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.

Load-independent index of diastolic filling: model-based derivation with in vivo validation in control and diastolic dysfunction subjects

2006 ◽  
Vol 101 (1) ◽  
pp. 92-101 ◽  
Author(s):  
Leonid Shmuylovich ◽  
Sándor J. Kovács
Keyword(s):  
Diastolic Dysfunction ◽  
Driving Force ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Tilt Table ◽  
Resistive Force ◽  
Force Peak

Maximum elastance is an experimentally validated, load-independent systolic function index stemming from the time-varying elastance paradigm that decoupled extrinsic load from (intrinsic) contractility. Although Doppler echocardiography is the preferred method of diastolic function (DF) assessment, all echo-derived indexes are load dependent, and no invasive or noninvasive load-independent index of filling (LIIF) exists. In this study, we derived and experimentally validated a LIIF. We used a kinematic filling paradigm (the parameterized diastolic filling formalism) to predict and derive the (dimensionless) dynamic diastolic efficiency M, defined by the slope of the peak driving force [maximum driving force ( kx o) ∝ peak atrioventricular (AV) gradient] to maximum viscoelastic resistive force [peak resistive force ( cEpeak)] relation. To validate load independence, we analyzed E-waves recorded while load was varied via tilt table (head up, horizontal, and head down) in 16 healthy volunteers. For the group, linear regression of E-wave derived kx o vs. cEpeak yielded kx o = M ( cEpeak) + B, r2 = 0.98; where M = 1.27 ± 0.09 and B = 5.69 ± 1.70. Effects of diastolic dysfunction (DD) on M were assessed by analysis of preexisting simultaneous cath-echo data in six DD vs. five control subjects. Average M for the DD group ( M = 0.98 ± 0.07) was significantly lower than controls ( M = 1.17 ± 0.05, P < 0.001). We conclude that M is a LIIF because it uncouples intrinsic DF (i.e., the pressure-flow relation) from extrinsic load (left ventricular end-diastolic pressure). Larger M values imply better DF in that increasing AV pressure gradient results in relatively smaller increases in peak resistive losses ( cEpeak). Conversely, lower M implies that increasing AV gradient leads to larger increases in resistive losses. Further prospective validation characterizing M in well-defined pathological states is warranted.

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.

scholarly journals Myocardial lysyl oxidase regulation of cardiac remodeling in a murine model of diet-induced metabolic syndrome

2009 ◽  
Vol 297 (3) ◽  
pp. H976-H982 ◽  
Author(s):  
Sherma Zibadi ◽  
Randy Vazquez ◽  
Derek Moore ◽  
Douglas F. Larson ◽  
Ronald R. Watson
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Protein Expression ◽  
Diastolic Pressure ◽  
Lysyl Oxidase ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Cross Linking ◽  
Increased Risk

Metabolic syndrome (MetS) represents an increased risk of cardiovascular disease. Although its individual components adversely affect cardiac structure and function, the extent to which multiple components of MetS affect the cardiac extracellular matrix (ECM) has not been well characterized. Lysyl oxidase (LOX) is one of the cardiac ECM-modifying enzymes that catalyze the formation of collagen cross-linking. Our objective was to define the effect of diet-induced MetS on the LOX enzyme. MetS was induced in male C57BL/6 mice by administrating a high-fat, high-simple carbohydrate diet for 6 mo. Gene expression was determined by real-time PCR. The cardiac protein expression and enzymatic activity of LOX were measured. The severity of fibrosis was assessed by histology and hydroxylproline assay. Cardiac diastolic function was assessed by in vivo analysis of the pressure-volume relationship. LOX, matrix metalloproteinases, and their tissue inhibitors were analyzed, and of these three, LOX was most significantly changed in the MetS mice. Despite the blunted gene expression of LOX isoforms, MetS mice demonstrated a significant upregulation of bone morphogenetic protein-1. Correspondingly, there was an increase in the ratio of protein expression of mature to proenzyme LOX by 25.9%, enhanced LOX activity by 50.0%, and increased cardiac cross-linked collagen compared with the controls. This fibrotic response coincided with a marked increase in end-diastolic pressure, increased left ventricular stiffness, and impaired diastolic filling pattern. Our data signify that diet-induced MetS alters the remodeling enzymes, mainly LOX, thereby altering ECM structure by increasing the amount of cross-linking and inducing diastolic dysfunction.

scholarly journals Mechanics of intraventricular filling: study of LV early diastolic pressure gradients and flow velocities

1998 ◽  
Vol 275 (3) ◽  
pp. H1062-H1069 ◽  
Author(s):  
Otto A. Smiseth ◽  
Kjetil Steine ◽  
Gunnar Sandbæk ◽  
Marie Stugaard ◽  
Tor Ø. Gjølberg
Keyword(s):  
Pressure Gradient ◽  
Diastolic Pressure ◽  
Time Derivative ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Transmitral Flow ◽  
Intraventricular Flow ◽  
Artery Disease ◽  
Lv Volume ◽  
Flow Velocities

This study investigates mechanisms of left ventricular (LV) intracavitary flow during early, rapid filling. In eight coronary artery disease patients with normal LV ejection fraction we recorded simultaneous LV apical and outflow tract pressures and intraventricular flow velocities by color M-mode Doppler echocardiography. In five anesthetized dogs we also recorded left atrial pressure and LV volume by sonomicrometry. In patients, as the early diastolic mitral-to-apical filling wave arrived at the apex, we observed an apex-outflow tract pressure gradient of 3.5 ± 0.3 mmHg (mean ± SE). This pressure gradient correlated with peak early apex-to-outflow tract flow velocity ( r = 0.75, P < 0.05). The gradient was reproduced in the dog model and decreased from 3.1 ± 0.3 to 1.7 ± 0.5 mmHg ( P < 0.05) with caval constriction and increased to 4.2 ± 0.5 mmHg ( P < 0.001) with volume loading. The pressure gradient correlated with peak early transmitral flow (expressed as time derivative of LV volume; r = 0.95) and stroke volume ( r = 0.97). In conclusion, arrival of the early LV filling wave at the apex was associated with a substantial pressure gradient between apex and outflow tract. The pressure gradient was sensitive to changes in preload and correlated strongly with peak early transmitral flow. The significance of this gradient for intraventricular flow propagation in the normal and the diseased heart remains to be determined.

scholarly journals Acute stimulation of the soluble guanylate cyclase does not impact on left ventricular capacitance in normal and hypertrophied porcine hearts in vivo

2018 ◽  
Vol 315 (3) ◽  
pp. H669-H680 ◽  
Author(s):  
Alessio Alogna ◽  
Michael Schwarzl ◽  
Martin Manninger ◽  
Nazha Hamdani ◽  
Birgit Zirngast ◽  
...  
Keyword(s):  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Concentric Hypertrophy ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance ◽  
Stimulation Of

Experimental data indicate that stimulation of the nitric oxide-soluble guanylate cyclase(sGC)-cGMP-PKG pathway can increase left ventricular (LV) capacitance via phosphorylation of the myofilamental protein titin. We aimed to test whether acute pharmacological sGC stimulation with BAY 41-8543 would increase LV capacitance via titin phosphorylation in healthy and deoxycorticosteroneacetate (DOCA)-induced hypertensive pigs. Nine healthy Landrace pigs and 7 pigs with DOCA-induced hypertension and LV concentric hypertrophy were acutely instrumented to measure LV end-diastolic pressure-volume relationships (EDPVRs) at baseline and during intravenous infusion of BAY 41-8543 (1 and 3 μg·kg−1·min−1 for 30 min, respectively). Separately, in seven healthy and six DOCA pigs, transmural LV biopsies were harvested from the beating heart to measure titin phosphorylation during BAY 41-8543 infusion. LV EDPVRs before and during BAY 41-8543 infusion were superimposable in both healthy and DOCA-treated pigs, whereas mean aortic pressure decreased by 20–30 mmHg in both groups. Myocardial titin phosphorylation was unchanged in healthy pigs, but total and site-specific (Pro-Glu-Val-Lys and N2-Bus domains) titin phosphorylation was increased in DOCA-treated pigs. Bicoronary nitroglycerin infusion in healthy pigs ( n = 5) induced a rightward shift of the LV EDPVR, demonstrating the responsiveness of the pathway in this model. Acute systemic sGC stimulation with the sGC stimulator BAY 41-8543 did not recruit an LV preload reserve in both healthy and hypertrophied LV porcine myocardium, although it increased titin phosphorylation in the latter group. Thus, increased titin phosphorylation is not indicative of increased in vivo LV capacitance. NEW & NOTEWORTHY We demonstrate that acute pharmacological stimulation of soluble guanylate cyclase does not increase left ventricular compliance in normal and hypertrophied porcine hearts. Effects of long-term soluble guanylate cyclase stimulation with oral compounds in disease conditions associated with lowered myocardial cGMP levels, i.e., heart failure with preserved ejection fraction, remain to be investigated.

Effect of human urotensin-II infusion on hemodynamics and cardiac function

2003 ◽  
Vol 81 (2) ◽  
pp. 125-128 ◽  
Author(s):  
Ghada S Hassan ◽  
Fazila Chouiali ◽  
Takayuki Saito ◽  
Fu Hu ◽  
Stephen A Douglas ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Urotensin Ii ◽  
Ventricular Systolic Pressure ◽  
Wide Range ◽  
Dose Dependent Decrease

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by ±dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.Key words: urotensin-II, rat, infusion, heart.

Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts

1990 ◽  
Vol 259 (4) ◽  
pp. H1086-H1096 ◽  
Author(s):  
J. M. Capasso ◽  
T. Palackal ◽  
G. Olivetti ◽  
P. Anversa
Keyword(s):  
Ventricular Remodeling ◽  
Volume Fraction ◽  
Diastolic Pressure ◽  
Structural Characteristics ◽  
Myocardial Dysfunction ◽  
Pressure Rise ◽  
Wall Stress ◽  
Left Ventricular ◽  
Cross Sectional

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.

Left ventricular diastolic function of remodeled myocardium in dogs with pacing-induced heart failure

1998 ◽  
Vol 274 (3) ◽  
pp. H945-H954 ◽  
Author(s):  
Steven B. Solomon ◽  
Srdjan D. Nikolic ◽  
Stanton A. Glantz ◽  
Edward L. Yellin
Keyword(s):  
Heart Failure ◽  
Elastic Properties ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Elastic Recoil ◽  
Systolic Volume ◽  
Left Ventricular Chamber ◽  
Volume Relation

In patients with heart failure, decreased contractility resulting in high end-diastolic pressures and a restrictive pattern of left ventricular filling produces a decrease in early diastolic filling, suggesting a stiff ventricle. This study investigated the elastic properties of the myocardium and left ventricular chamber and the ability of the heart to utilize elastic recoil to facilitate filling during pacing-induced heart failure in the anesthetized dog. Elastic properties of the myocardium were determined by analyzing the myocardial stress-strain relation. Left ventricular chamber properties were determined by analyzing the pressure-volume relation using a logarithmic approach. Elastic recoil was characterized using a computer-controlled mitral valve occluder to prevent transmitral flow during diastole. We conclude that, during heart failure, the high end-diastolic pressures suggestive of a stiff ventricle are due not to stiffer myocardium but to a ventricle whose chamber compliance characteristics are changed due to geometric remodeling of the myocardium. The restrictive filling pattern is a result of the ventricle being forced to operate on the stiff portion of the diastolic pressure-volume relation to maintain cardiac output. Slowed relaxation and decreased contractility result in an inability of the heart to contract to an end-systolic volume below its diastolic equilibrium volume. Thus the left ventricle cannot utilize elastic recoil to facilitate filling during heart failure.

Regional diastolic mechanics of the left ventricle in the conscious dog

1979 ◽  
Vol 236 (2) ◽  
pp. H323-H330 ◽  
Author(s):  
D. Ling ◽  
J. S. Rankin ◽  
C. H. Edwards ◽  
P. A. McHale ◽  
R. W. Anderson
Keyword(s):  
Left Ventricle ◽  
Pressure Gradient ◽  
Regional Differences ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Transmural Pressure ◽  
Diastolic Filling ◽  
Rapid Phase ◽  
Conscious Dog ◽  
Dynamic Relationship

In eight chronically instrumented conscious dogs, apical and middle left ventricular transverse diameters were measured with pulse-transit ultrasonic dimension transducers. Intracavitary apical and midventricular pressures and intrapleural pressure were measured with micromanometers. Both diameters were normalized as a percent extension from the dimension at zero transmural pressure, determined during a transient vena caval occlusion. During the rapid phase of diastolic filling, there was a 2--5 mmHg pressure gradient from the midventricle to the apex. During late rapid filling, the apical transmural pressure and diameter increased more rapidly and reached diastasis 17 +/- 4 ms earlier than the corresponding midventricular measurements (P less than 0.01). The static diastolic pressure-dimension characteristics at the apical and midventricular levels were not significantly different (P greater than 0.30). The dynamic diastolic pressure-dimension relationship was also similar at the two levels and could be represented by a model incorporating parallel viscous properties. Because of regional differences in pressures and dimensions, however, the dynamic relationship could not be modeled when pressure was compared to the dimension at a different level. Thus, diastolic pressures should be measured at the same level as dimensions when assessing left ventricular diastolic mechanics.

Diverse regulation of IP3 and ryanodine receptors by pentazocine through σ1-receptor in cardiomyocytes

2013 ◽  
Vol 305 (8) ◽  
pp. H1201-H1212 ◽  
Author(s):  
Hideaki Tagashira ◽  
Md. Shenuarin Bhuiyan ◽  
Kohji Fukunaga
Keyword(s):  
Cardiac Hypertrophy ◽  
Diastolic Pressure ◽  
Ryanodine Receptors ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Female Rats ◽  
In Vivo Studies ◽  
Atp Production ◽  
Cultured Cardiomyocytes

Although pentazocine binds to σ1-receptor (σ1R) with high affinity, the physiological relevance of its binding remains unclear. We first confirmed that σ1R stimulation with pentazocine rescues contractile dysfunction following pressure overload (PO)-induced cardiac hypertrophy ovariectomized (OVX) female rats. In in vivo studies, vehicle, pentazocine (0.5–1.0 mg/kg ip), and NE-100 (1.0 mg/kg po), a σ1R antagonist, were administered for 4 wk (once daily) starting from the onset of aortic banding after OVX. We also examined antihypertrophic effects of pentazocine (0.5–1 μM) in cultured cardiomyocytes exposed to angiotensin II. Pentazocine administration significantly inhibited PO-induced cardiac hypertrophy and rescued hypertrophy-induced impairment of cardiac dysfunctions such as left ventricular end-diastolic pressure, left ventricular developed pressure, and left ventricular contraction and relaxation (±dp/dt) rates. Coadministration of NE-100 with pentazocine eliminated pentazocine-induced amelioration of heart dysfunction. Interestingly, pentazocine administration inhibited PO-induced σ1R reduction and inositol-1,4,5-trisphosphate (IP3) receptor type 2 (IP3R2) upregulation in heart. Therefore, the reduced mitochondrial ATP production following PO was restored by pentazocine administration. Furthermore, we found that σ1R binds to the ryanodine receptor (RyR) in addition to IP3 receptor (IP3R) in cardiomyocytes. The σ1R/RyR complexes were decreased following OVX-PO and restored by pentazocine administration. We noticed that pentazocine inhibits the ryanodine-induced Ca2+ release from sarcoplasmic reticulum (SR) in cultured cardiomyocytes. Taken together, the stimulation of σ1R by pentazocine rescues cardiac dysfunction by restoring IP3R-mediated mitochondrial ATP production and by suppressing RyR-mediated Ca2+ leak from SR in cardiomyocytes.

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