Dynamic Hemodynamic Energy Loss in Normal and Stenosed Aortic Valves

2010 ◽  
Vol 132 (2) ◽  
Author(s):  
Choon-Hwai Yap ◽  
Lakshmi P. Dasi ◽  
Ajit P. Yoganathan
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Energy Dissipation ◽  
Stroke Volume ◽  
Momentum Equation ◽  
Navier Stokes ◽  
Hydrodynamic Characteristics ◽  
Clinical Tool ◽  
Heart Rates

Aortic valve (AV) stenosis, if untreated, leads to heart failure. From a mechanics standpoint, heart failure can be interpreted as the failure of the heart to generate sufficient power to overcome energy losses in the circulation. Thus, energy efficiency-based measures for evaluating AV performance and disease severity have the advantage of being a direct measure of the contribution of the AV hydrodynamic characteristics toward heart failure. We present a new method for computing the rate of energy dissipation as a function of systolic time, by modifying the Navier–Stokes momentum equation. This method preserves the dynamic term of the Navier–Stokes momentum equation, and allows the investigation of the trend of the rate of energy dissipation over time. This method is applied to a series of in vitro experiments, where a trimmed porcine valve is exposed to various conditions: varying stroke volumes (50 ml to 90 ml) at the fixed heart rate; varying heart rates (60–80 beats/min) at fixed stroke volume; and varying stenosis levels (normal, mild stenosis, moderate stenosis). The results are: (1) energy dissipation waveform has a distinctive pattern of being skewed toward late systole, due to flow instabilities during deceleration phases; (2) increasing heart rate and stroke volume increases energy dissipation, but the normalized shape of the energy dissipation waveform is preserved across heart rates and stroke volumes; (3) increasing stenosis level increases energy dissipation, and also alters the normalized shape of the energy dissipation waveform. Since stenosis produces a signature energy dissipation waveform shape, dynamic energy dissipation analysis can potentially be extended into a clinical tool for AV evaluation.

scholarly journals Heart Rate–Induced Myocardial Ca 2+ Retention and Left Ventricular Volume Loss in Patients With Heart Failure With Preserved Ejection Fraction

2020 ◽  
Vol 9 (17) ◽  
Author(s):  
Daniel N. Silverman ◽  
Mehdi Rambod ◽  
Daniel L. Lustgarten ◽  
Robert Lobel ◽  
Martin M. LeWinter ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Sinus Rhythm ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Preserved Ejection Fraction ◽  
Volume Loss ◽  
Heart Rates ◽  
Patients With Heart Failure

Background Increases in heart rate are thought to result in incomplete left ventricular (LV) relaxation and elevated filling pressures in patients with heart failure with preserved ejection fraction (HFpEF). Experimental studies in isolated human myocardium have suggested that incomplete relaxation is a result of cellular Ca 2+ overload caused by increased myocardial Na + levels. We tested these heart rate paradigms in patients with HFpEF and referent controls without hypertension. Methods and Results In 22 fully sedated and instrumented patients (12 controls and 10 patients with HFpEF) in sinus rhythm with a preserved ejection fraction (≥50%) we assessed left‐sided filling pressures and volumes in sinus rhythm and with atrial pacing (95 beats per minute and 125 beats per minute) before atrial fibrillation ablation. Coronary sinus blood samples and flow measurements were also obtained. Seven women and 15 men were studied (aged 59±10 years, ejection fraction 61%±4%). Patients with HFpEF had a history of hypertension, dyspnea on exertion, concentric LV remodeling and a dilated left atrium, whereas controls did not. Pacing at 125 beats per minute lowered the mean LV end‐diastolic pressure in both groups (controls −4.3±4.1 mm Hg versus patients with HFpEF −8.5±6.0 mm Hg, P =0.08). Pacing also reduced LV end‐diastolic volumes. The volume loss was about twice as much in the HFpEF group (controls −15%±14% versus patients with HFpEF −32%±11%, P =0.009). Coronary venous [Ca 2+ ] increased after pacing at 125 beats per minute in patients with HFpEF but not in controls. [Na + ] did not change. Conclusions Higher resting heart rates are associated with lower filling pressures in patients with and without HFpEF. Incomplete relaxation and LV filling at high heart rates lead to a reduction in LV volumes that is more pronounced in patients with HFpEF and may be associated with myocardial Ca 2+ retention.

First clinical trial with etomoxir in patients with chronic congestive heart failure

2000 ◽  
Vol 99 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Stephan SCHMIDT-SCHWEDA ◽  
Christian HOLUBARSCH
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Sarcoplasmic Reticulum ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

In the failing human myocardium, both impaired calcium homoeostasis and alterations in the levels of contractile proteins have been observed, which may be responsible for reduced contractility as well as diastolic dysfunction. In addition, levels of a key protein in calcium cycling, i.e. the sarcoplasmic reticulum Ca2+-ATPase, and of the α-myosin heavy chain have been shown to be enhanced by treatment with etomoxir, a carnitine palmitoyltransferase inhibitor, in normal and pressure-overloaded rat myocardium. We therefore studied, for the first time, the influence of long-term oral application of etomoxir on cardiac function in patients with chronic heart failure. A dose of 80 mg of etomoxir was given once daily to 10 patients suffering from heart failure (NYHA functional class II–III; mean age 55±4 years; one patient with ischaemic heart disease and nine patients with dilated idiopathic cardiomyopathy; all male), in addition to standard therapy. The left ventricular ejection fraction was measured echocardiographically before and after a 3-month period of treatment. Central haemodynamics at rest and exercise (supine position bicycle) were defined by means of a pulmonary artery catheter and thermodilution. All 10 patients improved clinically; no patient had to stop taking the study medication because of side effects; and no patient died during the 3-month period. Maximum cardiac output during exercise increased from 9.72±1.25 l/min before to 13.44±1.50 l/min after treatment (P < 0.01); this increase was mainly due to an increased stroke volume [84±7 ml before and 109±9 ml after treatment (P < 0.01)]. Resting heart rate was slightly reduced (not statistically significant). During exercise, for any given heart rate, stroke volume was significantly enhanced (P < 0.05). The left ventricular ejection fraction increased significantly from 21.5±2.6% to 27.0±2.3% (P < 0.01). In acute studies, etomoxir showed neither a positive inotropic effect nor vasodilatory properties. Thus, although the results of this small pilot study are not placebo-controlled, all patients seem to have benefitted from etomoxir treatment. Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca2+-ATPase and the α-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction.

Pulsatile Flow Characteristics in a Stenotic Aortic Valve Model: An In Vitro Experimental Study

2019 ◽  
Author(s):  
Ruihang Zhang ◽  
Yan Zhang
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Aortic Valve ◽  
Pulsatile Flow ◽  
Heart Diseases ◽  
Flow Characteristics ◽  
Aortic Valve Area ◽  
Heart Rates ◽  
Valvular Heart Diseases

Abstract Aortic stenosis (AS) is one of the most common valvular heart diseases around the globe. The accurate assessment of AS severity is important and strongly associated with accurate interpretation of the hemodynamic parameters across the stenotic valve. In this study, we conducted in vitro fluid dynamic experiments to investigate the pulsatile flow characteristics of a stenotic aortic valve as a function of heart rate. An in vitro cardiovascular flow simulator was used to generate pulsatile flow with a prescribed waveform (40% systolic period and 4L/min cardiac output) under varied heart rates (50 bpm, 75 bpm and 100 bpm). The stenotic valve was constructed by molding silicone into three-leaflet aortic valve geometries wrapping around thin fabrics which increases its stiffness and tensile strength. Two-dimensional phase-locked particle image velocimetry (PIV) was employed to quantify the flow field characteristics of the stenotic valve. Pressure waveforms were recorded to evaluate the severity of the stenosis via the Gorlin and Hakki equations. Results suggest that as the heart rate increases, the peak pressure gradient across the stenotic aortic valve increases significantly under the same cardiac output. Analysis also shows the estimated aortic valve area (AVA) decreases as the heart rate increases under the same cardiac output using Gorlin equation estimation, while the trend is reversed using Hakki equation estimation. Under phase-locked conditions, quantitative flow characteristics, such as phase-averaged flow velocity, turbulence kinetic energy (TKE) for the stenotic aortic valve were analyzed based on the PIV data. Results suggest that the peak systolic jet velocity downstream of the valve increases as the heart rate increases, implying a longer pressure recovery distance as heart rate increases. While the turbulence at peak systole is higher under the slower heart rate, the faster heart rate contributes to a higher turbulence during the late systole and early diastole phases. Based on the comparison with no-valve cases, the differences in TKE was mainly related to the dynamics of leaflets under different heart rates. Overall, the results obtained in this study demonstrate that the hemodynamics of a stenotic aortic valve is complex and the assessment of AS could be significantly affected by the pulsating rate of the flow.

Effects of β-blockade with bisoprolol on heart rate variability in advanced heart failure: Analysis of scatterplots of R-R intervals at selected heart rates

1996 ◽  
Vol 132 (2) ◽  
pp. 369-375 ◽  
Author(s):  
Xavier Copie ◽  
Françoise Pousset ◽  
Philippe Lechat ◽  
Patrice Jaillon ◽  
Louis Guize ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Failure Analysis ◽  
Advanced Heart Failure ◽  
Heart Rates

Left atrial assist device function at various heart rates using a mock circulation loop

2020 ◽  
pp. 039139882097750
Author(s):  
Yuichiro Kado ◽  
Anthony R Polakowski ◽  
Barry D Kuban ◽  
David J Horvath ◽  
Takuma Miyamoto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Atrial ◽  
Diastolic Heart Failure ◽  
New Left ◽  
Aortic Pressure ◽  
Normal Heart ◽  
Assist Device ◽  
Heart Rates ◽  
Mock Circulation

We are developing a new left atrial assist device (LAAD) for patients who have heart failure with preserved ejection fraction (HFpEF). This study aimed to assess the hemodynamic effects of the LAAD under both normal heart conditions and various diastolic heart failure (DHF) conditions using a mock circulatory loop. A continuous-flow pump that simulates LAAD, was placed between the left atrial (LA) reservoir and a pneumatic ventricle that simulated a native left ventricle on a pulsatile mock loop. Normal heart (NH) and mild, moderate, and severe DHF conditions were simulated by adjusting the diastolic drive pressures of the pneumatic ventricle. With the LAAD running at 3200 rpm, data were collected at 60, 80, and 120 bpm of the pneumatic ventricle. Cardiac output (CO), mean aortic pressure (AoP), and mean LA pressure (LAP) were compared to evaluate the LAAD performance. With LAAD support, the CO and AoP rose to a sufficient level at all heart rates and DHF conditions (CO; 3.4–3.8 L/min, AoP; 90–105 mm Hg). Each difference in the CO and the AoP among various heart rates was minuscule compared with non-pump support. The LAP decreased from 21–23 to 17–19 mm Hg in all DHF conditions (difference not significant). Furthermore, hemodynamic parameters improved for all DHF conditions, independent of heart rate. The LAAD can provide adequate flow to maintain the circulation status at various heart rates in an in vitro mock circulatory loop.

scholarly journals Impact of heart rate on cross-bridge cycling kinetics in failing and nonfailing human myocardium

2019 ◽  
Vol 317 (3) ◽  
pp. H640-H647
Author(s):  
Jae-Hoon Chung ◽  
Nima Milani-Nejad ◽  
Jonathan P. Davis ◽  
Noah Weisleder ◽  
Bryan A. Whitson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Human Myocardium ◽  
Force Frequency ◽  
Human Heart Failure ◽  
Relaxation Kinetics ◽  
Heart Rates ◽  
Cross Bridge ◽  
Maximal Activation

The force-frequency relationship (FFR) is an important regulatory mechanism that increases the force-generating capacity as well as the contraction and relaxation kinetics in human cardiac muscle as the heart rate increases. In human heart failure, the normally positive FFR often becomes flat, or even negative. The rate of cross-bridge cycling, which has been reported to affect cardiac output, could be potentially dysregulated and contribute to blunted or negative FFR in heart failure. We recently developed and herein use a novel method for measuring the rate of tension redevelopment. This method allows us to obtain an index of the rate of cross-bridge cycling in intact contracting cardiac trabeculae at physiological temperature and assess physiological properties of cardiac muscles while preserving posttranslational modifications representative of those that occur in vivo. We observed that trabeculae from failing human hearts indeed exhibit an impaired FFR and a reduced speed of relaxation kinetics. However, stimulation frequencies in the lower spectrum did not majorly affect cross-bridge cycling kinetics in nonfailing and failing trabeculae when assessed at maximal activation. Trabeculae from failing human hearts had slightly slower cross-bridge kinetics at 3 Hz as well as reduced capacity to generate force upon K+ contracture at this frequency. We conclude that cross-bridge kinetics at maximal activation in the prevailing in vivo heart rates are not majorly impacted by frequency and are not majorly impacted by disease. NEW & NOTEWORTHY In this study, we confirm that cardiac relaxation kinetics are impaired in filing human myocardium and that cross-bridge cycling rate at resting heart rates does not contribute to this impaired relaxation. At high heart rates, failing myocardium cross-bridge rates are slower than in nonfailing myocardium.

scholarly journals To Balloon or Not to Balloon? The Effects of an Intra-Aortic Balloon-Pump on Coronary Artery Flow during Extracorporeal Circulation Simulating Normal and Low Cardiac Output Syndromes

2021 ◽  
Vol 10 (22) ◽  
pp. 5333
Author(s):  
Philippe Reymond ◽  
Karim Bendjelid ◽  
Raphaël Giraud ◽  
Gérald Richard ◽  
Nicolas Murith ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Low Cardiac Output ◽  
Coronary Artery Flow ◽  
Artery Flow

ECMO is the most frequently used mechanical support for patients suffering from low cardiac output syndrome. Combining IABP with ECMO is believed to increase coronary artery blood flow, decrease high afterload, and restore systemic pulsatile flow conditions. This study evaluates that combined effect on coronary artery flow during various load conditions using an in vitro circuit. In doing so, different clinical scenarios were simulated, such as normal cardiac output and moderate-to-severe heart failure. In the heart failure scenarios, we used peripheral ECMO support to compensate for the lowered cardiac output value and reach a default normal value. The increase in coronary blood flow using the combined IABP-ECMO setup was more noticeable in low heart rate conditions. At baseline, intermediate and severe LV failure levels, adding IABP increased coronary mean flow by 16%, 7.5%, and 3.4% (HR 60 bpm) and by 6%, 4.5%, and 2.5% (HR 100 bpm) respectively. Based on our in vitro study results, combining ECMO and IABP in a heart failure setup further improves coronary blood flow. This effect was more pronounced at a lower heart rate and decreased with heart failure, which might positively impact recovery from cardiac failure.

The importance of nervous and humoral mechanisms in the control of cardiac performance in the Atlantic cod Gadus morhua at rest and during non-exhaustive exercise

1988 ◽  
Vol 137 (1) ◽  
pp. 287-301 ◽  
Author(s):  
M. Axelsson
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Gadus Morhua ◽  
Positive Inotropic Effect ◽  
Atlantic Cod ◽  
Inotropic Effect ◽  
Response Curves

The nervous regulation of heart rate and stroke volume in the Atlantic cod Gadus morhua was investigated both in vivo, during rest and exercise, and in vitro. The cholinergic and adrenergic influences on the heart were estimated in experiments with injections of atropine and sotalol. At rest the cholinergic and adrenergic tonus on the heart were 38% and 21%, respectively (ratio 1.81:1). At the end of an exercise period, the cholinergic tonus had decreased to 15% but the adrenergic tonus had increased to 28% (ratio 0.54:1). The results suggest that variation of the cholinergic tonus on the heart is a major factor in the regulation of the heart rate. In one group of fish, cardiac output was also measured, allowing calculation of stroke volume. Cardiac output increased significantly during exercise, and this effect persisted in the presence of both atropine and sotalol, although the increase in heart rate was reduced or abolished. The persisting increase in cardiac output during exercise is due to an increase in stroke volume, reflecting a Starling relationship. In the presence of the adrenergic neurone-blocking agent bretylium, a positive inotropic effect on isolated, paced atrial and ventricular strips was observed. In the atrial preparations the effect persisted after 24 h. The effect was prevented by pretreatment with sotalol or cocaine, but potentiated by phentolamine pretreatment. This shows that bretylium exerts its neurone-blocking action after being taken up into the adrenergic nerves, and suggests that the positive inotropic effect of bretylium observed in vivo is due to release of endogenous catecholamines. The concentration-response curves for adrenaline on isolated spontaneously beating atrial preparations showed that the concentrations of catecholamines necessary to produce appreciable effects on the heart are higher than the concentrations found in cod plasma during ‘stress’ situations (handling and exhaustive swimming).

Automation of the Harvard Apparatus Pulsatile Blood Pump

2012 ◽  
Vol 6 (4) ◽  
Author(s):  
Charles E. Taylor ◽  
Zachary W. Dziczkowski ◽  
Gerald E. Miller
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Mechanical Design ◽  
Blood Pump ◽  
Cardiac Assist ◽  
Usb Communication ◽  
And Performance ◽  
Vitro Analysis ◽  
Pulsatile Blood Pump

Producing accurate physiological circulatory conditions in vitro is integral to the evaluation of cardiac assist technologies. The ability to simulate cardiac function, normal or pathological, is dependent on the capabilities of the pump deployed for this purpose. Presented is a reference standard for this in vitro analysis, with automation features targeted for robust bench-top testing. Cardiac performance is typically described in terms of stroke volume, heart rate, and percent systole. Respectively, these three settings prescribe the volume of fluid ejected, the rate of pumping, and the percentage of the pumping cycle spent in ejection. A pump that provides settings for each of these parameters and precise repeatability allows for accurate construction of simulation conditions. These capabilities are present in the commercially available Harvard Apparatus 1423 pulsatile blood pump. Modifications have been made to this particular model that allow for the automation of its function and real-time performance determination. Discussed in this publication is the design and performance of a modified 1423 pump that employs universal serial bus (USB) communication in the control of its stroke volume, heart rate, and percent systole. The percent systole is denoted as the phase ratio on the hardware. Utilization of an embedded microcontroller (MCU) allows for not only the digital communication via a computer terminal, but process control of the subsystems maintaining each parameter. Care was taken to preserve the mechanical design employed by Harvard Apparatus; the modifications were not invasive to the mechanical driveline of the pump. Electromechanical design characterization was performed in Simulink® using the following Simscape™ block sets: Simscape™ Foundation Library, SimElectronics®, and SimMechanics™. This provided an accurate model of the systems during the design process, which assisted in the deployment of the process controllers with minimal prototype construction. Communication with the MCU is achieved with American Standard Code for Information Interchange (ASCII) commands delivered through a LabVIEW VI interface. Continuous readbacks on fill/ejection rate, pump rate (HR), percent systole (PS), and stroke volume (SV) are possible with these modifications. The deployed upgrade allows for complete automation of the Harvard Apparatus 1423 pulsatile blood pump, with the capability to run sequences of conditions without the need for manual intervention.

Exhaustion of Frank-Starling mechanism in conscious dogs with heart failure

1993 ◽  
Vol 265 (4) ◽  
pp. H1119-H1131 ◽  
Author(s):  
K. Komamura ◽  
R. P. Shannon ◽  
T. Ihara ◽  
Y. T. Shen ◽  
I. Mirsky ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Heart Failure ◽  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Ventricular Dilatation ◽  
Cross Sectional ◽  
Control State

The goal of this study was to elucidate the ability of the left ventricle to accommodate an increase in preload (Frank-Starling mechanism) in the presence of congestive heart failure (CHF) but in the absence of the complicating effects of hypertrophy and fibrosis. To accomplish this, the effects of volume loading were examined in eight conscious dogs during the control state and after 3 wk of right ventricular pacing (240 beats/min). CHF increased heart rate (by 16 +/- 5 from 92 +/- 5 beats/min), left ventricular (LV) end-diastolic pressure (by 17 +/- 2 from 10 +/- 1 mmHg), and LV end-diastolic volume (EDV; by 23 +/- 4 from 57 +/- 3 ml). Despite reduced LV ejection fraction (from 54 +/- 3 to 31 +/- 3%), there was no significant change in cardiac output (2.5 +/- 0.3 l/min) compared with control (2.7 +/- 0.2 l/min). Stroke volume was preserved (control 19 +/- 2 ml; CHF 18 +/- 2 ml) at a constant heart rate by a shift to the right in the relationship between LV stroke volume and EDV, indicating the importance of chronic ventricular dilatation in maintaining pump performance. In the control state, acute volume load increased LV EDV (by 17 +/- 2 ml) and stroke volume (by 11 +/- 2 ml), whereas in CHF it did not increase LV EDV or stroke volume. Scanning electron microscopy revealed areas of reduced collagen weave pattern surrounding myofibers. Myocyte cross-sectional area by transmission electron microscopy was significantly reduced, and there were multiple electron-dense expansions of the Z lines with disruption of the normal lateral sarcomere alignment. These morphological findings suggest that chronic ventricular dilatation utilized in CHF results from myocyte stretch and morphological intracellular rearrangement. Furthermore, the failing heart cannot further augment stroke volume by acutely increasing EDV in CHF, suggesting that the Frank-Starling reserve is essentially exhausted.

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