Myocardial interaction between the ventricles

1976 ◽  
Vol 41 (3) ◽  
pp. 362-368 ◽  
Author(s):  
W. P. Santamore ◽  
P. R. Lynch ◽  
G. Meier ◽  
J. Heckman ◽  
A. A. Bove
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
The Other ◽  
Volume Increase ◽  
Lv Volume ◽  
Developed Pressure ◽  
Pressure Changes

The myocardial interaction between the ventricles was studied using isolated, flow-perfused, paced rabbit hearts beating isovolumically. In general, increasing left ventricular (LV) volume increased right ventricular (RV) diastolic and developed pressures. In particular, with a peak RV volume (RVV), increasing LV volume (LVV) from zero to two-thirds of its peak volume increase RV diastolic pressure by 1.7 mmHg (N=10, P less than 0.001) and RV developed pressure by 1.5 mmHg (N=10,P less than 0.001). For the LV, small RVV caused LV diastolic and developed pressure to increase, while large RVV increased LV diastolic pressure but decreased LV developed pressure. With a LVV held at two-third of peak volume, increasing RVV from zero to its peak volume caused LV diastolic pressure to increase by 2.5 mmHg (N=10,P less than 0.001) and LV developed pressure to decrease by 2.0 mmHg (N=10, P less than 0.001). The position of the interventricular septum correlated with LV diastolic pressure and RV diastolic and developed pressure changes (P less than 0.01). The results demonstrate that the diastolic and developed pressure-volume relationships of either ventricle can be acutely altered by varying the volume of the other ventricle.

Effects of sequential biventricular pacing during acute right ventricular pressure overload

2006 ◽  
Vol 291 (5) ◽  
pp. H2380-H2387 ◽  
Author(s):  
T. Alexander Quinn ◽  
George Berberian ◽  
Santos E. Cabreriza ◽  
Lauren J. Maskin ◽  
Alan D. Weinberg ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Biventricular Pacing ◽  
Interventricular Septum ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Ventricular Contractility ◽  
Rate Of Increase ◽  
Control State

Temporary sequential biventricular pacing (BiVP) is a promising treatment for postoperative cardiac dysfunction, but the mechanism for improvement in right ventricular (RV) dysfunction is not understood. In the present study, cardiac output (CO) was optimized by sequential BiVP in six anesthetized, open-chest pigs during control and acute RV pressure overload (RVPO). Ventricular contractility was assessed by the maximum rate of increase of ventricular pressure (dP/d tmax). Mechanical interventricular synchrony was measured by the area of the normalized RV-left ventricular (LV) pressure diagram ( APP). Positive APP indicates RV pressure preceding LV pressure, whereas zero indicates complete synchrony. In the control state, CO was maximized with nearly simultaneous stimulation of the RV and LV, which increased RV ( P = 0.006) and LV dP/d tmax ( P = 0.002). During RVPO, CO was maximized with RV-first pacing, which increased RV dP/d tmax ( P = 0.007), but did not affect LV dP/d tmax, and decreased the left-to-right, end-diastolic pressure gradient ( P = 0.023). Percent increase of RV dP/d tmax was greater than LV dP/d tmax ( P = 0.014). There were no increases in end-diastolic pressure to account for increases in dP/d tmax. In control and RVPO, RV dP/dtmax was linearly related to APP ( r = 0.779, P < 0.001). The relation of CO to APP was curvilinear, with a peak in CO with positive APP in the control state ( P = 0.004) and with APP approaching zero during RVPO ( P = 0.001). These observations imply that, in our model, BiVP optimization improves CO by augmenting RV contractility. This is mediated by changes in mechanical interventricular synchrony. Afterload increases during RVPO exaggerate this effect, making CO critically dependent on simultaneous pressure generation in the RV and LV, with support of RV contractility by transmission of LV pressure across the interventricular septum.

Left ventricular effects on right ventricular developed pressure

1976 ◽  
Vol 41 (6) ◽  
pp. 925-930 ◽  
Author(s):  
W. P. Santamore ◽  
P. R. Lynch ◽  
J. L. Heckman ◽  
A. A. Bove ◽  
G. D. Meier
Keyword(s):  
Coronary Artery ◽  
Right Ventricular ◽  
Left Coronary Artery ◽  
Coronary Occlusion ◽  
Left Ventricular ◽  
Free Wall ◽  
Wall Function ◽  
Lv Volume ◽  
Developed Pressure ◽  
Rv Function

The possibility that left ventricular (LV) performance might affect right ventricular (RV) function through the myocardium was examined by using isolated, flow-perfused, paced rabbit hearts beating isovolumically. ReducingLV volume from its optimal volume to zero caused a 5.7% decrease (N = 10, Pless than 0.001) in right ventricular developed pressure (RVDP). Ligatingthe anterior ventricular branches of the left coronary artery which in the rabbit supply the LV free wall resulted in an additional 9.3% decrease in RVDP (N = 5, P = 0.05) within 3 min of ligation. Finally, cutting the LV free wall from the atrioventricular orifice to the apex (thereby preventing any developed LV free wall force during systole) caused a 45% further decrease in RVDP (N = 2, P less than 0.02). Cineradiographic study showed that the alterations in RVDP resulting from changes in LV volume and coronary occlusion correlated significantly (N = 5, P less than 0.01) with the magnitude ofseptal bulging into the RV cavity during systole. The results indicate thatalteration in LV free wall function and changes in LV volume can directly effect RVDP through the myocardium.

scholarly journals Heart in Acromegaly: The Echocardiographic Characteristics of Patients Diagnosed with Acromegaly in Various Stages of the Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Agata Popielarz-Grygalewicz ◽  
Jakub S. Gąsior ◽  
Aleksandra Konwicka ◽  
Paweł Grygalewicz ◽  
Maria Stelmachowska-Banaś ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Healthy Volunteers ◽  
Global Longitudinal Strain ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Volume Index ◽  
Control Group ◽  
Glucose Metabolism Disorders ◽  
Acromegalic Cardiomyopathy ◽  
The Right

To determine whether the echocardiographic presentation allows for diagnosis of acromegalic cardiomyopathy. 140 patients with acromegaly underwent echocardiography as part of routine diagnostics. The results were compared with the control group comprising of 52 age- and sex-matched healthy volunteers. Patients with acromegaly presented with higher BMI, prevalence of arterial hypertension, and glucose metabolism disorders (i.e., diabetes and/or prediabetes). In patients with acromegaly, the following findings were detected: increased left atrial volume index, increased interventricular septum thickness, increased posterior wall thickness, and increased left ventricular mass index, accompanied by reduced diastolic function measured by the following parameters: E’med., E/E’, and E/A. Additionally, they presented with abnormal right ventricular systolic pressure. All patients had normal systolic function measured by ejection fraction. However, the values of global longitudinal strain were slightly lower in patients than in the control group; the difference was statistically significant. There were no statistically significant differences in the size of the right and left ventricle, thickness of the right ventricular free wall, and indexed diameter of the ascending aorta between patients with acromegaly and healthy volunteers. None of 140 patients presented systolic dysfunction, which is the last phase of the so-called acromegalic cardiomyopathy. Some abnormal echocardiographic parameters found in acromegalic patients may be caused by concomitant diseases and not elevated levels of GH or IGF-1 alone. The potential role of demographic parameters like age, sex, and/or BMI requires further research.

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.

Abstract 13055: Impact of New Pacing Requirement on Echocardiographic Outcomes After Transcatheter Aortic Valve Replacement With Sapien-3 Valve

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yasser Sammour ◽  
Rama D Gajulapalli ◽  
Hassan Mehmood Lak ◽  
Sanchit Chawla ◽  
Arnav Kumar ◽  
...  
Keyword(s):  
Interventricular Septum ◽  
Cleveland Clinic ◽  
Vena Cava ◽  
Left Ventricular ◽  
The Other ◽  
Volume Index ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Sapien 3 ◽  
The Impact

Introduction: New permanent pacemaker (PPM) requirement has been linked with left ventricular dysfunction after TAVR. Objective: We sought to study the impact of new PPM on echocardiographic outcomes after TAVR with SAPIEN-3 (S3) valve. Methods: We included consecutive patients who underwent TAVR with S3 valve at the Cleveland Clinic between April 2015 and December 2018. Patients with prior PPM were excluded. Echocardiograms were reviewed to determine left ventricular ejection fraction (LVEF), left ventricular end diastolic volume index (LVEDVi), left ventricular end systolic volume index (LVESVi), left ventricular dimension during diastole (LVDd), posterior wall thickness during diastole (PWTd), interventricular septum during diastole (IVSd), right ventricular systolic pressure (RVSP), inferior vena cava (IVC) diameter and tricuspid regurgitation (TR) grade. Results: Among 886 patients, the rate of 30-day PPM was 10.2%. Baseline LVEF was similar between new PPM and no PPM (55.4 ± 12.7% vs. 57.2 ± 11.2%; p = 0.188). There were no differences in the other studied echocardiographic parameters at baseline. Among patients with new PPM, LVEF was lower at both 30 days (54.4 ± 11.3% vs. 58.4 ± 10.1%; p = 0.001) and 1 year (54.2 ± 12% vs. 59.1 ± 11.3%; p = 0.009) compared to no PPM with Δ LVEF -0.9% vs. +1.4%; p = 0.023. There were no differences in LVEDVi (52 ± 20.8 vs. 48.3 ± 17.6; p = 0.186) at 1 year. LVESVi was higher with new PPM (24.8 ± 16.1 vs. 20.2 ± 10.9; p = 0.038). However, Δ LVESVi was similar between the 2 groups (-1.6 vs. -2.6; p = 0.517). There were no differences in RVSP (38.9 ± 14.1 vs. 40 ± 14; p = 0.58). LVIDd, PWTd, IVSd and IVC diameter also did not show variations whether patients were paced or not. Moderate to severe TR rates were similar as well (17.7% vs. 21.5%; p = 0.407). Conclusion: Among S3 TAVR recipients, new pacing requirement had a detrimental impact on LVEF at both 30 days and 1 year. However, it did not seem to affect the other studied echocardiographic outcomes after TAVR.

Abstract P109: Alteration in Intracellular Calcium During Cardiac Arrest

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Satoshi Takeda ◽  
Hiroshi Yoshida ◽  
Takeki Ogawa
Keyword(s):  
Cardiac Arrest ◽  
Intracellular Calcium ◽  
Cell Injury ◽  
Diastolic Pressure ◽  
Pulseless Electrical Activity ◽  
Left Ventricular Pressure ◽  
Cardiac Metabolism ◽  
Left Ventricular ◽  
Free Calcium ◽  
Developed Pressure

AIM: A cytosolic free calcium is an important regulator of cardiac metabolism and contractility, and an increased [Ca2+]i has been implicated in irreversible cell injury and contractile dysfunction. We investigated intracellular calcium ([Ca2+]i) dynamics during cardiac arrest, especially in pulseless electrical activity (PEA) and asystole. METHODS: Rat hearts (n=18) were perfused with a Langendorff system and loaded with Fura-2/AM, as a [Ca2+]i marker, and BCECF/AM, as a pHi marker. Surface fluorescence of the heart was recorded with an intracellular ion analyzer. A latex balloon was inserted into the left ventricle to monitor left ventricular pressure. Sustained normo-thermic cardiac arrest was induced for 20 min by clamping the aortic cannula. RESULTS: After clamping (cardiac arrest), the left ventricular developed pressure decreased significantly, from 84.3±11 mmHg to 3.88±0.7 mmHg (p<0.01) at 2min. The rhythm was PEA in all cases in this period, followed by asystole. The amplitude of the [Ca2+]i transient (0.30±0.03) was maintained at 2 min, but further significant increases were observed in both systolic (1.14±0.04, p<0.01) and diastolic levels of [Ca2+]i (0.84±0.04, p<0.05), when compared with pre-arrest levels. The [Ca2+]i transient disappeared 4.7±0.6 min. The diastolic [Ca2+]i increased gradually after 5 min to 20 min. This diastolic [Ca2+]i increase was parallel with the increase in left ventricular end diastolic pressure (indicated ischemic contracture). The pHi increased (to 7.6±1.0) immediately after clamping. Thereafter pHi decreased rapidly and remained steady (at pH 6.6±0.6). CONCLUSIONS: The change in the [Ca2+]i-pressure relationship rather than change in the amplitude of the [Ca2+]i transient was the main contributor in the early cardiac arrest phase. The diastolic [Ca2+]i increase might induce irreversible cell injury in the late cardiac arrest phase.

Direct diastolic ventricular interaction gain measured with sudden hemodynamic transients

1989 ◽  
Vol 256 (2) ◽  
pp. H567-H573 ◽  
Author(s):  
B. K. Slinker ◽  
Y. Goto ◽  
M. M. LeWinter
Keyword(s):  
Confidence Interval ◽  
Right Ventricular ◽  
Diastolic Pressure ◽  
Direct Interaction ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Base Line ◽  
Right Ventricular Volume ◽  
Ventricular Interaction ◽  
Venae Cavae

Changes in right ventricular volume affect left ventricular function via direct ventricular interaction mediated by the septum, common myocardial fibers in the free wall, and the pericardium, and also via series interaction mediated by changes in right ventricular output reaching the left ventricle through the pulmonary circulation. To study direct interaction, series interaction must be held constant or removed from the experimental preparation. Because there has been no way to directly measure direct ventricular interaction in the intact circulation, we developed a new method to experimentally separate these two components of ventricular interaction by combining abrupt occlusion of both venae cavae and quick withdrawal of 10-15 ml of blood from the right ventricle. This procedure decreased right ventricular end-diastolic pressure (RVEDP) on the next beat without changing pulmonary venous flow, left ventricular end-diastolic segment lengths, or left ventricular systolic function. The direct interaction gains, quantified as delta LVEDP/delta RVEDP, where LVEDP is left ventricular end-diastolic pressure, and delta refers to the change between the beats before and after reducing right ventricular volume, were (means +/- SD) 0.32 +/- 0.32 at steady-state LVEDP = 5 mmHg, 0.38 +/- 0.23 at LVEDP = 10 mmHg, and 0.28 +/- 0.32 at LVEDP = 15 mmHg. These gains were not significantly different (P greater than 0.50). Therefore, we calculated an overall average gain by pooling data from the three base-line LVEDP conditions. This value is 0.33 with 95% confidence interval 0.16-0.51. This 95% confidence interval indicates our data are consistent with many previous reports of diastolic direct interaction.

Protective effect of hypoxia on mechanical and metabolic changes induced by hydrogen peroxide in rat hearts

1995 ◽  
Vol 268 (2) ◽  
pp. H614-H620 ◽  
Author(s):  
A. Hara ◽  
Y. Abiko
Keyword(s):  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Receptor Antagonist ◽  
Katp Channel ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Metabolic Changes ◽  
Constant Flow Rate ◽  
Adenosine Receptor Antagonist ◽  
Developed Pressure

The effect of hypoxia (20% O2 for 5 min) on the hydrogen peroxide (H2O2)-induced myocardial change was studied in the Langendorff rat heart, which was perfused at a constant flow rate and driven electrically. H2O2 decreased the left ventricular developed pressure, increased the left ventricular end-diastolic pressure, and decreased the myocardial ATP level. These mechanical and metabolic alterations induced by H2O2 were less prominent in the hypoxia-reoxygenated heart than in the normoxic heart (i.e., hypoxia had a protective effect on the H2O2-induced change). Both 8-phenyltheophylline (8-PT), a nonselective adenosine-receptor antagonist, and glyburide (Gly), an inhibitor of the ATP-sensitive potassium (KATP) channel, significantly reduced the protective effect of hypoxia. The adenosine A1-receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DP-CPX) reduced the protective effect of hypoxia incompletely. Gly, 8-PT, and DPCPX did not affect the mechanical function and energy metabolism of the hypoxia-reoxygenated heart without H2O2. These results suggest that brief and mild hypoxia attenuates the H2O2-induced mechanical and metabolic changes and that the protective effect of hypoxia is probably mediated by activation of the adenosine receptors, which open the KATP channel.

End-systolic and end-diastolic ventricular interaction

1986 ◽  
Vol 251 (5) ◽  
pp. H1062-H1075 ◽  
Author(s):  
B. K. Slinker ◽  
S. A. Glantz
Keyword(s):  
Right Ventricular ◽  
Interventricular Septum ◽  
Systolic Pressure ◽  
Direct Interaction ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Physiological Mechanisms ◽  
In Series ◽  
The Right ◽  
Transient And Steady State

Right ventricular volume affects left ventricular volume via direct interaction across the interventricular septum and series interaction because the right and left hearts are connected in series through the lungs. Because it is difficult to sort out complex physiological mechanisms in the intact circulation, the relative importance of these two effects is unknown. We used statistical analyses of transient changes in left and right ventricular pressures and dimensions following pulmonary artery and venae caval constrictions to separate and quantitate the direct (immediate) from the series (delayed) interaction effects on left ventricular size at end systole and end diastole. With the pericardium closed, direct interaction was one-half as important as series interaction at end diastole and was one-third as important at end systole. With the pericardium removed, direct interaction was one-fifth as important as series interaction at end diastole and one-sixth as important at end systole. These results suggest that differences between transient and steady-state end-systolic pressure-volume relationships are largely explained by direct interaction and that direct end-systolic interaction is important for maintaining balanced right and left heart outputs.

Preservation of left ventricular function by insulin in experimental catecholamine cardiomyopathy

1980 ◽  
Vol 238 (2) ◽  
pp. H257-H262
Author(s):  
J. C. Werner ◽  
J. C. Lee ◽  
S. E. Downing
Keyword(s):  
Left Ventricular Function ◽  
Ventricular Function ◽  
Myocardial Injury ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Initial Slope ◽  
Histological Findings ◽  
Aortic Constriction ◽  
The Mean ◽  
Lv Volume

We have shown previously that insulin reduces myocardial injury associated with norepinephrine (NE) infusion in the rabbit (Am. J. Pathol. 93:399--353, 1978). In the present study, left ventricular function (LVF) was assessed from afterload curves obtained by progressive aortic constriction 2--4 days following NE infusion. The initial slope of the function curves (SFC), maximum dP/dt and left ventricular end-diastolic pressure at 120 mmHg ((LVEDP120) were used for comparison. In 4 controls, SFC averaged 23.8 mmHg/cmH2O. In 10 rabbits given NE, the mean slope was 8.4 (P less than 0.01). However, animals pretreated with insulin before being given NE did not differ from controls (SFC, 19.7 mmHg/cmH2O). These performance data were supported by measurements of LVEDP120, which were 2.8, 12.3 and 3.1 cmH2O, respectively (P less than 0.05 and less than 0.02). In spite of the higher LVEDP, max dP/dt120 was significantly lower in the NE group than in the group given insulin. Histological findings and postmortem measurements of LV volume and mass were consistent with the observed differences in LVF. It is concluded that NE damage reduces LVF and this is largely prevented by pretreatment with insulin.

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