Experimental assessment of a new research tool for the estimation of two-dimensional myocardial strain.

One-dimensional strain imaging has been shown to be angle dependent. To address this problem, a new methodology, 2D-strain, has become available. The aim of this study was to validate this methodology in an in vivo set-up against sonomicrometry. In five open chest sheep, ultrasound gray-scale images were acquired of the inferolateral wall from two different angles. The longitudinal and radial strain components were simultaneously extracted using the novel 2D-strain methodology. The extracted values were compared with sonomicrometry using Bland-Altman statistics and correlation coefficients. A good agreement was found for the longitudinal strain component, while, for the radial strain estimates, the accuracy was less. 2D-strain is a fast and accurate tool to assess longitudinal strain from apical views. Further improvements are needed for the method to be sufficiently accurate in estimating the deformation perpendicular or close to perpendicular to the ultrasound beam.

Hemodynamic effects of different lung-protective ventilation strategies in closed-chest pigs with normal lungs.

OBJECTIVE: The benefits of lung-protective ventilation strategies used for acute respiratory distress syndrome in subjects with normal lungs are uncertain. The purpose of this study was to investigate the hemodynamic effects of conventional lung-protective ventilation (CLPV) and high-frequency oscillatory ventilation (HFOV) in a normal lung animal model. DESIGN: Prospective laboratory investigation. SETTING: Animal laboratory in a university medical center. SUBJECTS: Seven landrace pigs (mean weight 41 kg). INTERVENTIONS: Pigs were ventilated at random conventionally with positive end-expiratory pressure 2-3 cm H2O and tidal volume 10-12 mL/kg (control), with CLPV (positive end-expiratory pressure 10 cm H2O, tidal volume 6 mL/kg), or with HFOV. Hemodynamics were analyzed after insertion of biventricular conductance catheters and a pulmonary artery catheter. MEASUREMENTS AND MAIN RESULTS: The protective strategies led to higher mean airway pressures and severe hypercapnia with acidosis, which was only significant with CLPV. Compared with control, oxygenation was worse with CLPV and HFOV. With HFOV and CLPV, mean arterial pressure, cardiac output, and stroke volume decreased significantly; pulmonary arterial elastance increased. The slope of the end-diastolic pressure volume relationship for the left and right ventricle remained unchanged (preserved ventricular function), whereas the intercept increased with both protective strategies (augmented intrathoracic pressure); left and right end-diastolic volumes decreased significantly. CONCLUSIONS: In the absence of a fluid resuscitation strategy, CLPV and HFOV caused decreased mean arterial pressure, cardiac output, and stroke volume and worsened oxygenation in this normal lung animal model. This resulted primarily from a biventricular decrease in preload.

Longitudinal but not circumferential deformation reflects global contractile function in the right ventricle with open pericardium.

The clinical evaluation of right ventricular (RV) contractility is problematic because instantaneous RV volumetry is difficult to achieve. Our aim was to test whether global RV contractility can be assessed by using regional indexes in the longitudinal and/or circumferential axis. Six anesthetized adult ewes were instrumented with a RV conductance catheter and four RV free wall sonomicrometry crystals (interrogating the longitudinal and circumferential axes). Global and regional preload recruitable stroke work (PRSW) were measured by using acute vena cava occlusions at baseline, during esmolol and dobutamine infusion, and during stable low-preload and high-afterload conditions. The agreement between regional and global PRSW was assessed with regression and Bland-Altman analysis. Both regional PRSW indexes correlated well with global PRSW in baseline conditions, during inotropic modulation (R(2) = 0.83 and 0.74 for longitudinal and circumferential regional PRSW, respectively), and during preload reduction (R(2) = 0.62 and 0.83, respectively), but only longitudinal regional PRSW correlated with global PRSW in increased afterload conditions (R(2) = 0.59 and 0.13 for longitudinal and circumferential regional PRSW, respectively). We conclude that in the open-chest, open-pericardium animal model, deformation in the longitudinal axis accurately reflects global RV contractile function in baseline conditions and during acute load modulation, whereas circumferential motion is influenced by changes in afterload.

Experimental validation of a new ultrasound method for the simultaneous assessment of radial and longitudinal myocardial deformation independent of insonation angle.

BACKGROUND: Strain and strain rate have been proposed as tools to quantify regional myocardial function. One of the major pitfalls of the current methodology is its angle dependency. To overcome this problem, we have developed a new method for the estimation of strain, independent of angle. The aim of this study was to validate this new methodology in an experimental setting using sonomicrometry. METHODS AND RESULTS: In 5 open-chest sheep, ultrasound data were acquired. The new methodology was used to perform simultaneous measurements of radial and longitudinal strain in the inferolateral wall. Segment-length sonomicrometry crystals were used as the reference. After baseline acquisitions, deformation was modulated by pharmacologically changing the inotropic state of the myocardium and by inducing ischemia. Ultrasonically estimated radial and longitudinal strain were validated against sonomicrometry by means of Bland-Altman analysis and the intraclass correlation coefficient. For both strain components, good agreements were found between the ultrasound and the sonomicrometry measurements as shown by Bland-Altman statistics. The intraclass correlation coefficients were found to be 0.72 and 0.80 for the radial and longitudinal components, respectively. CONCLUSIONS: A new technique for the estimation of myocardial deformation was validated. It was shown that the current problem of angle dependency was solved and that 2 deformation components could be estimated simultaneously and accurately. Furthermore, the technique was less time-consuming, because anatomic tracking was performed automatically. This approach could potentially accelerate the clinical acceptance of ultrasound deformation imaging in cardiology.

Effects of levosimendan on right ventricular function and ventriculovascular coupling in open chest pigs.

OBJECTIVE: Levosimendan is a promising calcium sensitizer that potentially could be useful in settings of pulmonary vasoconstriction and right ventricular dysfunction. There is a shortage of information concerning its effects on right ventricular function and ventriculovascular coupling. The aim of the present study was to characterize the effects of levosimendan on right ventricular and pulmonary vascular function by means of pressure-volume and pulsatile flow analysis. DESIGN: Prospective laboratory investigation. SETTING: University hospital laboratory. SUBJECTS: Eight landrace pigs (mean weight, 37 kg). INTERVENTIONS: Following instrumentation with biventricular conductance catheters, pulmonary and right coronary artery flow probes, a high-fidelity pulmonary pressure catheter, and a right coronary venous catheter, hemodynamic measurements were performed in baseline conditions and during levosimendan infusion at three increasing plasma concentrations (mean values, 27.5, 67.6, and 142.5 ng/mL). MEASUREMENTS AND MAIN RESULTS: Levosimendan increased heart rate and cardiac output, reduced systemic vascular resistance, and had a positive inotropic effect on the left ventricle and increased left ventricular mechanical efficiency. Moreover, levosimendan increased right ventricular contractility and hydraulic power. However, total pulmonary vascular resistance and characteristic impedance did not change throughout the protocol, and right ventricular mechanical efficiency decreased slightly at the highest concentration of levosimendan. CONCLUSIONS: At clinical concentrations in the present model, levosimendan increases right ventricular contractility and performance without significantly influencing pulmonary vascular tone. Further studies are required in a model of pulmonary vasoconstriction to disclose possible pulmonary vasodilator effects of levosimendan.

Determinants of left ventricular preload-adjusted maximal power.

Maximal left ventricular (LV) hydraulic power output (PWR(max)), corrected for preload as PWR(max)/(V(ed))(beta) (where V(ed) is the end-diastolic volume and beta is a constant coefficient), is an index of LV contractility. Whereas preload-adjusted maximal power (PAMP) is usually calculated with beta = 2, there is uncertainty about the optimal value of beta (beta = 1 for the normal LV and 2 for the dilated LV). The aim of this work is to study the determining factors of beta. The data set consisted of 245 recordings (steady state and vena cava occlusion) in 10 animals in an ischemic heart pig model. The occlusion data yielded the slope (E(es); 2.01 +/- 0.77 mmHg/ml, range 0.71-4.16 mmHg/ml) and intercept (V(0); -11.9 +/- 22.6 ml; range -76 to 39 ml) of the end-systolic pressure-volume relation, and the optimal beta-factor (assessed by fitting an exponential curve through the V(ed)-PWR(max) relation) was 1.94 +/- 0.88 (range 0.29-4.73). The relation of beta with V(ed) was weak [beta = 0.60 + 0.02(V(ed)); r(2) = 0.20]. In contrast, we found an excellent exponential relation between V(0) and beta [beta = 2.16e(0.0189(V(0))), r(2) = 0.70]. PAMP, calculated from the steady-state data, was 0.64 +/- 0.40 mW/ml(2) (range 0.14-2.83 mW/ml(2)) with a poor correlation with E(es) (r = 0.30, P < 0.001). An alternative formulation of PAMP as PWR(max)/(V(ed) - V(0))(2), incorporating V(0), yielded 0.47 +/- 0.26 mW/ml(2) (range 0.09-1.42 mW/ml(2)) and was highly correlated with E(es) (r = 0.89, P < 0.001). In conclusion, correct preload adjustment of maximal LV power requires incorporation of V(0) and thus of data measured under altered loading conditions.

Effects of vasopressin on right ventricular function in an experimental model of acute pulmonary hypertension.

OBJECTIVE: Arginine vasopressin is a promising systemic vasopressor in settings such as vasodilatory shock and cardiopulmonary resuscitation. The evidence that arginine vasopressin may also have a pulmonary vasodilatory effect makes it an attractive drug for the treatment of circulatory shock secondary to right ventricular failure and pulmonary hypertension. In the present study, we evaluated the effects of arginine vasopressin on right ventricular function and ventriculovascular coupling in the setting of moderate acute pulmonary hypertension and compared these effects with those of phenylephrine. DESIGN: Prospective laboratory investigation using an established model of acute pulmonary hypertension. SETTING: University hospital laboratory. SUBJECTS: Seven adult beagle dogs weighing 8-14 kg. INTERVENTIONS: After acute instrumentation to measure right ventricular pressure and volume with the conductance technique and pulmonary artery flow and pressure with high-fidelity transducers, the stable thromboxane analogue U46619 was infused continuously to obtain stable pulmonary hypertension. Phenylephrine and arginine vasopressin were administered consecutively in continuous infusions at doses titrated to achieve a 25% increase in aortic pressure. MEASUREMENTS AND MAIN RESULTS: Phenylephrine and arginine vasopressin both increased total pulmonary vascular resistance and arterial elastance without influencing characteristic impedance. Both drugs decreased cardiac output and stroke volume. Right ventricular hydraulic power output was reduced by arginine vasopressin but not by phenylephrine. Most importantly, arginine vasopressin caused a 31% decrease in right ventricular contractility measured as the slope of the preload recruitable stroke work relationship, whereas contractility was preserved during phenylephrine infusion. CONCLUSIONS: In the present model, arginine vasopressin causes pulmonary vascular constriction and exerts an important negative inotropic effect on the right ventricle. These findings suggest that one should be cautious in the use of arginine vasopressin when right ventricular function is compromised.

Preload-adjusted maximal power of right ventricle: contribution of end-systolic P-V relation intercept.

To assess whether preload-adjusted maximal power (PAMP), which is calculated as W(max)/V (where W(max) is maximal power and V(ed) is end-diastolic volume with beta = 2) is an index of right ventricular (RV) contractility, we measured RV pressure (P) and volume (V) and pulmonary artery pressure and flow in 10 dogs at baseline and after inotropic stimulation. PAMP was derived from steady-state data, whereas the slope (E(es)) and intercept (V(d)) of the end-systolic P-V relationship were derived from data obtained during vena caval occlusion. Inotropic stimulation increased E(es) (from 0.96 +/- 0.25 to 1.62 +/- 0.28 mmHg/ml; P < 0.001) and V(d) (from -3.0 +/- 17.2 to 12.4 +/- 10.8 ml; P < 0.05) but not PAMP (from 0.24 +/- 0.10 to 0.36 +/- 0.22 mW/ml(2); P = 0.09). We found a strong relationship between the optimal beta-factor for preload adjustment and V(d). A corrected PAMP, PAMP(c) = W(max)/(V(ed) - V(d))(2), which incorporated the V(d) dependency, was sensitive to the inotropic changes (from 0.23 +/- 0.12 to 0.54 +/- 0.17 mW/ml(2); P < 0.001) with a good correlation with E(es) (r = 0.88; P < 0.001).

The limitations of preload-adjusted maximal power as an index of right ventricular contractility.

UNLABELLED: Right ventricular (RV) dysfunction is an important cause of perioperative morbidity and mortality, particularly in cardiac surgery. However, assessment of RV contractility remains difficult in clinical practice. Our goal in this study was to examine the value of preload-adjusted maximal power (PWR(max)/end-diastolic volume [EDV](2); PAMP) as an alternative to the load-independent pressure-volume-derived indices of contractility in the RV. In anesthetized dogs, RV end-systolic elastance and preload-recruitable stroke work were studied as "gold standards" by using the conductance technique. PAMP was calculated with pulmonary artery flow and RV pressure measurements. Changes in these indices were compared after modulation of the inotropic state (dobutamine infusion; n = 12) and loading conditions (pulmonary artery and inferior caval vein occlusion; n = 14). All indices increased dose-dependently with dobutamine. PAMP was slightly influenced by preload reduction (the slope of the relation between PAMP and EDV was 0.00397 +/- 0.01026 W. mL(-3). 0.10(-4); mean +/- SD). PAMP decreased significantly during pulmonary artery banding (from 1.1 +/- 0.7 to 0.7 +/- 0.5 W. mL(-2). 0.10(-4); mean +/- SD), whereas end-systolic elastance and preload-recruitable stroke work did not change. We conclude that the value of PAMP as an index of RV contractility is limited in the open-chest/open-pericardium setting, primarily by its sensitivity to alterations in afterload. IMPLICATIONS: Preload-adjusted maximal power (PAMP), a load-independent contractile index in the left ventricle, could offer a solution to the problem of measuring right ventricular (RV) contractility in clinical practice. However, this study in open-chest dogs suggests that PAMP is unreliable for assessment of RV contractility because of its sensitivity to afterload changes.