Left Ventricular Pressure-volume Measurements Research Articles

Therapeutic effects of interleukin-37 and induced cardiosphere on treating myocardial ischemia-reperfusion injury

BackgroundsMyocardial ischemia-reperfusion injury (MI-RI) has many adverse complications with high mortality rate. In the current study, we investigated the therapeutic advantages of delivering Interleukin-37 (IL-37) by induced cardiospheres (iCS), generated from adult skin fibroblasts via somatic reprogramming, in treating the mice model MI-RI. MethodsThe mouse model of MI-RI was established and the iCS cells with IL-37 overexpression (iCS-IL37) were transplanted into the mice via tail-vein injection. Left ventricular (LV) dimensions and LV pressure-volume measurements were assessed by parasternal long-axis echocardiography and hemodynamic assessment. The infarct size was determined by histology analysis. And the inflammatory responses were analyzed by using enzyme-linked immunosorbent assay (ELISA). ResultsThe LV function was significantly improved after the iCS-IL37 transplantation when compared to the vehicle control group and iCS group, including the end-systolic pressure and dP/dtMax. Furthermore, the infarct size was significantly decreased after the iCS-IL37 transplantation. The protein levels of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), were down-regulated by the iCS-IL37 transplantation. ConclusionThe present study indicated that the iCS with IL-37 overexpression had therapeutic effects on the mice model of MI-RI.

Experimental validation of the prestretch-strain relationship as a non-invasive index of left ventricular myocardial contractility.

BackgroundThe slope of the relationship between segmental PreS and total systolic shortening (S) has been proposed as a non-invasive index of left ventricular contractility. The aim of this study was to correlate this novel parameter to invasive gold standard measurements of contractility and to investigate how it is influenced by afterload.MethodsIn domestic pigs, afterload was increased by either balloon inflation in the aorta or by administration of phenylephrine while contractility was increased by dobutamine infusion. During all interventions, left ventricular pressure-volume measurements and trans-diaphragmatic two-dimensional echocardiographic images were acquired. The PreS-S slope was constructed from 18 segmental strain curves obtained by speckle tracking analysis and compared to the slope of the end systolic PV relationship (Emax) and the pre-load recruitable stroke work (PRSW).ResultsSixteen datasets of increased contractility and afterload were analyzed. During dobutamine infusion, the LV volumes decreased (p<0.05) while ejection fraction increased (p<0.05). Emax, PRSW and the slope of the intra-ventricular PreS-S relation increased significantly during dobutamine infusion. Afterload increase led to increase in systolic blood pressure (105±16mmHg vs. 138±25mmHg; p<0.01) and decrease of LV stroke volume and ejection fraction (p<0.01). The PreS-S slope was not influenced by loading conditions in concordance with the PRSW findings. The absolute values of the PreS-S slope did not correlate with Emax or PRSW. However, the change of the PreS-S slope in relation with different interventions demonstrated good correlation with changes in PRSW or Emax, (r = 0.66, p<0.05 and r = 0.69, p<0.05).ConclusionsThe slope of the PreS-S relationship is sensitive to changes in inotropy and is less load-dependent than conventional non-invasive parameters of left ventricular function. The magnitude of the change of this slope correlates well with changes in invasive contractility measurements making it an attractive parameter to assess contractile reserve or contractile changes during longitudinal follow-up of patients.

Protective effects of induced cardiosphere on myocardial ischemia-reperfusion injury through secreting interleukin 10

BackgroundsMyocardial ischemia-reperfusion injury (MI-RI) has many adverse complications with high mortality rate. It has been demonstrated that the induced cardiospheres (iCS), generated from adult skin fibroblasts via somatic reprogramming, represents a novel source for cell therapy in myocardial infarction. However, whether the iCS could also be applied to treat MI-RI remains unclear. Thus, we investigated the therapeutic application of iCS in the mice model MI-RI. MethodsThe mice model of MI-RI was established and the iCS cells were transplanted to the mice via tail-vein injection. Left ventricular (LV) dimensions and LV pressure-volume measurements were assessed by parasternal long-axis echocardiography. The infarct size was determined by histology analysis. And the inflammatory responses were analyzed by using enzyme-linked immunosorbent assay (ELISA). ResultsThe LV function was significantly improved after the iCS transplantation when compared to the vehicle control group, including the end-systolic pressure and dP/dtMax. Furthermore, the infarct size was significantly decreased after the iCS transplantation. The protein levels of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), were down-regulated by the iCS transplantation while the IL-10 was up-regulated. The anti-inflammatory factor IL-10 was found to be expressed and secreted by the iCS cells and knocking down the IL-10 in iCS would significantly impair the therapeutic effects of iCS in the mice model of MI-RI. ConclusionThe present study indicated that the iCS had therapeutic effects on the mice model of MI-RI through secreting the IL-10.

Acute Effects of Pacing at Different Ventricular Sites on Left Ventricular Rotational Mechanics in a Porcine Model.

The purpose of this study was to examine the acute effects of pacing at different ventricular sites on hemodynamics and left ventricular (LV) rotational mechanics using speckle-tracking echocardiography (STE) in a porcine model. A prospective laboratory investigation. University research laboratory. Yorkshire pigs. In 9 pigs, after midline sternotomy, epicardial pacing was performed from the right ventricular outflow tract (RVOT), right ventricular apex (RVA), and LV free wall. Two-dimensional STE and conductance catheter-derived LV pressure-volume measurements were made to determine the impact of pacing from various sites on LV rotational parameters (twist/untwist) and hemodynamics. RVOT pacing caused the least decrease in end-systolic pressure from baseline (-9.5%), when compared with RVA (-19.1%) and LV (-23.4%). Systolic and diastolic parameters (Emax, Tau) also were different among RVOT (4.7±0.8 mmHg/mL, 32±4 ms), RVA (3.9±0.7 mmHg/mL, 37±6 ms), and LV sites (3.6±0.8 mmHg/mL, 42±7 ms). Similar to the effects of pacing on hemodynamics, RVOT pacing better preserved LV twist (11.1±1.8 v 8.6±1.7, 5.9±0.7 °) and untwisting rate (64.6±8.5 v 56.2±5.3, 48.2±8.5 °/s) when compared with RV apical pacing and LV pacing. Furthermore, prolongation of conduction from LV lateral to anteroseptal at LV base (26.5±3.8 v 13.8±3.3 ms, p<0.05) and LV midpapillary muscle level (35.6±5.6 v 14.1±2.4 ms, p<0.05) was observed with LV pacing compared with RVOT pacing. The present data showed that the LV twist/untwist and cardiac systolic and diastolic function were least affected by RVOT pacing. This finding may be explained by the proximity of this location to the native ventricular conduction system.

The Structure-Function Analysis of Myosin Pseudo-Phosphorylation in Mouse Model of FHC

Familial hypertrophic cardiomyopathy (FHC) is a disease of the heart caused by autosomal dominant mutations in genes coding for all major sarcomeric proteins, including the myosin regulatory light chain (RLC). In this report, we have explored the rescue strategies to ameliorate the malignant cardiomyopathy phenotype induced by an aspartic acid to valine substitution (D166V) in the RLC. Previous studies on porcine reconstituted preparations showed that the phosphorylation mimic (S15D) in the background of the D166V mutation (S15D-D166V) restored the calcium sensitivity of force and improved Vmax of myosin ATPase that were largely compromised by the D166V mutation. Transgenic carrying the S15D-D166V mutation have been generated and subjected to structural and functional measurements. Small angle X-ray studies on freshly skinned papillary muscle fibers revealed that a D166V-induced reorganization in cross-bridge mass distribution was partially reversed in Rescue Mice (abnormally increased I1,1/I1,0 ratio observed in Tg-D166V fibers returned to the value near Tg-WT). Noteworthy, pseudo-phosphorylation of D166V significantly restored fiber elasticity allowing for changes in the cross-bride mass distribution on stretch. In vivo cardiac morphology and function were assessed by non-invasive echocardiography followed by invasive left ventricular pressure-volume measurements (P-V loops). Echocardiography assessment confirmed hypertrophy in Tg-D166V mice showing an increased posterior wall thickness in systole. Invasive hemodynamics showed diastolic and systolic dysfunction in Tg-D166V mice. The end-systolic P-V relationship, a measure of heart contractility, which was largely reduced in Tg-D166V mice was completely ameliorated in Rescue Mice. In addition, the maximum dP/dt - End-Diastolic Volume relation, which was compromised in Tg-D166V was fully reversed in Rescue Mice. In conclusion, our results suggest that pseudo-phosphorylation of myosin RLC can mitigate both the structural and functional abnormalities of the FHC heart. Supported by NIH-HL108343 and HL071778 (DSC).

Extent of load-independence of pressure-normalized stress in swine

A load-independent index of myocardial contractility provides a measure of cardiac function. Previous contractility indices have been shown to be either load-dependent or invasive. We sought to determine the extent of load (preload and afterload)-independence of dσ*/dtmax (σ* is pressure-normalized stress) in comparison with other well-established indices. Six anaesthetized pigs underwent left ventricular pressure-volume measurements under various load conditions. The average preload was decreased by 70.0 ± 15.0% (from 39.2 ± 6.4 mL to 11.7 ± 7.7 mL) and increased by 49.3 ± 5.9% (from 35.1 ± 7.4 mL to 51.7 ± 8.9 mL). The average afterload was increased by 74.3 ± 43.5% (from 3.3 ± 0.6 mmHg/mL to 5.7 ± 1.7 mmHg/mL). When preload was reduced within an average of 21.7% (39.2 ± 6.4 mL to 30.7 ± 6.2 mL) using occlusion of the inferior vena cava, dσ*/dt max did not change significantly (6.50 ± 1.10 s⁻¹ vs 6.60 ± 0.90 s⁻¹, P = non-significant [NS]). When preload was increased within an average of 29.3% (35.1 ± 7.4 mL to 45.4 ± 7.3 mL) from infusion of normal saline, dσ*/dt max did not change significantly (7.04 ± 1.00 s⁻¹ vs 7.29 ± 1.10 s⁻¹, P = NS). When afterload was increased within an average of 42.4% (3.3 ± 0.6 mmHg/mL to 4.7 ± 1.0 mmHg/mL) using intra-aortic balloon occlusion, dσ*/dtmax did not change significantly (6.72 ± 1.18 s⁻¹ vs 6.89 ± 1.28 s⁻¹, P = NS). As expected, dσ*/dtmax was significantly increased with dobutamine. A linear regression showed no correlation between dσ*/dtmax and preload (r² = 0.02, P = 0.17) within a maximum range of -30% to +50% of preload change, or between dσ*/dtmax and afterload (r² = 0.03, P = 0.36) within maximum range of 0-100% of afterload increase, respectively. In conclusion, dσ*/dtmax is independent of loading conditions within an average of 21.7% of preload decrease, 29.3% of preload increase, 42.4% of afterload increase, and sensitive to dobutamine infusion.

Effect of stellate ganglia stimulation on global and regional left ventricular function as assessed by speckle tracking echocardiography

Left ventricular (LV) twist mechanics and regional strain during cardiac sympathetic efferent activation are poorly understood. The purpose of this study was to compare the effects of left stellate ganglia (LSG) and right stellate ganglia (RSG) stimulation on cardiac twist/untiwst mechanics and regional strain. In nine pigs, echocardiographic imaging and LV pressure-volume measurements were performed before and during unilateral and bilateral stellate ganglion stimulation. LSG and RSG stimulation significantly augmented LV end-systolic pressure by 24% and 22% (P < 0.01), maximal rate of LV pressure change by 167% and 165% (P < 0.01), and time constant of LV relaxation by 20% and 12% (P < 0.01), respectively. RSG stimulation resulted in a greater chronotropic response than LSG stimulation (RSG: 68% vs. LSG: 12%, P < 0.01). Both LSG and RSG stimulation significantly increased global epicardial and endocardial LV rotation and diastolic untwisting rate and reduced the time to peak rotation (P < 0.05). However, LSG stimulation predominantly increased radial and circumferential strain in the LV inferoseptal, inferior, posterior, and lateral regions, whereas RSG stimulation primarily increased radial and circumferential strain in the anteroseptal, anterior, and lateral LV regions. Stimulation of both stellate ganglia led to a uniform increase in all LV segments. Our data suggest that LSG and RSG stimulation lead to a global increase in LV twist, driven by distinct regional strain heterogeneity that may result from myocardial innervation from the LSG and RSG. These findings provide a better understanding of the global and regional functional consequences of regional myocardial innervation from the LSG and RSG.

The effect of repeated ischaemic periods on left ventricular dynamics during percutaneous coronary intervention

To study online left ventricular (LV) dynamic effects of transmural ischaemia and reperfusion during consecutive balloon coronary occlusions in the setting of percutaneous coronary intervention (PCI). In 10 consecutive unselected patients with stable angina (seven males, mean age 62 ± 3 years) who underwent elective PCI, LV dynamics were continuously recorded using a pressure-conductance catheter to simultaneously measure pressure and volume (PV-loop). The effects of a prolonged balloon coronary occlusion (148 ± 19 s) and a second occlusion on various LV function parameters were studied, as well as recovery of these parameters after reperfusion. Ischaemia caused an immediate (<5 s) decrease in diastolic function, followed by a decrease in contractile function, indicated by a rightward shift of the PV-loop, and a decreased dP/dtmax and ejection fraction. All parameters recovered within two minutes after reperfusion. The second occlusion caused a more rapid and more pronounced decrease in systolic and global LV function, while the 12-lead ECG showed less ST-segment deviation. Online LV pressure-volume measurements during elective PCI show that prolonged balloon coronary occlusion causes a phased ischaemic response of diastolic dysfunction, and then systolic dysfunction with more pronounced deterioration during a consecutive ischaemic period, paradoxical to the ischaemic electrocardiographic signs.

Abstract 5052: Attenuation of Ventricular Remodeling and Improvement of Left Ventricular Systolic Function by Injection of Human Fetal Cardiomyocyte Progenitor Cells After Acute Myocardial Infarction

Introduction: The human cardiomyocyte progenitor cell (hCMPC) is part of a population of stem cells located in the human heart. Isolates of hCMPCs from human fetal hearts showed differentiation into functional cardiomyocytes in vitro. In the present study we investigated the potential of hCMPCs to restore ischemic myocardium and improve left ventricular (LV) function in a myocardial infarction (MI) model in mice. Methods: MI was induced in immune-compromised NOD/scid mice, immediately followed by injection of hCMPCs labeled with eGFP (hCMPC group) or vehicle only (control group). From sham operated mice we obtained reference values. Cardiac performance was measured 2 and 14 days after MI using 9.4 Tesla MRI. LV pressure-volume measurements were performed at day 15 followed by extensive immunohistological analysis. Results: Animals injected with hCMPCs after MI demonstrated a significantly higher LV ejection fraction, a lower LV end-systolic volume and a smaller ô (relaxation time constant), compared to animals from the control group (by 17%, by 22% and by 24% respectively, P&lt;0.05). A trend towards a lower LV end-diastolic volume was also observed, although this did not reach significance (P=0.14). Both the infarct zone and border zone of the hCMCP group showed a significant increase in total blood vessel density (6.67%±0.85% and 9.13%±0.46%) compared to control (3.35%±1.13% and 4.31%±1.08%, P&lt;0.01 in either zone). The infarct and border zone of the hearts injected with hCMPCs also had a diminished collagen type III density (1.07±0.06 and 1.11±0.07), compared to the control group (1.45±0.05 and 1.51±0.08, P&lt;0.01 in either zone). Furthermore, nuclear PCNA expression indicated an increased rate of mitosis in the infarct (37.76%±2.23%) and border zone (48.84%±2.07%) compared to the infarct (25.48%±4.83%, P&lt;0.01) and border zone (32.03%±1.03%, P&lt;0.01) of the control group. Conclusions: Fetal hCMPCs engraft into infarcted myocardium where they improve LV systolic function and attenuate ventricular remodeling. Increased blood vessel density, elevated mitosis rate and decreased collagen III deposition may be involved in this process. These results indicate that hCMPCs are promising candidates for cell-based therapy.

Expression of a transgene encoding mutant p193/CUL7 preserves cardiac function and limits infarct expansion after myocardial infarction

Background:Transgenic mice expressing the dominant interfering p193 protein in cardiomyocytes (MHC-1152stop mice) exhibit an induction of cell cycle activity and altered remodelling after experimental myocardial infarction (MI).Objective:To determine whether the...

Forced Myocardin Expression Enhances the Therapeutic Effect of Human Mesenchymal Stem Cells After Transplantation in Ischemic Mouse Hearts

Human mesenchymal stem cells (hMSCs) have only a limited differentiation potential toward cardiomyocytes. Forced expression of the cardiomyogenic transcription factor myocardin may stimulate hMSCs to acquire a cardiomyogenic phenotype, thereby improving their possible therapeutic potential. hMSCs were transduced with green fluorescent protein (GFP) and myocardin (hMSC(myoc)) or GFP and empty vector (hMSC). After coronary ligation in immune-compromised NOD/scid mice, hMSC(myoc) (n = 10), hMSC (n = 10), or medium only (n = 12) was injected into the infarct area. Sham-operated mice (n = 12) were used to determine baseline characteristics. Left ventricular (LV) volumes and ejection fraction (EF) were serially (days 2 and 14) assessed using 9.4-T magnetic resonance imaging. LV pressure-volume measurements were performed at day 15, followed by histological evaluation. At day 2, no differences in infarct size, LV volumes, or EF were observed among the myocardial infarction groups. At day 14, left ventricular ejection fraction in both cell-treated groups was preserved compared with the nontreated group; in addition, hMSC(myoc) injection also reduced LV volumes compared with medium injection (p < .05). Furthermore, pressure-volume measurements revealed a significantly better LV function after hMSC(myoc) injection compared with hMSC treatment. Immunohistochemistry at day 15 demonstrated that the engraftment rate was higher in the hMSC(myoc) group compared with the hMSC group (p < .05). Furthermore, these cells expressed a number of cardiomyocyte-specific markers not observed in the hMSC group. After myocardial infarction, injection of hMSC(myoc) improved LV function and limited LV remodeling, effects not observed after injection of hMSC. Furthermore, forced myocardin expression improved engraftment and induced a cardiomyocyte-like phenotype hMSC differentiation.

Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction

Cardiomyocyte loss is a major contributor to the decreased cardiac function observed in diseased hearts. Previous studies have shown that cardiomyocyte-restricted cyclin D2 expression resulted in sustained cell cycle activity following myocardial injury in transgenic (MHC-cycD2) mice. Here, we investigated the effects of this cell cycle activation on cardiac function following myocardial infarction (MI). MI was induced in transgenic and non-transgenic mice by left coronary artery occlusion. At 7, 60, and 180 days after MI, left ventricular pressure-volume measurements were recorded and histological analysis was performed. MI had a similar adverse effect on cardiac function in transgenic and non-transgenic mice at 7 days post-injury. No improvement in cardiac function was observed in non-transgenic mice at 60 and 180 days post-MI. In contrast, the transgenic animals exhibited a progressive and marked increase in cardiac function at subsequent time points. Improved cardiac function in the transgenic mice at 60 and 180 days post-MI correlated positively with the presence of newly formed myocardial tissue which was not apparent at 7 days post-MI. Intracellular calcium transient imaging indicated that cardiomyocytes present in the newly formed myocardium participated in a functional syncytium with the remote myocardium. These findings indicate that cardiomyocyte cell cycle activation leads to improvement of cardiac function and morphology following MI and may represent an important clinical strategy to promote myocardial regeneration.

Delayed erythropoietin therapy reduces post-MI cardiac remodeling only at a dose that mobilizes endothelial progenitor cells

We examined the cardiac effects of chronic erythropoietin (EPO) therapy initiated 7 days after myocardial infarction (MI) in rats. A single high dose of EPO has been shown to reduce infarct size by preventing apoptosis when injected immediately after myocardial ischemia. The proangiogenic potential of EPO has also been reported, but the effects of chronic treatment with standard doses after MI are unknown. In this study, rats underwent coronary occlusion followed by reperfusion or a sham procedure. Infarcted rats were assigned to one of three treatment groups: 1) 0.75 microg/kg darbepoetin (MI+darb 0.75, n = 12); 2) 1.5 microg/kg darbepoetin (MI+darb 1.5, n = 12); 3) vehicle (MI+PBS, n = 16), once a week from day 7 postsurgery. Sham rats received the vehicle alone (n = 10). After 8 wk of treatment, the animals underwent echocardiography, left ventricular pressure-volume measurements, and peripheral blood endothelial progenitor cell (EPC) counting. MI size and capillary density in the border zone and the area at risk (AAR) were measured postmortem. The AAR was similar in the three MI groups. Compared with MI+PBS, the MI+darb 1.5 group showed a reduction in the MI-to-AAR ratio (20.8% vs. 38.7%; P < 0.05), as well as significantly reduced left ventricle dilatation and improved cardiac function. This reduction in post-MI remodeling was accompanied by increased capillary density (P < 0.05) and by a higher number of EPC (P < 0.05). Both darbepoetin doses increased the hematocrit, whereas MI+darb 0.75 did not increase EPC numbers or capillary density and had no functional effect. We found that chronic EPO treatment reduces MI size and improves cardiac function only at a dose that induces EPC mobilization in blood and that increases capillary density in the infarct border zone.

Cardiovascular dysfunction caused by cecal ligation and puncture is attenuated in CD8 knockout mice treated with anti-asialoGM1

The present study was designed to assess hemodynamics and myocardial function at 18 h after injury caused by cecal ligation and puncture (CLP) in CD8-knockout mice treated with anti-asialoGM1 (CD8KO/alphaAsGM1 mice). Arterial pressure was measured by carotid artery cannulation, and left ventricular pressure-volume measurements were obtained by use of a 1.4-Fr conductance catheter. Blood acid-base balance and indexes of hepatic, renal, and pulmonary injury were also measured. CD8KO/alphaAsGM1 mice exhibited higher mean arterial pressure and increased systemic vascular resistance compared with wild-type mice. Cardiac output was significantly decreased in wild-type, but not CD8KO/alphaAsGM1, mice compared with sham controls. Myocardial function was better preserved in CD8KO/alphaAsGM1 mice as indicated by less impairment of left ventricular pressure development over time, time varying maximum elastance, end-systolic pressure-volume relationship, and preload recruitable stroke work. The impairment in myocardial function was associated with induction of proinflammatory cytokine mRNAs in the hearts of wild-type mice. The hemodynamic derangements in wild-type mice were coupled with significant metabolic acidosis and elevated serum creatinine levels. Overall, this study shows that cardiovascular collapse and shock characterized by hypotension, myocardial depression, low systemic vascular resistance, and metabolic acidosis occurs after CLP in wild-type mice but is attenuated in CD8KO/alphaAsGM1 mice. These observations likely explain, in part, the previously observed survival advantage of CD8KO/alphaAsGM1 mice following CLP.

Physiological loading of isolated feline cardiac muscle. The interaction between muscle contraction and vascular impedance in the production of pressure and flow waves.

HomeCirculation ResearchVol. 44, No. 4Physiological loading of isolated feline cardiac muscle. The interaction between muscle contraction and vascular impedance in the production of pressure and flow waves. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBPhysiological loading of isolated feline cardiac muscle. The interaction between muscle contraction and vascular impedance in the production of pressure and flow waves. W J Paulus, V A Claes and D L Brutsaert W J PaulusW J Paulus Search for more papers by this author , V A ClaesV A Claes Search for more papers by this author and D L BrutsaertD L Brutsaert Search for more papers by this author Originally published1 Apr 1979https://doi.org/10.1161/01.RES.44.4.491Circulation Research. 1979;44:491–497 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Avolio A and Butlin M (2016) Indices of central aortic pressure waveform and ventricular function, Journal of Hypertension, 10.1097/HJH.0000000000000883, 34:4, (634-636), Online publication date: 1-Apr-2016. Campbell K, Wu Y, Simpson A, Kirkpatrick R, Shroff S, Granzier H and Slinker B (2005) Dynamic myocardial contractile parameters from left ventricular pressure-volume measurements, American Journal of Physiology-Heart and Circulatory Physiology, 10.1152/ajpheart.01045.2004, 289:1, (H114-H130), Online publication date: 1-Jul-2005. Sørhus V, Sys S, Natåns A, Demolder M and Angelsen B (2000) Controlled Auxotonic Twitch in Papillary Muscle: A New Computer-Based Control Approach, Computers and Biomedical Research, 10.1006/cbmr.2000.1551, 33:6, (398-415), Online publication date: 1-Dec-2000. Guccione J, Le Prell G, de Tombe P and Hunter W (1997) Measurements of active myocardial tension under a wide range of physiological loading conditions, Journal of Biomechanics, 10.1016/S0021-9290(96)00122-4, 30:2, (189-192), Online publication date: 1-Feb-1997. Campbell K, Campbell L, Pinto J and Burton T (1994) Contractile-based model interpretation of pressure-volume dynamics in the constantly activated (Ba2+) isolated heart, Annals of Biomedical Engineering, 10.1007/BF02368284, 22:6, (550-567), Online publication date: 1-Nov-1994. Waldman L (1987) Modeling of the Coupling of the Left Ventricle to the Peripheral Circulation Ventricular/Vascular Coupling, 10.1007/978-1-4613-8634-6_14, (301-333), . Campbell K, Ringo J, Neti C and Alexander J (1984) Informational analysis of left-ventricle/systemic-arterial interaction, Annals of Biomedical Engineering, 10.1007/BF02584231, 12:2, (209-231), Online publication date: 1-Mar-1984. Avolio A, Chen S, Wang R, Zhang C, Li M and O'Rourke M (1983) Effects of aging on changing arterial compliance and left ventricular load in a northern Chinese urban community., Circulation, 68:1, (50-58), Online publication date: 1-Jul-1983.Elzinga G and Westerhof N (1982) Isolated cat trabeculae in a simulated feline heart and arterial system. Contractile basis of cardiac pump function., Circulation Research, 51:4, (430-438), Online publication date: 1-Oct-1982.Elzinga G and Westerhof N (1981) "Pressure-volume" relations in isolated cat trabecula., Circulation Research, 49:2, (388-394), Online publication date: 1-Aug-1981.Paulus W and Brutsaert D (1980) Comments on "How to quantify pump function of the heart"., Circulation Research, 46:2, (303-304), Online publication date: 1-Feb-1980.Paulus W, Claes V and Brutsaert D (1980) End-systolic pressure-volume relation estimated from physiologically loaded cat papillary muscle contractions., Circulation Research, 47:1, (20-26), Online publication date: 1-Jul-1980. April 1, 1979Vol 44, Issue 4 Advertisement Article InformationMetrics Copyright © 1979 by American Heart Associationhttps://doi.org/10.1161/01.RES.44.4.491 Originally publishedApril 1, 1979 PDF download Advertisement