scholarly journals E-wave asymmetry elucidates diastolic ventricular stiffness-relaxation coupling: model-based prediction with in vivo validation

2021 ◽  
Vol 320 (1) ◽  
pp. H181-H189
Author(s):  
Junedh M. Amrute ◽  
David Zhang ◽  
William M. Padovano ◽  
Sándor J. Kovács
Keyword(s):  
Heart Rate ◽  
Dimensionless Parameter ◽  
Coupling Model ◽  
Diastolic Filling ◽  
Inertial Oscillation ◽  
Diastolic Stiffness ◽  
Doppler Data ◽  
Simultaneous Change ◽  
Deceleration Time

Although diastolic stiffness and relaxation are considered independent chamber properties, the cardio-hemic inertial oscillation that generates E-waves obeys Newton’s law. E-waves vary with heart rate requiring simultaneous change in stiffness and relaxation. By retrospective analysis of human heart-rate varying transmitral Doppler-data, we show that diastolic stiffness and relaxation are coupled and that the coupling manifests through E-wave asymmetry, quantified through a parametrized diastolic filling model-derived dimensionless parameter, which only depends on deceleration time and acceleration time, readily obtainable via standard echocardiography.

Chamber properties from transmitral flow: prediction of average and passive left ventricular diastolic stiffness

2001 ◽  
Vol 91 (1) ◽  
pp. 154-162 ◽  
Author(s):  
Jennifer B. Lisauskas ◽  
Jasvindar Singh ◽  
Andrew W. Bowman ◽  
Sándor J. Kovács
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Excellent Correlation ◽  
Transmitral Flow ◽  
Flow Prediction ◽  
Diastolic Stiffness ◽  
Pressure Interval ◽  
Deceleration Time

A chamber stiffness ( KLV)-transmitral flow (E-wave) deceleration time relation has been invasively validated in dogs with the use of average stiffness [(ΔP/ΔV)avg]. KLVis equivalent to kE, the (E-wave) stiffness of the parameterized diastolic filling model. Prediction and validation of 1) (ΔP/ΔV)avgin terms of kE, 2) early rapid-filling stiffness [(ΔP/ΔV)E] in terms of kE, and 3) passive (postdiastasis) chamber stiffness [(ΔP/ΔV)PD] from A waves in terms of the stiffness parameter for the Doppler A wave ( kA) have not been achieved. Simultaneous micromanometric left ventricular (LV) pressure (LVP) and transmitral flow from 131 subjects were analyzed. (ΔP)avgand (ΔV)avgutilized the minimum LVP-LV end-diastolic pressure interval. (ΔP/ΔV)Eutilized ΔP and ΔV from minimum LVP to E-wave termination. (ΔP/ΔV)PDutilized atrial systolic ΔP and ΔV. E- and A-wave analysis generated kEand kA. For all subjects, noninvasive-invasive relations yielded the following equations: kE= 1,401 · (ΔP/ΔV)avg+ 59.2 ( r = 0.84) and kE= 229.0 · (ΔP/ΔV)E+ 112 ( r= 0.80). For subjects with diastasis ( n = 113), kA= 1,640 · (ΔP/ΔV)PD− 8.40 ( r = 0.89). As predicted, kAshowed excellent correlation with (ΔP/ΔV)PD; kEcorrelated highly with (ΔP/ΔV)avg. In vivo validation of average, early, and passive chamber stiffness facilitates quantitative, noninvasive diastolic function assessment from transmitral flow.

Adverse Effects of Hypoxaemia on Diastolic Filling in Humans

1995 ◽  
Vol 89 (2) ◽  
pp. 165-169 ◽  
Author(s):  
Robert I. Cargill ◽  
David G. Kiely ◽  
Brian J. Lipworth
Keyword(s):  
Heart Rate ◽  
Relaxation Time ◽  
Confidence Interval ◽  
Left Ventricular ◽  
Mean Difference ◽  
Oxygen Mixture ◽  
Diastolic Filling ◽  
Isovolumic Relaxation Time ◽  
Isovolumic Relaxation ◽  
Deceleration Time

1. Abnormalities of myocardial relaxation may occur as a consequence of myocyte hypoxia. We have therefore examined the effects of hypoxaemia on right and left ventricular diastolic function in 10 healthy male subjects. 2. After resting to reach baseline haemodynamics, subjects were rendered hypoxaemic by breathing a variable nitrogen/oxygen mixture. Oxygen saturation (SaO2) was maintained at 85–90% for 20 min and then at 75–80% for a further 20 min. Haemodynamic and diastolic filling parameters were measured non-invasively at baseline and at the end of each period of hypoxaemia. 3. Diastolic filling of both ventricles was significantly impaired by hypoxaemia. In comparison with baseline, left ventricular isovolumic relaxation time and transmitral E-wave deceleration time corrected for heart rate were significantly prolonged at SaO2 75–80%: mean difference in corrected relaxation time, 9.8 ms (95% confidence interval 1–19); mean difference in corrected deceleration time, 34 ms (95% confidence interval 11–56). Similarly, right ventricular isovolumic relaxation time and transtricuspid E-wave deceleration time were significantly prolonged at SaO2 values of 75–80% compared with baseline: mean difference in relaxation time, 20.3 ms (95% confidence interval 3–38); mean difference in deceleration time, 33 ms (95% confidence interval 11–55). 4. During hypoxaemia there were dose-related increases in heart rate, cardiac output and mean pulmonary artery pressure, but no effects on mean arterial pressure. 5. Hypoxaemia significantly impairs relaxation of left and right ventricles in normal humans. These changes may reflect impairment of intracellular calcium transport secondary to the effects of myocyte hypoxia.

scholarly journals Focused Genetic Recombination of Bacteriophage T4 Initiated by Double-Strand Breaks

Genetics ◽  
2002 ◽  
Vol 162 (2) ◽  
pp. 543-556
Author(s):  
Victor Shcherbakov ◽  
Igor Granovsky ◽  
Lidiya Plugina ◽  
Tamara Shcherbakova ◽  
Svetlana Sizova ◽  
...  
Keyword(s):  
Genetic Recombination ◽  
Bacteriophage T4 ◽  
Proximal Part ◽  
Coupling Model ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Strand Breaks ◽  
The Right ◽  
Frequency Distance

Abstract A model system for studying double-strand-break (DSB)-induced genetic recombination in vivo based on the ets1 segCΔ strain of bacteriophage T4 was developed. The ets1, a 66-bp DNA fragment of phage T2L containing the cleavage site for the T4 SegC site-specific endonuclease, was inserted into the proximal part of the T4 rIIB gene. Under segC+ conditions, the ets1 behaves as a recombination hotspot. Crosses of the ets1 against rII markers located to the left and to the right of ets1 gave similar results, thus demonstrating the equal and symmetrical initiation of recombination by either part of the broken chromosome. Frequency/distance relationships were studied in a series of two- and three-factor crosses with other rIIB and rIIA mutants (all segC+) separated from ets1 by 12-2100 bp. The observed relationships were readily interpretable in terms of the modified splice/patch coupling model. The advantages of this localized or focused recombination over that distributed along the chromosome, as a model for studying the recombination-replication pathway in T4 in vivo, are discussed.

scholarly journals Heart rate reduction with ivabradine promotes shear stress-dependent anti-inflammatory mechanisms in arteries

2016 ◽  
Vol 116 (07) ◽  
pp. 181-190 ◽  
Author(s):  
Luong Le ◽  
Hayley Duckles ◽  
Torsten Schenkel ◽  
Marwa Mahmoud ◽  
Jordi Tremoleda ◽  
...  
Keyword(s):  
Heart Rate ◽  
Shear Stress ◽  
Carotid Arteries ◽  
Vascular Inflammation ◽  
Protective Effects ◽  
En Face ◽  
Inflammatory Activation ◽  
Anti Inflammatory ◽  
Stress Dependent

SummaryBlood flow generates wall shear stress (WSS) which alters endothelial cell (EC) function. Low WSS promotes vascular inflammation and atherosclerosis whereas high uniform WSS is protective. Ivabradine decreases heart rate leading to altered haemodynamics. Besides its cardio-protective effects, ivabradine protects arteries from inflammation and atherosclerosis via unknown mechanisms. We hypothesised that ivabradine protects arteries by increasing WSS to reduce vascular inflammation. Hypercholesterolaemic mice were treated with ivabradine for seven weeks in drinking water or remained untreated as a control. En face immunostaining demonstrated that treatment with ivabradine reduced the expression of pro-inflammatory VCAM-1 (p<0.01) and enhanced the expression of anti-inflammatory eNOS (p<0.01) at the inner curvature of the aorta. We concluded that ivabradine alters EC physiology indirectly via modulation of flow because treatment with ivabradine had no effect in ligated carotid arteries in vivo, and did not influence the basal or TNFα-induced expression of inflammatory (VCAM-1, MCP-1) or protective (eNOS, HMOX1, KLF2, KLF4) genes in cultured EC. We therefore considered whether ivabradine can alter WSS which is a regulator of EC inflammatory activation. Computational fluid dynamics demonstrated that ivabradine treatment reduced heart rate by 20 % and enhanced WSS in the aorta. In conclusion, ivabradine treatment altered haemodynamics in the murine aorta by increasing the magnitude of shear stress. This was accompanied by induction of eNOS and suppression of VCAM-1, whereas ivabradine did not alter EC that could not respond to flow. Thus ivabradine protects arteries by altering local mechanical conditions to trigger an anti-inflammatory response.

Cardiovascular Responding during Anger and Fear Imagery

1982 ◽  
Vol 50 (1) ◽  
pp. 219-230 ◽  
Author(s):  
Richard J. Roberts ◽  
Theodore C. Weerts
Keyword(s):  
College Students ◽  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Scene Change ◽  
Emotional Responding ◽  
Analysis Of Change ◽  
Screening Interview

This study was designed to determine if visualization of anger- and fear-provoking scenes produced differential physiological patterns similar to those produced by in vivo manipulations. Normotensive college students were selected on the basis of their responses to newly developed Anger and Fear/Anxiety questionnaires and for their ability to construct arousing scenes during a screening interview. In a 2 × 2 design (intensity × emotion), four scenes (high and low anger, high and low fear) were constructed individually for each of 16 subjects to imagine. Diastolic blood pressure, systolic blood pressure, and heart rate were monitored during visualization of each scene. Change in diastolic blood pressure was significantly greater for high anger than for high fear as predicted. Analysis of change in heart rate and systolic blood pressure showed significant effects for intensity only. These results provide further support for the concept of physiological differentiation in human emotion and suggest the utility of imagery for systematic study of human emotional responding.

Cerebral oxygen availability by NIR spectroscopy during transient hypoxia in humans

1990 ◽  
Vol 69 (3) ◽  
pp. 907-913 ◽  
Author(s):  
N. B. Hampson ◽  
E. M. Camporesi ◽  
B. W. Stolp ◽  
R. E. Moon ◽  
J. E. Shook ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Volume ◽  
Near Infrared ◽  
Cerebral Blood Volume ◽  
Minute Ventilation ◽  
Nir Spectroscopy ◽  
Redox Status ◽  
Total Blood ◽  
Arterial Ph

The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PETCO2) 36.9 +/- 2.6 to 34.9 +/- 3.4 Torr] or hypocapnia (PETCO2 32.8 +/- 0.6 to 23.7 +/- 0.6 Torr) by an 8-min rebreathing technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (PaO2, 89.1 +/- 3.5 to 34.1 +/- 0.1 Torr) with stable PETCO2, arterial PCO2 (PaCO2), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progressively decreasing PaO2 (100.2 +/- 3.6 to 28.9 +/- 0.1 Torr), with progressive reduction in PaCO2 (39.0 +/- 1.6 to 27.3 +/- 1.9 Torr), and an increase in arterial pH (7.41 +/- 0.02 to 7.53 +/- 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia. PaCO is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.

Heart rate variability in patients with agoraphobia with or without panic disorder remains stable during CBT but increases following in-vivo exposure

2019 ◽  
Vol 64 ◽  
pp. 16-23
Author(s):  
Jennifer Lara Maria Mumm ◽  
Lena Pyrkosch ◽  
Jens Plag ◽  
Patrick Nagel ◽  
Moritz Bruno Petzold ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Panic Disorder

Heart Rate Is the Major Determinant of Diastolic Filling Pattern During Growth: A Radionuclide Ventriculography Assessment

2002 ◽  
Vol 23 (4) ◽  
pp. 378-387 ◽  
Author(s):  
G. Arsos ◽  
E. Moralidis ◽  
N. Karatzas ◽  
I. Iakovou ◽  
S. Georga ◽  
...  
Keyword(s):  
Heart Rate ◽  
Radionuclide Ventriculography ◽  
Major Determinant ◽  
Diastolic Filling ◽  
Filling Pattern

scholarly journals Regulation of murine myocardial energy metabolism during adrenergic stress studied by in vivo 31P NMR spectroscopy

2003 ◽  
Vol 285 (5) ◽  
pp. H1976-H1979 ◽  
Author(s):  
A. V. Naumova ◽  
R. G. Weiss ◽  
V. P. Chacko
Keyword(s):  
Heart Rate ◽  
Cardiac Metabolism ◽  
High Energy ◽  
Dobutamine Stress ◽  
Resonance Spectroscopy ◽  
31P Nmr Spectroscopy ◽  
Adult Mice ◽  
The Mean ◽  
Large Animals

Image-guided, spatially localized 31P magnetic resonance spectroscopy (MRS) was used to study in vivo murine cardiac metabolism under resting and dobutamine-induced stress conditions. Intravenous dobutamine infusion (24 μg · min–1 · kg body wt–1) increased the mean heart rate by ∼39% from 482 ± 46 per min at baseline to 669 ± 77 per min in adult mice. The myocardial phosphocreatine (PCr)-to-ATP (PCr/ATP) ratio remained unchanged at 2.1 ± 0.5 during dobutamine stress, compared with baseline conditions. Therefore, we conclude that a significant increase in heart rate does not result in a decline in the in vivo murine cardiac PCr/ATP ratio. These observations in very small mammals, viz., mice, at extremely high heart rates are consistent with studies in large animals demonstrating that global levels of high-energy phosphate metabolites do not regulate in vivo myocardial metabolism during physiologically relevant increases in cardiac work.

Sign in / Sign up

Export Citation Format

Share Document