Ejecting deactivation does not affect O2 consumption-pressure-volume area relation in dog hearts

1993 ◽  
Vol 265 (3) ◽  
pp. H934-H942 ◽  
Author(s):  
O. Kawaguchi ◽  
Y. Goto ◽  
S. Futaki ◽  
Y. Ohgoshi ◽  
H. Yaku ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Generation Process ◽  
Ejection Velocity ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume

We studied the effects of ejection velocity and resistive properties of the left ventricle (LV) on myocardial oxygen consumption (VO2) in 13 excised cross-circulated dog hearts. Increases in peak ejection velocity (-dV/dt) from 4.0 +/- 1.3 (SD) end-diastolic volume (EDV)/s to 12.7 +/- 5.3 EDV/s with constant EDV and end-systolic volume (velocity run) induced systolic pressure deficit. This decreased pressure-volume area (PVA; a measure of ventricular mechanical energy) and LV end-systolic elastance (Emax) by 47 +/- 14 and 38 +/- 15%, respectively. Unchanged maximum rate of left ventricular pressure rise and time-varying elastance during the isovolumic contraction period at the same EDV indicated that these contractions started with the same contractile state although the quicker ejection caused the greater deactivation. If the PVA deficit due to systolic pressure deficit is attributable to an internal energy-dissipating resistive element, VO2 in the velocity run will not as much decrease in proportion to PVA as in the isovolumic or slowly ejecting control run. However, the decreases in PVA due to increased -dV/dt decreased VO2 to the same extent as in the control run. This result negated the possibility that the pressure and PVA deficits would be caused by a mechanical energy-losing process. The same results were obtained whether or not Emax was decreased by quick ejection. We conclude that the pressure and PVA deficits and the proportionally decreased VO2 during quick ejection are mainly attributable to suppression of a ventricular mechanical energy generation process, but not of mechanical energy-losing process, by ejecting deactivation.

Effects of reduced resistive afterload on left ventricular pressure-volume relationship

1985 ◽  
Vol 248 (2) ◽  
pp. H163-H169
Author(s):  
J. Ducas ◽  
U. Schick ◽  
L. Girling ◽  
R. M. Prewitt
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Base Line ◽  
Resistive Load ◽  
Systolic Volume ◽  
Arteriovenous Fistulas ◽  
End Diastolic Volume ◽  
End Systolic Volume

In seven anesthetized, beta-blocked dogs, we investigated the effects of a reduction in systemic vascular resistance (SVR) on left ventricular (LV) systolic mechanics. LV pressure and volumes (scintigraphic techniques) were measured in base-line condition, after opening one and then two arteriovenous fistulas (AVF). Volume was infused to maintain LV end-systolic pressure (LVESP). Despite a constant ESP, the mean end-systolic volume (LVESV) fell from 42 to 31 ml (P less than 0.025) when the SVR fell from 81 to 48 units (P less than 0.0025), and the LVESV fell further to 24 ml (P less than 0.0025) when the SVR was decreased to 30 units (P less than 0.025). In six similarly prepared dogs, aortic flow was measured, and when resistive afterload decreased, instantaneous flow increased. Since end-diastolic volume was not significantly changed when resistive afterload decreased, instantaneous LV volume decreased despite constant systolic LV pressure. In two of these dogs, LV pressure-volume (PV) trajectories were drawn for the ejection period. When SVR decreased there was a marked leftward shift of the PV trajectory as the end of ejection was approached. It is concluded that at a given contractile state and ventricular pressure, alterations in resistive load directly affect rate and extent of ventricular shortening.

Dimensional analysis of the left ventricle: effects of acute aortic regurgitation

1975 ◽  
Vol 228 (2) ◽  
pp. 536-542 ◽  
Author(s):  
SJ Leshin ◽  
LD Horwitz ◽  
JH Mitchell
Keyword(s):  
Left Ventricle ◽  
Aortic Regurgitation ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Systolic Volume ◽  
Severe Aortic Regurgitation ◽  
End Diastolic Volume ◽  
Catheter Technique ◽  
End Systolic Volume

The effects of acute severe aortic regurgitation on the left ventricle were investigated in conscious, chronically instrumented dogs. Left ventricular dimensions and volumes were measured from biplane cineradiographs of beads positioned near the endocardium. Data were collected before and after the production of aortic regurgitation by a catheter technique. The aortic regurgitation resulted in increases in mean aortic pulse pressure from 44 to 73 mmHg (P smaller than 0.001), heart rate from 87 to 122 beats/min (P smaller than 0.02), and left ventricular end-diastolic pressure from 11 to 25 mmHg (P smaller than 0.05). Mean end-diastolic volume rose from 61 to 69 cc (P smaller than 0.001), while end-systolic volume remained unchanged at 37 cc. The end-diastolic dilatation following regurgitation was asymmetrical in that the increase in size was due principally to an increase in the septal-lateral axis. The acute volume load of aortic regurgitation was accomplished by an increase in end-diastolic volume, i.e., the Frank-Starling mechanism. The tachycardia probably reflects augmented cardiac sympathetic activity, but the constant end-systolic volume at a similar mean systolic pressure suggests that the net contractile state was unchanged.

Effect of vasopressin on left ventricular performance

1993 ◽  
Vol 264 (1) ◽  
pp. H53-H60
Author(s):  
C. P. Cheng ◽  
Y. Igarashi ◽  
H. S. Klopfenstein ◽  
R. J. Applegate ◽  
Z. Shihabi ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Performance ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
The Right

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 microns.kg-1 x min-1 for 2 min) the plasma AVP was elevated from 3.9 +/- 0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1 x min, P < 0.01) and arterial elastance (Ea) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dtmax)-end-diastolic volume (VED) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg.s-1 x ml-1, P < 0.05), and the stroke work-VED relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in Ea produced by methoxamine did not depress LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)

P5581In patients with aortic valve regurgitation, left ventricular geometry and strain, more than pulmonary artery systolic pressure, affect right ventricular function

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Abdelgawad ◽  
M A Abdelhay ◽  
S Ashour ◽  
M Shehata ◽  
M Previato ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Pulmonary Artery Systolic Pressure ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
Sphericity Index ◽  
End Systolic Volume ◽  
Rv Function

Abstract Background Left ventricular (LV) overload due to aortic valve (AR) regurgitation may affect right ventricular (RV) function. Elevation of pulmonary artery pressures secondary to isolated AR is not common. Thus, the effects of chronic LV overload due to AR on RV function remains to be clarified. Purpose To assess the determinants of RV dysfunction in chronic AR. Methods We studied 36 patients with moderate or severe AR (53±18 years, 81% were men). We used 3D echocardiography to acquire multi-beat, full-volume data sets of LV and RV and to measure volumes and EF. RV fractional area change (FAC) was calculated. LV global longitudinal strain (GLS) and RV peak longitudinal strain (RVLS) were assessed by 2D speckle tracking echocardiography. Results RV EF and RV FAC were 40±6% and 34±9%. LV GLS and peak RVLS were reduced (Table). LV EDVi showed negative correlations with RV function (RV EF: r=−0.545, p<0.001; RV FAC: r=−0.816, p<0.001). LV sphericity index showed negative correlations with RV function (RVFAC: r=−0.608, P=0.001; RV EF: r=−0.469, P=0.004). Moreover, LV GLS and RVLS correlated positively with RV function (FAC: for GLS: r=0.475, p=0.003 and for RVLS: r=0.389, p=0.019) (RV EF: for GLS: r=0.526, p=0.001 and for RVLS: r=0.475, p=0.003). On multivariable linear regression analysis, LV EDVi, LV sphericity index, LV GLS and peak RVLS were found to be the only independent predictors of RV EF and FAC. Left and right ventricular volumes and function in patients with chronic aortic regurgitation AR (n=36) Control (n=25) p value LV end-diastolic volume (ml/m2) 106±36 56±8 <0.001 LV end-systolic volume (ml/m2) 50±28 22±4 <0.001 LV ejection fraction (%) 54±10 60±4 <0.001 LV sphericity index 0.53±0.11 0.38±0.08 <0.001 Pulmonary artery systolic pressure (mm Hg) 27±8 RV end-diastolic volume (ml/m2) 59±12 35±7 <0.001 RV end-systolic volume (ml/m2) 31±9 17±3 <0.001 RV ejection fraction (%) 40±6 50±4 <0.001 RV fractional area change (%) 34±9 44±6 <0.001 LV GLS (%) −18±3 21±1 <0.001 Peak RVLS (%) −26±5 −31±3 <0.001 Conclusions RV remodeling in chronic LV overload due to AR occurs independent on PASP values. LV size, shape and strain are the only independent predictors of RV function.

Endotoxin-induced left ventricular depression is blocked by nitrogen mustard or dimethylthiourea in rabbits

1995 ◽  
Vol 269 (3) ◽  
pp. H1098-H1105
Author(s):  
Y. Nishikawa ◽  
W. Y. Lew
Keyword(s):  
Nitrogen Mustard ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Free Radical Scavenger ◽  
Control Group ◽  
Radical Scavenger ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume

We examined endotoxin-induced myocardial depression in 31 anesthetized rabbits using left ventricular end-systolic and end-diastolic pressure-volume relationships (sonomicrometers). In the control group, endotoxin (100 micrograms/kg iv) induced systolic depression (> 10% increase in end-systolic volume at matched end-systolic pressure) in 9 of 16 and diastolic dilation (> 10% increase in end-diastolic volume at matched end-diastolic pressure) in 8 of 16 rabbits within 7 h, unrelated to hypotension, acidosis, or hypoxia. Seven rabbits were pretreated with nitrogen mustard (1-2 mg/kg iv 4 and 2 days before) to decrease circulating neutrophils and monocytes by 98%. Endotoxin did not induce systolic depression in any rabbit (P = 0.01 compared with control), and diastolic dilation developed in one rabbit (P = 0.12). In eight rabbits pretreated with dimethylthiourea (DMTU; 500 mg/kg iv 30 min before), an intracellular free radical scavenger, systolic depression developed in one (P = 0.05) and diastolic dilation in five (P = 0.44). We conclude that cells inhibited by nitrogen mustard (e.g., neutrophils, monocytes, or macrophages) mediate endotoxin-induced left ventricular systolic depression. DMTU inhibited endotoxin-induced systolic but not diastolic dysfunction.

Independent effects of preload, afterload, and contractility on left ventricular torsion

1999 ◽  
Vol 277 (3) ◽  
pp. H1053-H1060 ◽  
Author(s):  
Sheng-Jing Dong ◽  
Paul S. Hees ◽  
Wen-Mei Huang ◽  
Sam A. Buffer ◽  
James L. Weiss ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Dobutamine Infusion ◽  
Windkessel Model ◽  
Systolic Volume ◽  
Left Ventricular Torsion ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
Ventricular Torsion ◽  
Magnetic Resonance Imaging Mri

Shortening of oblique left ventricular (LV) fibers results in torsion. A unique relationship between volume and torsion is therefore expected, and the effects of load and contractility on torsion should be predictable. However, volume-independent behavior of torsion has been observed, and the effects of load on this deformation remain controversial. We used magnetic resonance imaging (MRI) with tagging to study the relationships between load and contractility, and torsion. In ten isolated, blood-perfused canine hearts, ejection was controlled by a servopump: end-diastolic volume (EDV) was controlled by manipulating preload parameters and end-systolic volume (ESV) by manipulating afterload using a three-element windkessel model. MRI was obtained at baseline, two levels of preload alteration, two levels of afterload alteration, and dobutamine infusion. An increase in EDV resulted in an increase in torsion at constant ESV (preload effect), whereas an increase in ESV resulted in a decrease in torsion at constant EDV (afterload effect). Dobutamine infusion increased torsion in association with an increase in LV peak-systolic pressure (PSP), even at identical EDV and ESV. Multiple regression showed correlation of torsion with preload (EDV), afterload (ESV), and contractility (PSP; r = 0.67). Furthermore, there was a close linear relationship between torsion and stroke volume (SV) and ejection fraction (EF) during load alteration, but torsion during dobutamine infusion was greater than expected for the extent of ejection. Preload and afterload influence torsion through their effects on SV and EF, and there is an additional direct inotropic effect on torsion that is independent of changes in volume but rather is force dependent. There is therefore potential for the torsion-volume relation to provide a load-independent measure of contractility that could be measured noninvasively.

A Systematic Review and Meta-analysis : Safety and Efficacy of Mesenchymal stem Cells Therapy for Heart Failure

2020 ◽  
Vol 15 ◽  
Author(s):  
Tiantian Shen ◽  
Lin Xia ◽  
Wenliang Dong ◽  
Jiaxue Wang ◽  
Feng Su ◽  
...  
Keyword(s):  
Heart Failure ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Safety And Efficacy ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume

Background: Preclinical and clinical evidence suggests that mesenchymal stem cells (MSCs) may be beneficial in treating heart failure (HF). However, the effects of stem cell therapy in patients with heart failure is an ongoing debate and the safety and efficacy of MSCs therapy is not well-known. We conducted a systematic review of clinical trials that evaluated the safety and efficacy of MSCs for HF. This study aimed to assess the safety and efficacy of MSCs therapy compared to the placebo in heart failure patients. Methods: We searched PubMed, Embase, Cochrane library systematically, with no language restrictions. Randomized controlled trials(RCTs) assessing the influence of MSCs treatment function controlled with placebo in heart failure were included in this analysis. We included RCTs with data on safety and efficacy in patients with heart failure after mesenchymal stem cell transplantation. Two investigators independently searched the articles, extracted data, and assessed the quality of the included studies. Pooled data was performed using the fixed-effect model or random-effect model when it appropriate by use of Review Manager 5.3. The Cochrane risk of bias tool was used to assess bias of included studies. The primary outcome was safety assessed by death and rehospitalization and the secondary outcome was efficacy which was assessed by six-minute walk distance and left ventricular ejection fraction (LVEF)，left ventricular end-systolic volume（LVESV），left ventricular end-diastolic volume（LVEDV） and brain natriuretic peptide（BNP） Results: A total of twelve studies were included, involving 823 patients who underwent MSCs or placebo treatment. The overall rate of death showed a trend of reduction of 27% (RR [CI]=0.73 [0.49, 1.09], p=0.12) in the MSCs treatment group. The incidence of rehospitalization was reduced by 47% (RR [CI]=0.53[0.38, 0.75], p=0.0004). The patients in the MSCs treatment group realised an average of 117.01m (MD [95% CI]=117.01m [94.87, 139.14], p<0.00001) improvement in 6MWT.MSCs transplantation significantly improved left ventricular ejection fraction (LVEF) by 5.66 % (MD [95% CI]=5.66 [4.39, 6.92], p<0.00001), decreased left ventricular end-systolic volume (LVESV) by 14.75 ml (MD [95% CI]=-14.75 [-16.18, -12.83], p<0.00001 ) and left ventricular end-diastolic volume (LVEDV) by 5.78 ml (MD [95% CI]=-5.78[-12.00, 0.43], p=0.07 ) ,in the MSCs group , BNP was decreased by 133.51 pg/ml MD [95% CI]= -133.51 [-228.17,-38.85], p=0.54, I2= 0.0%) than did in the placebo group. Conclusions: Our results suggested that mesenchymal stem cells as a regenerative therapeutic approach for heart failure is safe and effective by virtue of their self-renewal potential, vast differentiation capacity and immune modulating properties. Allogenic MSCs have superior therapeutic effects and intracoronary injection is the optimum delivery approach. In the tissue origin, patients who received treatment with umbilical cord MSCs seem more effective than bone marrow MSCs. As to dosage injected, (1-10)*10^8 cells were of better effect.

Use of the Frank-Starling mechanism during submaximal versus maximal upright exercise

1986 ◽  
Vol 251 (6) ◽  
pp. H1101-H1105 ◽  
Author(s):  
G. D. Plotnick ◽  
L. C. Becker ◽  
M. L. Fisher ◽  
G. Gerstenblith ◽  
D. G. Renlund ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Blood Pool ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Vigorous Exercise ◽  
Systolic Volume ◽  
Early Exercise ◽  
End Diastolic Volume ◽  
Blood Pool Scintigraphy ◽  
End Systolic Volume

To evaluate the extent to which the Frank-Starling mechanism is utilized during successive stages of vigorous upright exercise, absolute left ventricular end-diastolic volume and ejection fraction were determined by gated blood pool scintigraphy at rest and during multilevel maximal upright bicycle exercise in 30 normal males aged 26-50 yr, who were able to exercise to 125 W or greater. Left ventricular end-systolic volume, stroke volume, and cardiac output were calculated at rest and during each successive 3-min stage of exercise [25, 50, 75, 100, and 125–225 W (peak)]. During early exercise (25 W), end-diastolic and stroke volumes increased (+17 +/- 1 and +31 +/- 4%, respectively), with no change in end-systolic volume. With further exercise (50–75 W) end-diastolic volume remained unchanged as end-systolic volume decreased (-12 +/- 4 and -24 + 5%, respectively). At peak exercise end-diastolic volume decreased to resting level, stroke volume remained at a plateau, and end-systolic volume further decreased (-48 +/- 7%). Thus the Frank-Starling mechanism is used early in exercise, perhaps because of a delay in sympathetic mobilization, and does not appear to play a role in the later stages of vigorous exercise.

scholarly journals The effect of left ventricle ischemia severity on cardiac performance appeared on ejection fraction using radioactive TC 99m MIBI in comparison with echocardiography

2021 ◽  
Vol 2114 (1) ◽  
pp. 012006
Author(s):  
M K Mohammed ◽  
S I Essa
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Mean Value ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
Significant Difference ◽  
End Systolic Volume ◽  
The Mean

Abstract Ischemic heart disease is a major causes of heart failure. Heart failure patients have predominantly left ventricular dysfunction (systolic or diastolic dysfunction, or both). Acute heart failure is most commonly caused by reduced myocardial contractility, and increased LV stiffness. We performed echocardiography and gated SPECT with Tc99m MIBI within 263 patients and 166 normal individuals. Left ventricular end systolic volume (LVESV), left ventricular end diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF) were measured. For all degrees of ischemia, there was a significant difference between ejection fraction values measured by SPECT and echocardiography, and there were no significant differences among end systolic volume and end diastolic volume value calculated by two methods for all cases. The mean value for EDV (ECHO)/EDV (SPECT) was 1.07 ± 0.31 for degree (1, 2); in the degree 3 the mean value was 1.02 ± 0.08, and 1.005 ± 0.07 for degree 4. The mean value for ESV (ECHO)/ESV (SPECT) was 1.08 ± 0.34 for degree (1, 2); while 1.03 ± 0.12, 1.021 ± 0.128 for degree 3 and 4 respectively. This study was showed a good relation between left ventricular size and ejection fraction measured by SPECT with Tc99m, and echocardiography.

Comparison of left ventricular volumes by dye dilution and angiographic methods in the dog

1963 ◽  
Vol 204 (3) ◽  
pp. 446-450 ◽  
Author(s):  
Franz J. Hallermann ◽  
G. C. Rastelli ◽  
H. J. C. Swan
Keyword(s):  
Stroke Volume ◽  
Left Ventricular ◽  
Dilution Method ◽  
Left Ventricular Volumes ◽  
Heart Rates ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
Fundamental Error ◽  
Indicator Dye

In each of 12 mongrel dogs, data for end-diastolic volume, end-systolic volume, and stroke volume of the left ventricle were obtained by two independent methods: the indicator dilution method and a radiographic method. While the values for stroke volume showed good agreement between the two methods, a significant and directionally constant difference was found between values for end-diastolic volume and end-systolic volume calculated by the two different methods. This was observed in dogs with fast heart rates (exceeding 150 beats/min), as well as in dogs with heart rates of about 100 beats/min. The findings strongly suggest that a fundamental error is present in estimations of volume based on the washout of an indicator dye.

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