Academic literature on the topic 'Carotid Arterial Pulse Pressure Waveform (CAPPW)'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Carotid Arterial Pulse Pressure Waveform (CAPPW).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Carotid Arterial Pulse Pressure Waveform (CAPPW)"

1

Liu, Chengyu, Tao Zhuang, Lina Zhao, Faliang Chang, Changchun Liu, Shoushui Wei, Qiqiang Li, and Dingchang Zheng. "Modelling Arterial Pressure Waveforms Using Gaussian Functions and Two-Stage Particle Swarm Optimizer." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/923260.

Full text
Abstract:
Changes of arterial pressure waveform characteristics have been accepted as risk indicators of cardiovascular diseases. Waveform modelling using Gaussian functions has been used to decompose arterial pressure pulses into different numbers of subwaves and hence quantify waveform characteristics. However, the fitting accuracy and computation efficiency of current modelling approaches need to be improved. This study aimed to develop a novel two-stage particle swarm optimizer (TSPSO) to determine optimal parameters of Gaussian functions. The evaluation was performed on carotid and radial artery pressure waveforms (CAPW and RAPW) which were simultaneously recorded from twenty normal volunteers. The fitting accuracy and calculation efficiency of our TSPSO were compared with three published optimization methods: the Nelder-Mead, the modified PSO (MPSO), and the dynamic multiswarm particle swarm optimizer (DMS-PSO). The results showed that TSPSO achieved the best fitting accuracy with a mean absolute error (MAE) of 1.1% for CAPW and 1.0% for RAPW, in comparison with 4.2% and 4.1% for Nelder-Mead, 2.0% and 1.9% for MPSO, and 1.2% and 1.1% for DMS-PSO. In addition, to achieve target MAE of 2.0%, the computation time of TSPSO was only 1.5 s, which was only 20% and 30% of that for MPSO and DMS-PSO, respectively.
APA, Harvard, Vancouver, ISO, and other styles
2

Salvi, Paolo, Filippo Valbusa, Anna Kearney-Schwartz, Carlos Labat, Andrea Grillo, Gianfranco Parati, and Athanase Benetos. "Non-Invasive Assessment of Arterial Stiffness: Pulse Wave Velocity, Pulse Wave Analysis and Carotid Cross-Sectional Distensibility: Comparison between Methods." Journal of Clinical Medicine 11, no. 8 (April 15, 2022): 2225. http://dx.doi.org/10.3390/jcm11082225.

Full text
Abstract:
Background: The stiffening of large elastic arteries is currently estimated in research and clinical practice by propagative and non-propagative models, as well as parameters derived from aortic pulse waveform analysis. Methods: Common carotid compliance and distensibility were measured by simultaneously recording the diameter and pressure changes during the cardiac cycle. The aortic and upper arm arterial distensibility was estimated by measuring carotid–femoral and carotid–radial pulse wave velocity (PWV), respectively. The augmentation index and blood pressure amplification were derived from the analysis of central pulse waveforms, recorded by applanation tonometry directly from the common carotid artery. Results: 75 volunteers were enrolled in this study (50 females, average age 53.5 years). A significant inverse correlation was found between carotid distensibility and carotid–femoral PWV (r = −0.75; p < 0.001), augmentation index (r = −0.63; p < 0.001) and central pulse pressure (r = −0.59; p < 0.001). A strong correlation was found also between the total slope of the diameter/pressure rate carotid curves and aortic distensibility, quantified from the inverse of the square of carotid–femoral PWV (r = 0.67). No correlation was found between carotid distensibility and carotid–radial PWV. Conclusions: This study showed a close correlation between carotid–femoral PWV, evaluating aortic stiffness by using the propagative method, and local carotid cross-sectional distensibility.
APA, Harvard, Vancouver, ISO, and other styles
3

Shibata, Shigeki, and Benjamin D. Levine. "Biological aortic age derived from the arterial pressure waveform." Journal of Applied Physiology 110, no. 4 (April 2011): 981–87. http://dx.doi.org/10.1152/japplphysiol.01261.2010.

Full text
Abstract:
Indexes for arterial stiffness are, by their nature, influenced by the ambient blood pressure due to the curvilinear nature of arterial compliance. We developed a new concept of the “Modelflow aortic age,” which is, theoretically, not influenced by the ambient blood pressure and provides an easily understood context (biological vs. chronological age) for measures of arterial stiffness. The purpose of the present study was to validate this pressure-independent index for aortic stiffness in humans. Twelve sedentary elderly (65–77 yr), 11 Masters athletes (65–73 yr), and 12 sedentary young individuals (20–42 yr) were studied. Modelflow aortic ages were comparable with chronological ages in both sedentary groups, indicating that healthy sedentary individuals have age-appropriate aortas. In contrast, Masters athletes showed younger Modelflow aortic ages than their chronological ages. The coefficient of variation of sedentary subjects was three times smaller with the Modelflow aortic age (21%) than with other indexes, such as static systemic arterial stiffness (61%), central pulse wave velocity (61%), or carotid β-stiffness index (58%). The typical error was very small and two times smaller in the Modelflow aortic age (<7%) than in static systemic arterial stiffness (>13%) during cardiac unloading by lower body negative pressure. The Modelflow aortic age can more precisely and reliably estimate aortic stiffening with aging and modifiers, such as life-long exercise training compared with the pressure-dependent index of static systemic arterial stiffness, and provides a physiologically relevant and clinically compelling context for such measurements.
APA, Harvard, Vancouver, ISO, and other styles
4

van Houwelingen, Marc J., Daphne Merkus, Jan Hofland, Jan Bakker, Robert Tenbrinck, Maaike te Lintel Hekkert, Geert van Dijk, Arnold P. G. Hoeks, and Dirk J. Duncker. "A novel approach to assess hemorrhagic shock severity using the arterially determined left ventricular isovolumic contraction period." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 12 (December 15, 2013): H1790—H1797. http://dx.doi.org/10.1152/ajpheart.00504.2013.

Full text
Abstract:
Recently, the ventilatory variation in pre-ejection period (ΔPEP) was found to be useful in the prediction of fluid-responsiveness of patients in shock. In the present study we investigated the behavior of the ventilation-induced variations in the systolic timing intervals in response to a graded hemorrhage protocol. The timing intervals studied included the ventilatory variation in ventricular electromechanical delay (ΔEMD), isovolumic contraction period (determined from the arterial pressure waveform, ΔAIC), pulse travel time (ΔPTT), and ΔPEP. ΔAIC and ΔPEP were evaluated in the aorta and carotid artery (annotated by subscripts Ao and CA) and were compared with the responses of pulse pressure variation (ΔPPAo) and stroke volume variation (ΔSV). The graded hemorrhage protocol, followed by resuscitation using norepinephrine and autologous blood transfusion, was performed in eight anesthetized Yorkshire X Landrace swine. ΔAICAo, ΔAICCA, ΔPEPAo, ΔPEPCA, ΔPPAo, ΔPPCA, and ΔSV showed significant increases during the graded hemorrhage and significant decreases during the subsequent resuscitation. ΔAICAo, ΔAICCA, ΔPEPAo, and ΔPEPCA all correlated well with ΔPPAo and ΔSV (all r ≥ 0.8, all P < 0.001). ΔEMD and ΔPTT did not significantly change throughout the protocol. In contrast with ΔPEPAo, which was significantly higher than ΔPEPCA ( P < 0.01), ΔAICAo was not different from ΔAICCA. In conclusion, ventilation-induced preload variation principally affects the arterially determined isovolumic contraction period (AIC). Moreover, ΔAIC can be determined solely from the arterial pressure waveform, whereas ΔPEP also requires ECG measurement. Importantly, ΔAIC determined from either the carotid or aortic pressure waveform are interchangeable, suggesting that, in contrast with ΔPEP, ΔAIC may be site independent.
APA, Harvard, Vancouver, ISO, and other styles
5

Edwards, David G., Matthew S. Roy, and Raju Y. Prasad. "Wave reflection augments central systolic and pulse pressures during facial cooling." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 6 (June 2008): H2535—H2539. http://dx.doi.org/10.1152/ajpheart.01369.2007.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
6

Holewijn, Suzanne, Jenske J. M. Vermeulen, Majorie van Helvert, Lennart van de Velde, and Michel M. P. J. Reijnen. "Changes in Noninvasive Arterial Stiffness and Central Blood Pressure After Endovascular Abdominal Aneurysm Repair." Journal of Endovascular Therapy 28, no. 3 (April 9, 2021): 434–41. http://dx.doi.org/10.1177/15266028211007460.

Full text
Abstract:
Purpose: To evaluate the impact of elective endovascular aneurysm repair (EVAR) on the carotid-femoral pulse wave velocity (cfPWV) and central pressure waveform, through 1-year follow-up. Materials and Methods: A tonometric device was used to measure cfPWV and estimate the central pressure waveform in 20 patients with an infrarenal abdominal aortic aneurysm scheduled for elective EVAR. The evaluated central hemodynamic parameters included the central pressures, the augmentation index (AIx), and the subendocardial viability ratio (SEVR). AIx quantifies the contribution of reflected wave to the central systolic pressure, whereas SEVR describes the myocardial perfusion relative to the cardiac workload. Measurements were performed before EVAR, at discharge, and 6 weeks and 1 year after EVAR. Results: CfPWV was increased at discharge (12.4±0.4 vs 11.3±0.5 m/s at baseline; p=0.005) and remained elevated over the course of 1-year follow-up (6 weeks: cfPWV = 12.2±0.5 m/s; 1 year: cfPWV = 12.2±0.7 m/s, p<0.05). After an initial drop in systolic central pressure at discharge, all the central pressures increased thereafter up to 1 year, without significant differences compared with baseline. The same was observed for the AIx and SEVR. Conclusion: Endovascular aortic aneurysm repair caused an increase in pulse wave velocity compared with baseline, which remained elevated through 1 year follow-up, which may be related to an increased cardiovascular risk. However, no differences in central pressure, augmentation index, and subendocardial viability ration were observed during follow-up.
APA, Harvard, Vancouver, ISO, and other styles
7

Reesink, Koen D., Evelien Hermeling, M. Christianne Hoeberigs, Robert S. Reneman, and Arnold P. G. Hoeks. "Carotid artery pulse wave time characteristics to quantify ventriculoarterial responses to orthostatic challenge." Journal of Applied Physiology 102, no. 6 (June 2007): 2128–34. http://dx.doi.org/10.1152/japplphysiol.01206.2006.

Full text
Abstract:
Central blood pressure waveforms contain specific features related to cardiac and arterial function. We investigated posture-related changes in ventriculoarterial hemodynamics by means of carotid artery (CA) pulse wave analysis. ECG, brachial cuff pressure, and common CA diameter waveforms (by M-mode ultrasound) were obtained in 21 healthy volunteers (19–30 yr of age, 10 men and 11 women) in supine and sitting positions. Pulse wave analysis was based on a timing extraction algorithm that automatically detects acceleration maxima in the second derivative of the CA pulse waveform. The algorithm enabled determination of isovolumic contraction period (ICP) and ejection period (EP): ICP = 43 ± 8 (SD) ms (4-ms precision), and EP = 302 ± 16 (SD) ms (5-ms precision). Compared with the supine position, in the sitting position diastolic blood pressure (DBP) increased by 7 ± 4 mmHg ( P < 0.001) and R-R interval decreased by 49 ± 82 ms ( P = 0.013), reflecting normal baroreflex response, whereas EP decreased to 267 ± 19 ms ( P < 0.001). Shortening of EP was significantly correlated to earlier arrival of the lower body peripheral reflection wave ( r2 = 0.46, P < 0.001). ICP increased by 7 ± 7 ms ( P < 0.001), the ICP-to-EP ratio increased from 14 ± 3% (supine) to 19 ± 3% ( P < 0.001) and the DBP-to-ICP ratio decreased by 7% ( P = 0.023). These results suggest that orthostasis decreases left ventricular output as a result of arterial wave reflections and, presumably, reduced cardiac preload. We conclude that CA ultrasound and pulse wave analysis enable noninvasive quantification of ventriculoarterial responses to changes in posture.
APA, Harvard, Vancouver, ISO, and other styles
8

Yildiz, Mustafa. "Arterial Distensibility in Chronic Inflammatory Rheumatic Disorders." Open Cardiovascular Medicine Journal 4, no. 1 (February 23, 2010): 83–88. http://dx.doi.org/10.2174/1874192401004010083.

Full text
Abstract:
The pulse wave velocity (PWV), as an indicator of arterial distensibility, may play an important role in the stratification of patients based on the cardiovascular risk. PWV inversely correlates with arterial distensibility and relative arterial compliance. Decreased arterial distensibility alters arterial blood pressure and flow dynamics, and disturbes coronary perfusion. Systemic immune and inflammatory diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are associated with increased morbidity and mortality, predominantly due to adverse cardiovascular events. Systemic inflammation in these disorders may alter arterial compliance and arterial distensibility and, through this effect, lead to accelerated atherosclerosis. We have demonstrated an increase in the carotid-femoral (aortic) PWV that is a technique in which large artery elasticity is assessed from analysis of the peripheral arterial waveform, in patients with chronic inflammatory conditions such as RA, SLE, familial Mediterranean fever (FMF), Wegener’s granulomatosis (WG), sarcoidosis, psoriasis and psoriatic arthritis except Behçet’s disease (BD). In this review, the issue of arterial stiffness in RA, SLE, as well as WG, psoriasis, FMF, BD, sarcoidosis, systemic sclerosis (SS) and Takayasu's arteritis (TA) is overviewed.
APA, Harvard, Vancouver, ISO, and other styles
9

Paré, Mathilde, Rémi Goupil, Catherine Fortier, Fabrice Mac-Way, François Madore, Bernhard Hametner, Siegfried Wassertheurer, Martin G. Schultz, James E. Sharman, and Mohsen Agharazii. "Increased Excess Pressure After Creation of an Arteriovenous Fistula in End-Stage Renal Disease." American Journal of Hypertension 35, no. 2 (October 16, 2021): 149–55. http://dx.doi.org/10.1093/ajh/hpab161.

Full text
Abstract:
ABSTRACT BACKGROUND Reservoir-wave analysis (RWA) separates the arterial waveform into reservoir and excess pressure (XSP) components, where XSP is analogous to flow and related to left ventricular workload. RWA provides more detailed information about the arterial tree than traditional blood pressure (BP) parameters. In end-stage renal disease (ESRD), we have previously shown that XSP is associated with increased mortality and is higher in patients with arteriovenous fistula (AVF). In this study, we examined whether XSP increases after creation of an AVF in ESRD. METHODS Before and after a mean of 3.9 ± 1.2 months following creation of AVF, carotid pressure waves were recorded using arterial tonometry. XSP and its integral (XSPI) were derived using RWA through pressure wave analysis alone. Aortic stiffness was assessed by carotid–femoral pulse wave velocity (CF-PWV). RESURLTS In 38 patients (63% male, age 59 ± 15 years), after AVF creation, brachial diastolic BP decreased (79 ± 10 vs. 72 ± 12 mm Hg, P = 0.002), but the reduction in systolic BP, was not statistically significant (133 ± 20 vs. 127 ± 26 mm Hg, P = 0.137). However, carotid XSP (14 [12–19] to 17 [12–22] mm Hg, P = 0.031) and XSPI increased significantly (275 [212–335] to 334 [241–439] kPa∙s, P = 0.015), despite a reduction in CF-PWV (13 ± 3.6 vs. 12 ± 3.5 m/s, P = 0.025). CONCLUSIONS Creation of an AVF resulted in increased XSP in this population, despite improvement in diastolic BP and aortic stiffness. These findings underline the complex hemodynamic impact of AVF on the cardiovascular system.
APA, Harvard, Vancouver, ISO, and other styles
10

Tomasova, Lenka, Marian Grman, Anton Misak, Lucia Kurakova, Elena Ondriasova, and Karol Ondrias. "Cardiovascular “Patterns” of H2S and SSNO−-Mix Evaluated from 35 Rat Hemodynamic Parameters." Biomolecules 11, no. 2 (February 16, 2021): 293. http://dx.doi.org/10.3390/biom11020293.

Full text
Abstract:
This work is based on the hypothesis that it is possible to characterize the cardiovascular system just from the detailed shape of the arterial pulse waveform (APW). Since H2S, NO donor S-nitrosoglutathione (GSNO) and their H2S/GSNO products (SSNO−-mix) have numerous biological actions, we aimed to compare their effects on APW and to find characteristic “patterns” of their actions. The right jugular vein of anesthetized rats was cannulated for i.v. administration of the compounds. The left carotid artery was cannulated to detect APW. From APW, 35 hemodynamic parameters (HPs) were evaluated. H2S transiently influenced all 35 HPs and from their cross-relationships to systolic blood pressure “patterns” and direct/indirect signaling pathways of the H2S effect were proposed. The observed “patterns” were mostly different from the published ones for GSNO. Effect of SSNO−-mix (≤32 nmol kg−1) on blood pressure in the presence or absence of a nitric oxide synthase inhibitor (L-NAME) was minor in comparison to GSNO, suggesting that the formation of SSNO−-mix in blood diminished the hemodynamic effect of NO. The observed time-dependent changes of 35 HPs, their cross-relationships and non-hysteresis/hysteresis profiles may serve as “patterns” for the conditions of a transient decrease/increase of blood pressure caused by H2S.
APA, Harvard, Vancouver, ISO, and other styles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography