Hemodynamic evaluation of two models of coronary artery occlusion in pigs

in Acta Cardiologica (2007)

Single-beat evaluation of right ventricular contractility - Reply

in Critical Care Medicine (2005), 33(4), 918-918

Effect of a novel thromboxane A(2) inhibitor on right ventricular-arterial coupling in endotoxic shock

in Shock (2004), 21(1), 45-51

We investigated the effects of a dual thromboxane (TX)A(2) synthase inhibitor and TXA(2) receptor antagonist (BM-573) on right ventricular-arterial coupling in a porcine model of endotoxic shock. Thirty ... [more ▼]

We investigated the effects of a dual thromboxane (TX)A(2) synthase inhibitor and TXA(2) receptor antagonist (BM-573) on right ventricular-arterial coupling in a porcine model of endotoxic shock. Thirty minutes before the onset of 0.5 mg/kg endotoxin infusion, six pigs (Endo group) received an infusion with a placebo solution, and six other pigs (Anta group) with BM-573. Right ventricular pressure-volume loops were obtained by the conductance catheter technique. The slope (E-es) of the end-systolic pressure-volume relationship and its volume intercept at 25 mmHg were calculated as measures of right ventricular systolic function. RV afterload was quantified by pulmonary arterial elastance (E-a), and E-es/E-a ratio represented right ventricular-arterial coupling. Mechanical efficiency was defined as the ratio of stroke work and pressure-volume area. In this model of endotoxic shock, BM-573 blunted the early phase of pulmonary hypertension, improved arterial oxygenation, and prevented a decrease in right ventricular myocardial efficiency and right ventricular dilatation. However, the drug could not prevent the loss of homeometric regulation and alterations in right ventricular-arterial coupling. In conclusion, dual TXA(2) synthase inhibitor and receptor antagonists such as BM-573 have potential therapeutic applications, improving right ventricular efficiency and arterial oxygenation in endotoxic shock. [less ▲]

Systemic and pulmonary hemodynamics assessed with a lumped-parameter heart-arterial interaction model

in Journal of Engineering Mathematics (2003), 47(3-4), 185-199

Arterial pressure and flow result from the interaction between the ( actively) ejecting ventricle and the ( passive) arterial circulation. The main objective was to construct a model, accounting for this ... [more ▼]

Arterial pressure and flow result from the interaction between the ( actively) ejecting ventricle and the ( passive) arterial circulation. The main objective was to construct a model, accounting for this interaction, that is simple enough so that (i) model parameters can be derived from data measured in experimental and/or clinical conditions, and (ii) the model can be applied to support the analysis and interpretation of these data. It is demonstrated how an established conceptual model of ventricular function ( the time-varying elastance) can be coupled to a four-element windkessel model of the arterial system to yield an elegant model of heart-arterial interaction. The coupling leads to a set of three ordinary differential equations. The model allows the study of the effect of changes in cardiac and/or arterial properties on arterial pressure and flow. As an illustration, cardiac and arterial model parameters are derived from measured experimental data in the systemic circulation of a pig and in the pulmonary circulation of a dog. It is evaluated how well measured cardiac and arterial function actually adhere to their assumed theoretical models (time-varying elastance and four-element windkessel model). It is further assessed how well the simple model of heart-arterial interaction describes systemic and pulmonary hemodynamics by comparing simulated and measured experimental data. The limitations and pitfalls of the model, as well as possible applications in the clinical field, are discussed. [less ▲]

Effects of endotoxic shock on right ventricular systolic function and mechanical efficiency

in Cardiovascular Research (2003), 59(2), 412-418

Objective: To investigate the effects of endotoxin infusion on right ventricular (RV) systolic function and mechanical efficiency. Methods: Six anesthetized pigs (Endo group) received a 0.5 mg/kg ... [more ▼]

Objective: To investigate the effects of endotoxin infusion on right ventricular (RV) systolic function and mechanical efficiency. Methods: Six anesthetized pigs (Endo group) received a 0.5 mg/kg endotoxin infusion over 30 min and were compared with six other anesthetized pigs (Control group) receiving placebo for 5 h. RV pressure-volume (PV) loops were obtained by the conductance catheter technique and pulmonary artery flow and pressure were measured with high-fidelity transducers. Results: RV adaptation to increased afterload during the early phase of endotoxin-induced pulmonary hypertension (T30) was obtained by both homeometric and hetereometric regulations: the slope of the end-systolic PV relationship of the right ventricle increased from 1.4+/-0.2 mmHg/ml to 2.9+/-0.4 mmHg/ml (P<0.05) and RV end-diastolic volume increased from 56+/-6 ml to 64+/-11 ml (P<0.05). Consequently, right ventricular-vascular coupling was maintained at a maximum efficiency. Ninety minutes later (T120), facing the same increased afterload, the right ventricle failed to maintain its contractility to such an elevated level and, as a consequence, right ventricular-vascular uncoupling occurred. PV loop area, which is known to be highly correlated with oxygen myocardial consumption, increased from 1154+/-127 mmHg/ml (T0) to 1798+/-122 mmHg/ml (T180) (P<0.05) while RV mechanical efficiency decreased from 63+/-2% (T0) to 45+/-5% (T270) (P<0.05). Conclusions: In the very early phase of endotoxinic shock, right ventricular-vascular coupling is preserved by an increase in RV contractility. Later, myocardial oxygen consumption and energetic cost of RV contractility are increased, as evidenced by the decrease in RV efficiency, and right ventricular-vascular uncoupling occurs. Therefore, therapies aiming at restoring right ventricular-vascular coupling in endotoxic shock should attempt to increase RV contractility and to decrease RV afterload but also to preserve RV mechanical efficiency. (C) 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved. [less ▲]

effects of endotoxin infusion on right ventricular systolic function and mechanical efficiency

Poster (2003)

Arterial elastance and heart-arterial coupling in aortic regurgitation are determined by aortic leak severity

in American Heart Journal (2002), 144(4), 568-576

Background In aortic valve regurgitation (AR), aortic leak severity modulates left ventricle (LV) arterial system interaction. The aim of this study was to assess (1) how arterial elastance (E-a ... [more ▼]

Background In aortic valve regurgitation (AR), aortic leak severity modulates left ventricle (LV) arterial system interaction. The aim of this study was to assess (1) how arterial elastance (E-a), calculated as the ratio of LV end-systolic pressure and stroke volume, relates to arterial properties and leak severity and (2) the validity of E-a/E-max (with E-max the slope of the-end-systolic pressure-volume relation) as a heart-arterial coupling parameter in AR. Methods and Results Our work is based on human data obtained from a study on vascular adaptation in chronic AR. These data allowed us to assess the parameters of a computer model of heart-arterial interaction. In particular, total peripheral resistance (R) and aortic leak severity-expressed as leak resistance (R-L,R-ao)-were quantified for different patient subgroups (group I/IIa/IIb: E-max = 2.15/0.62/0.47 mm Hg/mL; E-a = 1.24/0.66/0.90 mm Hg/mL; R = 1.9/0.6/0.85 mm Hg-s/mL, R-L,R-ao = 0.35/0.05/0.20 mm Hg-s/mL). A parameter study demonstrated that R-L,R-ao was the main determinant of E-a. With all other parameters constant, valve repair would increase E-a to 2.81, 1.08, and 1.54 mm Hg/mL in groups I,IIa, and IIb, respectively. For a given E-a/E-max, LV pump efficiency (estimated as the ratio of stroke work and LV systolic pressure-volume area) was lower than the theoretical predicted value, except for the simulations with intact aortic valve. Conclusions In AR(a) E-a is determined by aortic leak severity rather than by arterial system properties. Using E-a/E-max as a coupling parameter in general or as a mechanico-energetic regulatory parameter in particular is questionable. [less ▲]