blood flow velocity (Vmean), SVI, cardiac index (CI), PPV, and SPV. Results: PPV (103 ± 89%, p < 0.05) and SPV (136 ± 117%, p < 0.05) increased with progression of central hypovolemia manifested by a reduction in thoracic admittance (11 ± 5%, p < 0.001), SVI (28 ± 6%, p < 0.001), CI (6 ± 8%, p < 0.001), and MCAVmean (17 ± 7%, p < 0.05) but not in arterial pressure. The reduction in MCAVmean correlated to the fall in SVI (R2 = 0.52, p < 0.0001) and inversely to PPV and SPV [R2 = 0.46 (p < 0.0001) and R2 = 0.45 (p < 0.0001), respectively]. PPV and SPV predicted a =15% reduction in MCAVmean and SVI with comparable sensitivity (67/67% vs. 63/68%, respectively) and specificity (89/94 vs. 89/94%, respectively). A rapid fluid challenge by tilt-back restored all parameters to baseline values within 1 min. Conclusion: In spontaneously breathing subjects, a reduction in MCAVmean was related to an increase in PPV and SPV during graded CBV depletion and repletion. Specifically, PPV and SPV predicted changes in both SVI and MCAVmean with comparable sensitivity and specificity, however the predictive value is limited in spontaneously breathing subjects. © 2014 Bronzwaer, Stok, Westerhof and van Lieshout. Source


Westerhof B.E.,BMEYE Inc | Westerhof B.E.,University of Amsterdam
Journal of Hypertension | Year: 2013

BACKGROUND:: The vasodilating beta-blocker nebivolol is thought to be superior in lowering wave reflection and central blood pressure (BP) compared to nonvasodilating beta-blockers. The results from studies comparing nebivolol with either metoprolol or atenolol, with or without hydrochlorothiazide (HCTZ), are not unequivocal. METHODS:: We examined the effects of nebivolol 5âŠmg and metoprolol 100âŠmg with HCTZ 12.5âŠmg on aortic wave augmentation, central BP and hemodynamics using a randomized, double-blind, crossover design. We included 22 patients (17 men, age 59.9⊱âŠ6.4 years) with office SBP of 155⊱âŠ16âŠmmHg and DBP of 93⊱âŠ10âŠmmHg. Radial applanation tonometry and noninvasive, continuous finger arterial BP measurement was performed at baseline and after 4 weeks of treatment with either drug regimen, separated by a 4-week washout period. RESULTS:: Neither treatment affected aortic wave augmentation significantly. Augmentation index increased 1.0⊱âŠ7.8% (PâŠ= âŠ0.5) for nebivolol/HCTZ and 2. 4⊱âŠ6.6% (PâŠ=âŠ0. 07) for metoprolol/HCTZ. Nebivolol/HCTZ lowered central SBP by 15.8⊱âŠ14.9âŠmmHg and DBP 10.5⊱âŠ8.4âŠmmHg, and with metoprolol/HCTZ by 13.5⊱âŠ12. 3âŠmmHg for SBP and 9.5⊱âŠ6. 8âŠmmHg for DBP (all PâŠ<âŠ0.001). Heart rate was lowered 8.1⊱âŠ5.4 beats/min by nebivolol/HCTZ and 8.6⊱âŠ4.9 beats/min by metoprolol/HCTZ. Peripheral BP was reduced to a similar extent as central BP. Peripheral BP decreased by 16.3⊱âŠ14. 9âŠmmHg systolic and 10.1⊱âŠ8. 2âŠmmHg diastolic with nebivolol/HCTZ, and by 15. 2⊱â̌13.0â̌mmHg systolic and 9.1â̌±âŠ6.9 mmHg diastolic with metoprolol/HCTZ. Both treatment modalities had a similar effect on stroke volume, cardiac output, left-ventricular contractility and peripheral resistance. CONCLUSION:: Nebivolol was not superior to metoprolol in reducing aortic wave augmentation or central BP when combined with HCTZ. © 2013 Wolkers Kluwer Health. Source


Westerhof N.,VU University Amsterdam | Segers P.,Ghent University | Westerhof B.E.,BMEYE Inc | Westerhof B.E.,Heart Failure Research Center
Hypertension | Year: 2015

Wave separation analysis and wave intensity analysis (WIA) use (aortic) pressure and flow to separate them in their forward and backward (reflected) waves. While wave separation analysis uses measured pressure and flow, WIA uses their derivatives. Because differentiation emphasizes rapid changes, WIA suppresses slow (diastolic) fluctuations of the waves and renders diastole a seemingly wave-free period. However, integration of the WIA-obtained forward and backward waves is equal to the wave separation analysis-obtained waves. Both the methods thus give similar results including backward waves spanning systole and diastole. Nevertheless, this seemingly wave-free period in diastole formed the basis of both the reservoir-wave concept and the Instantaneous wave-Free Ratio of (iFR) pressure and flow. The reservoir-wave concept introduces a reservoir pressure, Pres, (Frank Windkessel) as a wave-less phenomenon. Because this Windkessel model falls short in systole an excess pressure, Pexc, is introduced, which is assumed to have wave properties. The reservoir-wave concept, however, is internally inconsistent. The presumed wave-less Pres equals twice the backward pressure wave and travels, arriving later in the distal aorta. Hence, in contrast, Pexc is minimally affected by wave reflections. Taken together, Pres seems to behave as a wave, rather than Pexc. The iFR is also not without flaws, as easily demonstrated when applied to the aorta. The ratio of diastolic aortic pressure and flow implies division by zero giving nonsensical results. In conclusion, presumptions based on WIA have led to misconceptions that violate physical principles, and reservoir-wave concept and iFR should be abandoned. © 2015 American Heart Association, Inc. Source

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