Ambulatory arterial stiffness index is not a stiffness parameter but a ventriculo-arterial coupling factor.
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Arteries↗
Biomedical subjects
Berend E Westerhof
Publications and source records attributed to Berend E Westerhof.
A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations.
The twin-twin transfusion syndrome (TTTS) is a severe complication of monochorionic twin pregnancies caused by a net transfusion of blood from one twin (the donor) to the other (the recipient) through placental anastomoses. To examine the pathophysiology of TTTS evolving through clinical stages I to IV, we extended our mathematical model to include pulsating circulations propagating along the arterial tree as well as placental and cerebral vascular resistances, and arterial wall thickness and stiffness. The model demonstrates that abnormal umbilical arterial flow (TTTS stage III) in the donor twin results from increased placental resistance as well as reduced resistance in the cerebral arteries. In contrast, recipient twin abnormal umbilical arterial flow requires a significantly greater increase in placental resistance, resulting from the compressive effects of high amniotic fluid pressure. Thus simulated abnormalities of donor umbilical arterial pulsations occur in the donor more commonly and earlier than in the recipient. The "normal" staging sequence (I, II, III, IV) correlates with the presence of compensating placental anastomoses, constituting the majority of monochorionic twin placentas. However, TTTS stage III may occur before manifestations of stage II (lack of donor bladder filling), in our model correlating with severe TTTS from a single arteriovenous anastomosis, an infrequent occurring placental angioarchitecture. In conclusion, this mathematical model describes the onset and development of the four stages of TTTS, reproduces a variety of clinical manifestations, and may contribute to identifying the underlying pathophysiology of the staging sequence in TTTS.
Chorion↗
Arterial pressure transfer characteristics: effects of travel time.
We investigated the quantitative contribution of all local conduit arterial, blood, and distal load properties to the pressure transfer function from brachial artery to aorta. The model was based on anatomical data, Young's modulus, wall viscosity, blood viscosity, and blood density. A three-element windkessel represented the distal arterial tree. Sensitivity analysis was performed in terms of frequency and magnitude of the peak of the transfer function and in terms of systolic, diastolic, and pulse pressure in the aorta. The root mean square error (RMSE) described the accuracy in wave-shape prediction. The percent change of these variables for a 25% alteration of each of the model parameters was calculated. Vessel length and diameter are found to be the most important parameters determining pressure transfer. Systolic and diastolic pressure changed <3% and RMSE <1.8 mmHg for a 25% change in vessel length and diameter. To investigate how arterial tapering influences the pressure transfer, a single uniform lossless tube was modeled. This simplification introduced only small errors in systolic and diastolic pressures (1% and 0%, respectively), and wave shape was less well described (RMSE, approximately 2.1 mmHg). Local (arm) vasodilation affects the transfer function little, because it has limited effect on the reflection coefficient. Since vessel length and diameter translate into travel time, this parameter can describe the transfer accurately. We suggest that with a, preferably, noninvasively measured travel time, an accurate individualized description of pressure transfer can be obtained.
Aorta↗
Quantification of wave reflection in the human aorta from pressure alone: a proof of principle.
Wave reflections affect the proximal aortic pressure and flow waves and play a role in systolic hypertension. A measure of wave reflection, receiving much attention, is the augmentation index (AI), the ratio of the secondary rise in pressure and pulse pressure. AI can be limiting, because it depends not only on the magnitude of wave reflection but also on wave shapes and timing of incident and reflected waves. More accurate measures are obtainable after separation of pressure in its forward (P(f)) and reflected (P(b)) components. However, this calculation requires measurement of aortic flow. We explore the possibility of replacing the unknown flow by a triangular wave, with duration equal to ejection time, and peak flow at the inflection point of pressure (F(tIP)) and, for a second analysis, at 30% of ejection time (F(t30)). Wave form analysis gave forward and backward pressure waves. Reflection magnitude (RM) and reflection index (RI) were defined as RM=P(b)/P(f) and RI=P(b)/(P(f)+P(b)), respectively. Healthy subjects, including interventions such as exercise and Valsalva maneuvers, and patients with ischemic heart disease and failure were analyzed. RMs and RIs using F(tIP) and F(t30) were compared with those using measured flow (F(m)). Pressure and flow were recorded with high fidelity pressure and velocity sensors. Relations are: RM(tIP)=0.82RM(mf)+0.06 (R(2)=0.79; n=24), RM(t30)=0.79RM(mf)+0.08 (R(2)=0.85; n=29) and RI(tIP)=0.89RI(mf)+0.02 (R(2)=0.81; n=24), RI(t30)=0.83RI(mf)+0.05 (R(2)=0.88; n=29). We suggest that wave reflection can be derived from uncalibrated aortic pressure alone, even when no clear inflection point is distinguishable and AI cannot be obtained. Epidemiological studies should establish its clinical value.
Adult↗
Time course analysis of baroreflex sensitivity during postural stress.
Postural stress requires immediate autonomic nervous action to maintain blood pressure. We determined time-domain cardiac baroreflex sensitivity (BRS) and time delay (tau) between systolic blood pressure and interbeat interval variations during stepwise changes in the angle of vertical body axis (alpha). The assumption was that with increasing postural stress, BRS becomes attenuated, accompanied by a shift in tau toward higher values. In 10 healthy young volunteers, alpha included 20 degrees head-down tilt (-20 degrees), supine (0 degree), 30 and 70 degrees head-up tilt (30 degrees, 70 degrees), and free standing (90 degrees). Noninvasive blood pressures were analyzed over 6-min periods before and after each change in alpha. The BRS was determined by frequency-domain analysis and with xBRS, a cross-correlation time-domain method. On average, between 28 (-20 degrees) to 45 (90 degrees) xBRS estimates per minute became available. Following a change in alpha, xBRS reached a different mean level in the first minute in 78% of the cases and in 93% after 6 min. With increasing alpha, BRS decreased: BRS = -10.1.sin(alpha) + 18.7 (r(2) = 0.99) with tight correlation between xBRS and cross-spectral gain (r(2) approximately 0.97). Delay tau shifted toward higher values. In conclusion, in healthy subjects the sensitivity of the cardiac baroreflex obtained from time domain decreases linearly with sin(alpha), and the start of baroreflex adaptation to a physiological perturbation like postural stress occurs rapidly. The decreases of BRS and reduction of short tau may be the result of reduced vagal activity with increasing alpha.
Adaptation, Physiological↗
Abnormal arterial flows by a distributed model of the fetal circulation.
Modeling the propagation of blood pressure and flow along the fetoplacental arterial tree may improve interpretation of abnormal flow velocity waveforms in fetuses. The current models, however, either do not include a wide range of gestational ages or do not account for variation in anatomical, vascular, or rheological parameters. We developed a mathematical model of the pulsating fetoumbilical arterial circulation using Womersley's oscillatory flow theory and viscoelastic arterial wall properties. Arterial flow waves are calculated at different arterial locations from which the pulsatility index (PI) can be determined. We varied blood viscosity, placental and brain resistances, placental compliance, heart rate, stiffness of the arterial wall, and length of the umbilical arteries. The PI increases in the umbilical artery and decreases in the cerebral arteries, as a result of increasing placental resistance or decreasing brain resistance. Both changes in resistance decrease the flow through the placenta. An increased arterial stiffness increases the PIs in the entire fetoplacental circulation. Blood viscosity and peripheral bed compliance have limited influence on the flow profiles. Bradycardia and tachycardia increase and decrease the PI in all arteries, respectively. Umbilical arterial length has limited influence on the PI but affects the mean arterial pressure at the placental cord insertion. The model may improve the interpretation of arterial flow pulsations and thus may advance both the understanding of pathophysiological processes and clinical management.
Arteries↗
Changes in finger-aorta pressure transfer function during and after exercise.
Noninvasive finger blood pressure has become a surrogate for central blood pressure under widely varying circumstances. We tested the validity of finger-aorta transfer functions (TF) to reconstruct aortic pressure in seven cardiac patients before, during, and after incremental bicycle exercise. The autoregressive exogenous model method was used for calculating finger-aorta TFs. Finger pressure was measured noninvasively using Finapres and aortic pressure using a catheter-tip manometer. When applying the individual TFs found during rest for reconstruction of aortic pressure during all workloads, systolic pressure was increasingly underestimated, with large variation between subjects: +4.0 to -18.1 mmHg. In most subjects, diastolic pressure was overestimated: -3.9 to +5.5 mmHg. Pulse pressure estimation varied between +4.5 and -21.9 mmHg. In all cases, wave distortion was present. Postexercise, error in reconstructed aortic systolic pressure slowly declined, and diastolic pressure was overestimated. During rest, the TF gain had a minimum between 3.65 and 4.85 Hz (Fmin). During exercise, Fmin shifted to frequencies between 4.95 and 7.15 Hz at the maximum workload, with no change in gain. Postexercise, gain in most subjects shifted to values closer to unity, whereas Fmin did not return to resting values. Within each subject, aorta-Finapres travel time was linearly related to mean pressure. During exercise, Fmin was linearly related to both delay and heart rate. We conclude that, during increasing exercise, rest TFs give an increasingly unreliable reconstruction of aortic pressure, especially at higher heart rates.
Adult↗
Sublingual nitroglycerin used in routine tilt testing provokes a cardiac output-mediated vasovagal response.
OBJECTIVES: We set out to determine the effect of sublingual nitroglycerin (NTG), as used during routine tilt testing in patients with unexplained syncope, on hemodynamic characteristics and baroreflex control of heart rate (HR) and systemic vascular resistance (SVR). BACKGROUND: Nitroglycerin is used in tilt testing to elicit a vasovagal response. It is known to induce venous dilation and enhance pooling. Also, NTG is lipophilic and readily passes cell membranes, and animal studies suggest a sympatho-inhibitory effect of NTG on circulatory control. METHODS: Routine tilt testing was conducted in 39 patients with suspected vasovagal syncope (age 36 +/- 16 years, 18 females). Patients were otherwise healthy and free of medication. Before a loss of consciousness set in, oncoming syncope was cut short by tilt-back or counter-maneuvers. Finger arterial pressure was monitored continuously (Finapres). Left ventricular stroke volume (SV) was computed from the pressure pulsations (Modelflow). Spontaneous baroreflex control of HR was estimated in the time and frequency domains. RESULTS: During tilt testing, 22 patients developed presyncope. After NTG administration but before presyncope, SV and cardiac output (CO) decreased (p < 0.001), whereas SVR and HR increased (p < 0.001) in all patients. Arterial pressure was initially maintained. Baroreflex sensitivity decreased after NTG. On Cox regression analysis, the occurrence of a vasovagal response was related to a drop in SV after NTG (hazard ratio 0.86, p = 0.005). CONCLUSIONS: The cardiovascular response to NTG is similar in vasovagal and non-vasovagal patients, but more pronounced in those with tilt-positive results. The NTG-facilitated presyncope appears to be CO-mediated, and there is no evidence of NTG-induced sympathetic inhibition.
Administration, Sublingual↗
Beta-blocking therapy in patients with the Marfan syndrome and entire aortic replacement.
OBJECTIVE: Beta-blocking therapy is the standard therapy in non-operated Marfan patients, however its efficacy after entire aortic replacement is unknown. The aim of this study was to describe the influence of (nearly) entire aortic replacement and beta-blocking therapy on blood pressure and wave reflections in Marfan patients. METHODS: Four Marfan patients (mean age 31+/-3 years) and 8 age matched control subjects were studied. Blood pressure and wave reflections (reflection coefficient and augmentation index) were studied by means of magnetic resonance imaging, continuous non-invasive blood pressure measurements and applanation tonometry. Patients were studied with atenolol, labetalol and without beta-blocking therapy. RESULTS: In Marfan patients, aortic systolic pressure (129+/-13 vs 114+/-10 mmHg), pulse pressure (58+/-13 vs 40+/-5 mmHg), wave speed (11+/-3 vs 4+/-0.4 m s(-1)) and reflection coefficient (65+/-22 vs 41+/-5%) were significantly increased compared to controls. There was no difference in aortic pressure between various medications in Marfan patients (atenolol 129/76 mmHg, labetalol 121/75 mmHg and without beta-blocking therapy 129/71 mmHg). Higher reflection coefficients were seen in patients with atenolol compared to discontinued medication (73+/-18 vs 65+/-22%), and also the augmentation index was higher with atenolol compared to labetalol and discontinued medication (24+/-22 vs 17+/-17 vs 22+/-22%, respectively). CONCLUSION: Our results describe increased pulse pressure, systolic pressure, wave speed and wave reflections in four Marfan patients after entire aortic replacement. The use of atenolol or labetalol did not decrease aortic pressure and with atenolol increased wave reflections were observed. Therefore, the beneficial effect of atenolol in these patients is doubtful.
Adrenergic beta-Antagonists↗
Time-domain cross-correlation baroreflex sensitivity: performance on the EUROBAVAR data set.
OBJECTIVE: To test a new method (cross-correlation baroreflex sensitivity, xBRS) for the computation of time-domain baroreflex sensitivity on spontaneous blood pressure and heart interval variability using the EUROBAVAR data set. METHODS: We applied xBRS to the 42 records in the EUROBAVAR data set, obtained from 21 patients in the lying and standing positions. One patient had a recent heart transplant and one was diabetic with evident cardiac autonomic neuropathy. xBRS computes the correlation between beat-to-beat systolic blood pressure and R-R interval, resampled at 1 Hz, in a sliding 10 s window, with delays of 0-5 s for interval. The delay with the greatest positive correlation is selected and, when significant at P = 0.01, slope and delay are recorded as one xBRS value. Each 1 s of the recording is the start of a new computation. Non-parametric tests are used. RESULTS: With patients in the lying position, xBRS yielded a value of 12.4 ms/mmHg compared with the EUROBAVAR sequential 16.2 ms/mmHg, and for the standing positions the respective values were 6.2 and 6.7 ms/mmHg, giving lying to standing ratios of 1.96 and 2.10, respectively. xBRS yielded results for all files, with 20 values per minute on average at a lower within-patient variance. Best delays were 0, 1 and 2 s, and the delay increased by 102 ms when the patient was in the standing position. The xBRS method was successful in the patients with diabetes and the heart transplant. CONCLUSION: The xBRS method should be considered for experimental and clinical use, because it yielded values that correlated strongly with and were close to the EUROBAVAR averages, yielded more values per minute, had lower within-patient variance and measured baroreflex delay.
Adult↗
Finometer, finger pressure measurements with the possibility to reconstruct brachial pressure.
OBJECTIVE: To evaluate three methods aimed at the reconstruction of brachial pressure from non-invasive finger arterial pressure measurements as implemented in the Finometer trade mark, (FMS, Finapres Measurement Systems, Arnhem, Netherlands), the successor to the Finapres trade mark (TNO Biomedical Instrumentation, Amsterdam, Netherlands). METHODS: Finger arterial pressure (FinAP) may differ from intra-brachial pressure (BAP). Pulse shape differences are removed by applying a generalized waveform filter. Pressure level differences are corrected by a generalized level correction equation using filtered systolic and diastolic levels and by level calibration, which uses an additional return-to-flow (RTF) systolic pressure measurement on the ipsilateral upper arm for an individual calibration of the reconstructed brachial pressure. VALIDATION: These methods were validated in 37 subjects, aged 41 to 83 years after a cardiac catheterization procedure. Intra-brachial and Finometer pressures were recorded simultaneously. Finometer pressures were compared after application of waveform filtering and level correction (flcAP), and after an additional RTF calibration (reBAP). RESULTS: Finger arterial systolic, diastolic and mean pressures for the group differed from BAP by -9.7 +/- 13.0, -11.6 +/- 8.0 and -16.3 +/- 7.9 mmHg (mean +/- SD) respectively. Similarly flcAP differed by -1.1 +/- 10.7, -0.2 +/- 6.8 and -1.5 +/- 6.6 mmHg and reBAP differed by 3.1 +/- 7.6, 4.0 +/- 5.6 and 2.7 +/- 4.7 mmHg. CONCLUSION: Reconstruction of BAP from FinAP as implemented in the Finometer reduces the pressure differences, with an individual RTF calibration to well within AAMI requirements.
Adult↗
Variable day/night bias in 24-h non-invasive finger pressure against intrabrachial artery pressure is removed by waveform filtering and level correction.
BACKGROUND Twenty-four-hour finger arterial pressure (FAP) recordings show a negative bias against intrabrachial artery pressure (BAP) and the bias is greater during the night, thereby overestimating the nocturnal blood pressure dip. We have available a methodology with which to reconstruct BAP from FAP by waveform filtering (transfer function) and generalized level (bias) correction that reduces the bias for short-term blood pressure records. OBJECTIVE To investigate if this methodology also decreases the extra bias during the night, thereby yielding a better estimate of the nocturnal dip. METHODS Twenty-four-hour FAP and BAP blood pressure recordings were simultaneously obtained in eight healthy normotensive volunteers and 14 patients with hypertension (ages 19-60 years), during standardized scheduled activities. The data were analysed off-line, applying the brachial reconstruction technique (reBAP) consisting of a waveform filter and level correction. Simultaneous beats yielded systolic, diastolic and mean pressures that were averaged per 30 min, per day, per night, per activity, over the 24-h period, and for volunteers and patients separately. RESULTS Over the full 24 h, FAP systolic, diastolic and mean values for the total group differed from BAP by +1 +/- 10, -8 +/- 7 and -10 +/- 8 mmHg (mean +/- SD), respectively. Similarly, reBAPs differed by +1 +/- 11, -2 +/- 7 and -2 +/- 7 mmHg. BAPs dipped by 20 +/- 8, 13 +/- 6 and 15 +/- 6 mmHg, respectively, during the night. These dips were overestimated by +8, +4 and +4 mmHg by FAP, but not by reBAP: -1, +1 and +1 mmHg. The volunteer and the patient groups showed slight differences in results, but these were not statistically significant. CONCLUSIONS The generalized reconstruction technique to obtain near-brachial pressure from non-invasive FAP almost completely removed bias over the full 24-h day-night period and improved tracking of diurnal changes for all three blood pressure values.
Adult↗