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Biomedical subjects

S D Nikolic

Publications and source records attributed to S D Nikolic.

At least 19 recordsLinked to original sources
PubMed1999

Contraction-relaxation coupling: determination of the onset of diastole.

Left ventricular relaxation is dependent on afterload conditions during systole. An abrupt increase in afterload while the ventricle is actively contracting prolongs the duration of systole. An increase in afterload during ventricular relaxation shortens the duration of systole. Therefore, we hypothesized that the point during systole when an abrupt increase in afterload had no effect on the duration of systole represented the onset of ventricular relaxation. To determine when this point occurs, we performed aortic occlusions progressively throughout the duration of systole in six dogs. We determined the change in systolic time (t(sys)) after an intervention normalized to t(sys) of a control beat (t(sys,i)/t(sys, c)) as a function of systolic occlusion time as a percentage of total systolic time (t(occ)/t(sys,c)), where t(sys) is the duration from time of left ventricular end-diastolic pressure to the time of minimum first derivative of left ventricular pressure. Our results show the onset of left ventricular relaxation during normal ejection occurs at 34 +/- 3% of systolic time and approximately 16% after the onset of ejection. Thus the beginning of relaxation occurs soon after the beginning of ejection, suggesting that relaxation is modulated by variable loading conditions during ejection, significantly before what has been conventionally been assumed to be the beginning of ventricular relaxation.

Animals↗
PubMed1998

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

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 transmittral 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.

Animals↗
PubMed1998

Estimation of regional left ventricular wall stresses in intact canine hearts.

Left ventricular (LV) wall stress is an important element in the assessment of LV systolic function; however, a reproducible technique to determine instantaneous local or regional wall stress has not been developed. Fourteen dogs underwent placement of twenty-six myocardial markers into the ventricle and septum. One week later, marker images were obtained using high-speed biplane videofluoroscopy under awake, sedated, atrially paced baseline conditions and after inotropic stimulation (calcium). With a model taking into account LV pressure, regional wall thickness, and meridional and circumferential regional radii of curvature, we computed average midwall stress for each of nine LV sites. Regional end-systolic and maximal LV wall stress were heterogeneous and dependent on latitude (increasing from apex to base, P < 0.001) and specific wall (anterior > lateral and posterior wall stresses; P = 0. 002). Multivariate ANOVA demonstrated only a trend (P = 0.056) toward increased LV stress after calcium infusion; subsequent univariate analysis isolated significant increases in end-systolic LV wall stress with increased inotropic state at all sites except the equatorial regions. The model used in this analysis incorporates local geometric factors and provides a reasonable estimate of regional LV wall stress compared with previous studies. LV wall stress is heterogeneous and dependent on the particular LV site of interest. Variation in wall stress may be caused by anatomic differences and/or extrinsic interactions between LV sites, i.e., influences of the papillary muscles and the interventricular septum.

Animals↗
PubMed1997

Septal function during left ventricular unloading.

BACKGROUND: Left ventricular (LV) unloading with mechanical support devices alters biventricular geometry and impairs right ventricular (RV) contractility, but its effect on septal systolic function remains unknown. METHODS AND RESULTS: To evaluate the effects of LV volume and pressure unloading on septal geometry and function, LV preload was abruptly reduced by clamping left atrial pressure between 0 and -2 mm Hg in seven open-chest, anesthetized dogs by use of a pressure-control servomechanism to withdraw blood from the left atrium. With left atrial pressure clamping, maximal LV pressure decreased 30 +/- 12% (mean +/- SD) (P < .0001) and LV end-diastolic cross-sectional area (determined by two-dimensional echocardiography) decreased by 53 +/- 16% (P < .0001). This caused the septum to shift toward the left (RV septal free-wall dimension increased; P < .004) and flatten (radius of curvature increased; P < .0002), while LV septal free-wall dimension fell (P < .0001). Septal end-diastolic thickness increased 23 +/- 15% (P < .0005), reflecting a decline in septal preload. Systolic septal thickening decreased (P < .002), while systolic septal output (Septal Output = Septal Thickening x Heart Rate) fell from 30 +/- 17 to 15 +/- 22 cm/min (P < .002). This was associated with movement along the septal Frank-Starling equivalent (septal output versus end-diastolic septal thickness [preload] relation) to a less productive portion of the curve. CONCLUSIONS: LV unloading not only altered interventricular septal geometry but also reduced septal systolic thickening and output, all of which may contribute to impaired RV contractility during mechanical LV support.

Animals↗
PubMed1997

Redox potential measurements of plasma in patients undergoing coronary artery bypass graft and its clinical significance.

The apparent redox potentials (Em) of plasma as a marker of oxidant injury during coronary artery bypass graft (CABG) is determined, and their clinical significance is discussed. We measured plasma Em of normal volunteers (n = 20) and samples drawn at different time points from patients undergoing elective CABG (n = 60) directly and by adding 5 microl (20 mM) oxidants or reductants with known redox potential to plasma (95 microl), using a micro Pt/AgCl combination redox electrode. The Em value stays elevated up to 30 min during the surgery, after the administration of protamine it came down toward a more reduced state. Similar changes are seen with the lactate pyruvate ratio. Smaller changes of Em than normal are observed in plasma samples from patients treated with Aprotinin (antiprotease), Carmeda (heparin-coated) circuit and aspirin reflecting their protective effect. Redox potential (Em) measurements appear to be effective and useful in monitoring redox shifts wherever oxidative stress needs to be monitored.

Anticoagulants↗
PubMed1996

Time to dP/dtmax reflects both inotropic and chronotropic properties of cardiac contraction: a conscious dog study.

This study supports a mathematical model and previous findings indicating that td, the time from onset of contraction to dP/dtmax, reflects the time-dependent aspects of contraction and hence decreases with increasing contractility. Combined data from 20 conscious instrumented dogs create a highly significant inverse and linear td-HR (heart rate) relation. Both norepinephrine and isoproterenol decreased td values, but norepinephrine, in contrast to isoproterenol, decreased the heart rate by a reflex response. Despite the remarkable decline in heart rate (25.8%) td was decreased (16.5%). During wide spontaneous R-R variations longer preceding intervals gave shorter td values. The latter two facts indicate the dependence of td on the contractile state rather than it being merely interval dependent.

Adrenergic alpha-Agonists↗
PubMed1996

Left ventricular diastolic suction with zero left atrial pressure in open-chest dogs.

We investigated left ventricular (LV) diastolic volume changes (suction inflows) with left atrial pressure (LAP) clamped to ambient pressure in six open-chest, anesthetized dogs. The left atrium was cannulated and connected to a servo pump, and LAP was clamped to a set point near 0 mmHg for four beats by withdrawing blood. LAP averaged 5.88 +/- 1.44 mmHg before the clamp and fell to 0.74 +/- 0.61 mmHg (P < 0.0001) after the clamp. During the first clamped beat a transmitral pressure gradient of 1.0 +/- 0.6 mmHg was observed, resulting in LV filling of 2.6 +/- 1.8 ml. Subsequent beats developed suction-driven (mean negative LV pressure: -1.5 +/- 1.3 mmHg; P < 0.005 vs. zero) LV filling of 4.5 +/- 2.8 ml/beat with a peak transmitral pressure gradient of 1.7 +/- 0.6 mmHg. These data are consistent with the hypothesis that LV suction can be an important filling mechanism under condition in which LV end-systolic volume is reduced, e.g., reduced filling pressures, high heart rates, exercise, or increased inotropic drive.

Animals↗
PubMed1996

Viscoelastic behavior of the isolated guinea pig left ventricle in diastole.

To determine left ventricular (LV) viscoelastic properties during acute volume changes, the relaxation of LV pressure (2-Fr, Millar) at steady LV volume after a known volume change was measured in 14 isolated guinea pig left ventricles arrested in diastole. The left ventricle was loaded and unloaded by manual injection and withdrawal of saline in 10 x 0.1-ml steps, controlling the steadiness of LV volume by measuring LV major and minor diameters (ultrasonic crystals). Cyclic stepwise volume loading and unloading resulted in a hysteresis loop, the complexity of which was caused by stress relaxation at each steady volume. With the use of linear regression analysis, the gross elastic effect of the pressure signal was separated from the viscoelastic part, decomposed into the fast and the slow component with time constants of relaxation equal to 1 and 20 s, respectively. The amplitudes of the fast and the slow component showed that 1) stress relaxation is more expressed at higher LV volume and 2) it is asymmetric, i.e., it is well expressed during volume loading and almost absent during volume unloading. Both suggest that viscoelasticity of passive myocardium is not quasilinear, when the left ventricle is subjected to aperiodic volume loading to a high LV volume. The asymmetric viscoelastic behavior is consistent with the hypothesis of extracellular fluid filtration.

Animals↗
PubMed1996

Improving methods of chordal-sparing mitral valve replacement--Part II: Optimal tension for chordal resuspension.

BACKGROUND AND AIMS OF THE STUDY: Although chordal-sparing mitral valve replacement (MVR) is popular, the optimal tension for preserved or reattached chordae tendineae (CT) or for synthetic (ePTFE) CT is unknown. METHODS: Changes in left ventricular (LV) systolic and diastolic function in nine dogs with anterior CT preservation with different levels of end-diastolic chordal tension (0, 10, 20, 30, and 40 gm, measured by spring scale) were compared using an isovolumic double-balloon technique. RESULTS: LV function data at each level of tension were compared to control data using 0 gm of tension. Systolic function assessed as Emax (mmHg/ml) at 10, 20, 30, and 40 gm versus control was: 5.7 +/- 2.6/4.9 +/- 2.7, 4.7 +/- 2.2/4.7 +/- 2.7, 4.8 +/- 3.1/4.7 +/- 2.8, and 5.0 +/- 3.5/5.1 +/- 2.9; delta improvement from the control at 10 gm was larger than that at 20 gm (p < 0.05 by paired t-test). Diastolic function assessed as diastolic stiffness (Sd, mmHg/ml) at the same CT tensions versus control was: 0.56 +/- 0.23/0.56 +/- 0.34, 0.53 +/- 0.30/0.57 +/- 0.37, 0.56 +/- 0.39/0.52 +/- 0.38, and 0.60 +/- 0.36/0.58 +/- 0.39; delta Sd was smaller at 20 gm than at 30 gm (p = 0.05 by ANOVA). LV equilibrium volume (Veq, ml) was: 10.7 +/- 3.9/10.1 +/- 3.9, 9.6 +/- 3.4/9.9 +/- 3.8, 10.8 +/- 4.0/10.3 +/- 3.4, and 10.6 +/- 4.0/10.6 +/- 3.5; delta Veq was larger (i.e., more compliant chamber) at 10 gm than at 40 gm (p < 0.05 by rm-ANOVA). Arrhythmias precluding satisfactory measurements occurred in two dogs at 30 or 40 gm CT tension. CONCLUSIONS: With chordal tension exceeding 10 gm, which is barely palpable, there was no additional enhancement in LV systolic function compared to zero CT tension. Veq was largest at the lowest tension; LV diastolic function (assessed as Sd) deteriorated with tensions of 30 gm or higher. The optimal end-diastolic tension of preserved CT should enhance systolic LV performance without adversely affecting diastolic function; in this isovolumic model, minimal CT tension (10 gm) best met these goals. Excessive tension may negate the potential hemodynamic benefits of chordal preservation during mitral valve replacement.

Animals↗
PubMed1996

Improving methods of chordal-sparing mitral valve replacement--Part III: Optimal direction for artificial chordae.

BACKGROUND AND AIMS OF THE STUDY: The optimal direction to preserve artificial chordae tendineae (CT) during mitral valve replacement (MVR) is not known, especially in regard to the response to inotropic stimulation which simulates exercise conditions. METHODS: Using a non-distorting isovolumic balloon technique, we compared left ventricular (LV) systolic and diastolic mechanics in 11 dogs in a control state (no chordal sparing) and with four different methods of chordal preservation: posterior, anterior, oblique (anterior papillary muscle chordae directed anteriorly and others posteriorly, the direction which theoretically augments LV systolic twist), and counter-oblique (counter, chordae preserved in directions opposite to oblique). RESULTS: Before dobutamine, delta Emax from the control was: 0.32 +/- 0.82, 0.10 +/- 0.43, 0.64 +/- 1.07, and 0.51 +/- 0.78 (anterior, posterior, oblique, and counter method, respectively). With dobutamine (3 mg/kg/min), delta Emax (mmHg/ml) was: 0.41 +/- 1.21, -0.13 +/- 0.75, 0.59 +/- 0.82*, and -0.34 +/- 0.71. Before dobutamine, delta LV stiffness (Sd, mmHg/ml) was -0.01 +/- 0.09, -0.02 +/- 0.12, 0.02 +/- 0.10, and 0.01 +/- 0.12; with dobutamine it was 0.01 +/- 0.09, 0.00 +/- 0.15, 0.03 +/- 0.15, and -0.06 +/- 0.11. Similarly, before dobutamine delta LV equilibrium volume (Veq) was -1.2 +/- 3.8, -0.3 +/- 3.0, -0.7 +/- 2.7, and -0.2 +/- 3.5, whereas with dobutamine zeta eq was -0.1 +/- 1.1, -0.4 +/- 0.8, 0.6 +/- 1.7, and -0.4 +/- 1.1. (Mean +/- S.D.; *p = 0.005 posterior and counter by ANOVA; p = NS (< 0.06) versus counter and posterior by ANOVA). CONCLUSIONS: The oblique method enhanced systolic LV function both with and without dobutamine, while a tendency towards better diastolic LV function (Veq) was observed with dobutamine. The anterior method was next best in preserving systolic function, both with and without dobutamine. LV diastolic function tended to deteriorate with dobutamine in the posterior group. Systolic function with the counter method deteriorated with dobutamine. These results warrant further study in an ejecting model to investigate LV systolic and diastolic mechanics with the oblique method of CT preservation, including interactions with LV systolic twist and diastolic recoil.

Animals↗
PubMed1995

Left ventricular function, twist, and recoil after mitral valve replacement.

BACKGROUND: Preservation of the mitral subvalvular apparatus during mitral valve replacement (MVR) has become more popular, in part because of the clinically and experimentally demonstrated more optimal left ventricular (LV) performance after surgery; the mechanisms responsible for this beneficial influence, however, have not been clearly elucidated. METHODS AND RESULTS: Fourteen dogs underwent placement of 26 myocardial markers into the LV and septum. One week later, the animals were studied while awake, sedated, and atrially paced (120 beats per minute) both under baseline conditions and after inotropic stimulation (calcium). The animals then underwent MVR and were randomized into either chord-sparing (MVR-Intact) or chord-severing (MVR-Cut) techniques. Two weeks later, the animals were studied under the same conditions. LV systolic function was assessed by the slope of the end-systolic pressure-volume relation (Ees); early LV diastolic filling was analyzed by the pressure-time constant of relaxation (tau). The instantaneous longitudinal gradient of torsional deformation for the LV (twist) was also calculated, as were the changes in twist with respect to time during systole and early diastole (LV recoil). Intergroup comparison showed a trend toward increased contractility (Ees, P = .061, before versus after MVR), as well as faster relaxation for the MVR-Intact group. Concurrent analysis of LV systolic function and the rate of systolic twist revealed a significant inverse relation, which disappeared after MVR when the chordae were severed. CONCLUSIONS: These observations suggest that the mitral subvalvular apparatus acts as a modulator of LV systolic torsional deformation into LV pump (or ejection) performance.

Animals↗
PubMed1995

Origin of regional pressure gradients in the left ventricle during early diastole.

Left ventricular (LV) pressure (P)-diameter, LVP-area, or LVP-volume relationships used to evaluate LV diastolic function assume uniform LV wall motion and constant LVP. Contrary to these assumptions, there are significant differences in ventricular dynamic geometry and in LV pressures measured simultaneously in different parts of the LV, particularly during early diastole. We instrumented six anesthetized open-chest dogs with three pairs of orthogonal ultrasonic crystals (anterior-posterior and septal-free wall minor axes, and base-apex major axis) and two micromanometers (in the apex and in the LV base). The mitral valve occluder was implanted during standard cardiopulmonary bypass in the mitral annulus. Data were recorded during 11 transient vena caval occlusions. The mitral valve was occluded for 1 beat every 6-8 beats during each vena caval occlusion to produce nonfilling diastole. With the decrease of the LV end-systolic volume (Ves) below the equilibrium volume Veq (volume of the completely relaxed LV at LVP = 0); the minimum negative LVP in nonfilling beats increases, the shape of the ventricle is more ellipsoidal in both filling and nonfilling beats, and the base-to-apex pressure gradient at the time of LVP minimum increases regardless of the presence or absence of filling. Thus heterogeneous myocardial stresses during isovolumic relaxation and early diastole result in ventricular shape changes, intraventricular redistribution of chamber volume, local accelerations of blood, and associated intraventricular LVP gradients. The role of elastic recoil assumes greater importance at Ves smaller than Veq, when the left ventricle becomes more ellipsoidal in shape during isovolumic relaxation, leading, in turn, to greater shape changes and greater LVP gradient.

Animals↗
PubMed1995

A method to assess endocardial regional longitudinal curvature of the left ventricle.

Knowledge of the instantaneous geometry of the left ventricular (LV) chamber is necessary to calculate LV function and wall stresses. We describe a method utilizing myocardial markers that does not rely on any a priori assumptions of global LV geometry. Five dogs underwent placement of 25 endocardial and 3 epicardial miniature LV markers. Six weeks later, the animals were studied during conscious closed-chest conditions. The three-dimensional coordinates of the LV markers were used to compute longitudinal fitted curves for LV walls and septum during steady-state conditions; endocardial radii of curvature (rcurv) were then computed for each region at the midequatorial (rcurv-eq) and apical levels. There was a uniform decrease in rcurv in each LV wall during systole (compared with diastole, P < 0.01); at end systole, rcurv was regionally heterogeneous between opposing walls, e.g., anterior and posterior rcurv-eq values were 17.2 +/- 2.0 and 17.7 +/- 1.8 (SD) cm, respectively (P < 0.05). At end diastole, only septal-lateral rcurv-eq was different (16.9 +/- 2.1 vs. 18.7 +/- 1.3 cm: P < 0.05). Normalization of rcurv (to instantaneous LV volume) removed the systolic-diastolic differences, but a similar pattern of regional heterogeneity persisted. The data presented pertain to the LV endocardial surface, but the method described can be applied to the epicardial surface as well; this new method offers promise in assessing dynamic changes in longitudinal LV endocardial curvature.

Analysis of Variance↗
PubMed1994

Shifts in contractile regulatory protein subunits troponin T and troponin I in cardiac hypertrophy.

To examine the molecular basis of hypertrophied heart failure, we investigated the changes in cardiac contractile regulatory proteins. The guinea pigs were subjected to chronic pressure overload with aortic banding to induce ventricular hypertrophy, and in-situ pressure-volume relations were recorded together with biochemical characterizations to ascertain the contractile modifications. Immunoblots of left and right ventricular samples revealed four distinct troponin T isoforms, which underwent alterations during hypertrophy. The higher molecular weight bands TnT1 and TnT2 shifted towards the lower molecular weight isoforms TnT3 and TnT4. For TnI, a single prominent band was detected, whose intensity also increased with pump failure. The findings provide the first direct evidence of TnT and TnI shifts in an experimentally induced hypertrophied heart failure and has novel mechanistic implications for the future studies.

Animals↗
PubMed1994

Modeling the transient response to volume perturbations in the beating heart by the difference equation method.

Discrete theoretical methods, compatible with the discrete features of the beating heart, are used together with experimental study to attain a quantitative understanding of the transient response to a volume perturbation and of sustained mechanical alternans (SMA) in the beating heart. This is done in three stages. In stage A, a first-order difference equation describes the stroke volume (SV) response due to the Frank-Starling mechanism. It is shown that the value of gamma, the slope of the SV-end-diastolic volume curve, determines the type of response obtained because of a perturbation: 1) nonoscillatory decay for gamma < 1,2) oscillatory decay for 1 < gamma < 2, 3) SMA for gamma = 2, and 4) chaotic response for gamma > 2. In stage B, when the effect of each SV change on the successive end-diastolic aortic pressure (P) is considered, SV response to a perturbation is determined by a second-order difference equation. The solution of this equation shows that the response is determined by gamma and by the afterload factor lambda 1 = alpha 1.delta, where alpha 1 = delta Pj + 1/delta SVj and delta = delta SVj + 1/delta Pj + 1. The responses are a nonoscillatory decay for lambda 1 < 1 - gamma (type 1), oscillatory decay for 1 - (gamma/2) > lambda 1 > 1 - gamma (type 2), SMA for lambda 1 = 1 - gamma/2 (type 3), and 2:1 electrical-mechanical response for lambda 1 > 1 - gamma/2 (type 4). In stage C, a single volume perturbation, delta SVj, will directly affect not only Pj + 1 but also the subsequent values of P. Filling volume perturbations performed with a mitral valve occluder in eight anesthetized dogs led only to type 1 and 2 responses. The responses predicted by the model (using the experimental values of gamma and lambda 1) in each of the eight open-chest dogs are compatible with the experimental responses, suggesting that it is unlikely that SMA is initiated and maintained by variations in preload and afterload.

Animals↗
PubMed1994

Left atrial pressure-clamp servomechanism demonstrates LV suction in canine hearts with normal mitral valves.

A novel technique is presented to study suction of the in situ left ventricle in open-chest experimental animals without requiring cardiopulmonary bypass or disturbing the native mitral valvular apparatus. In 17 dogs, left ventricular pressure (LVP) and left atrial pressure (LAP) were measured, the left atrium was cannulated and connected to a servo pump, and LAP was controlled to a setpoint near 0 mmHg by withdrawing blood from the left atrium. Heart rate [103 +/- 17 (SD) min-1], peak pressure (100 +/- 13 mmHg), minimum pressure (1.4 +/- 0.8 mmHg), and maximum rate of change of pressure with respect to time during isovolumic contraction and relaxation (2,506 +/- 775 and -1,761 +/- 855 mmHg/s, respectively) were normal. Servo control of LAP was possible to +/- 1 mmHg. LV suction was demonstrated in each heart (mean negative LVP -2.3 +/- 1.1 mmHg; P < 0.0001). This new technique demonstrates that the left ventricle can generate negative diastolic suction pressures when examined in vivo and in situ with an undisturbed mitral valve and physiologically normal preload and afterload. This adds to a growing body of evidence that, under appropriate circumstances, the heart can suck blood into itself and thereby aid in its own filling.

Animals↗
PubMed1994

Left-to-right ventricular interaction with a noncontracting right ventricle.

UNLABELLED: Left ventricular systole is known to contribute to generation of right ventricular pressure and stroke volume. To study the interactions in a dilated noncontractile right ventricle after cardiopulmonary bypass we created a variable volume, neo-right ventricle by excision and replacement of the right ventricular free wall with a xenograft pericardial patch. We investigated the interactions in eight dogs with neo-right ventricle, instrumented to measure cardiac pressures and cardiac output in control conditions (n = 69) and during partial pulmonary artery occlusion (n = 50). RESULTS: The size of the neo-right ventricle was increased from original right ventricular volume V0 to V1 (V1 = V0 + 54 +/- 23 ml), V2 (V2 = V0 + 124 +/- 85 ml), and V3 (V3 = V0 + 223 +/- 162 ml). Cardiac output increased with increasing left ventricular end-diastolic pressure, indicating that the Frank-Starling mechanism was operating in the left ventricle. However, cardiac output decreased with increasing neo-right ventricular size (p < 0.001) and during pulmonary artery occlusion (p < 0.001). Maximal neo-right ventricular pressure was a linear function of the maximal left ventricular pressure at each neo-right ventricular size and decreased with the increase in neo-right ventricular size (p < 0.001), both in control conditions and during pulmonary artery occlusion (p < 0.004). Stroke work of the neo-right ventricle and left ventricle decreased with increasing neo-right ventricular size (p < 0.002). The relationship between neo-right ventricular stroke work and left ventricular stroke work at different neo-right ventricular sizes was linear both in control conditions and during pulmonary artery occlusion: in control Y = 0.24X (r = 0.968, n = 69); in pulmonary artery occlusion Y = 0.35X (r = 0.986, n = 50). In both conditions the intercept of the linear relationship was not significantly different from zero (p < 0.974 in control; p < 0.614 in pulmonary artery occlusion). The slope was significantly increased in pulmonary artery occlusion (p < 0.001). CONCLUSION: Left ventricular contraction contributes 24% of left ventricular stroke work to the generation of right ventricular stroke work via the septum in the absence of a contracting right ventricle; this increases to 35% in the face of increased pulmonary afterload. This mechanism can maintain adequate global cardiac function in the case of a noncontracting right ventricle while right ventricular volume is kept small and afterload is not increased. The interventricular interaction of the ventricles must be considered when patients with postbypass right ventricular failure are treated.

Animals↗