Ventricular Elastance Research Articles

Left ventricular-arterial coupling as a predictor of stroke volume response to norepinephrine in septic shock \u2013 a prospective cohort study

BackgroundLeft ventricular-arterial coupling (VAC), defined as the ratio of arterial elastance (Ea) to left ventricular end-systolic elastance (Ees), is a key determinant of cardiovascular performance. This study aims to evaluate whether left VAC can predict stroke volume (SV) response to norepinephrine (NE) in septic shock patients.MethodsThis was a prospective cohort study conducted in an intensive care unit of a tertiary teaching hospital in China. We recruited septic shock patients who had persistent hypotension despite fluid resuscitation and required NE to maintain mean arterial pressure (MAP) > 65 mmHg. Those patients in whom the target MAP was not reached after NE infusion were ineligible. Echocardiographic variables were measured before (baseline) and after NE infusion. SV responder was defined by a ≥ 15% increase in SV after NE infusion.ResultsOf 34 septic shock patients included, 19 (56%) were SV responders. Before NE infusion, SV responders had a lower Ees (1.13 ± 0.24 mmHg/mL versus 1.50 ± 0.46 mmHg/mL, P = 0.005) and a higher Ea/Ees ratio (1.47 ± 0.40 versus 1.02 ± 0.30, P = 0.001) than non-responders, and Ea in SV responders was comparable to that in non-responders (1.62 ± 0.36 mmHg/mL versus 1.43 ± 0.28 mmHg/mL, P = 0.092). NE significantly increased Ea and Ees in both groups. The Ea/Ees ratio was normalized by NE administration in SV responders but unchanged in non-responders. The baseline Ea/Ees ratio was positively correlated with NE-induced SV increases (r = 0.688, P < 0.001). Logistic regression analysis indicated that the baseline Ea/Ees ratio was a predictor of SV increases induced by NE (odd ratio 0.008, 95% confidence interval (CI): 0.000 to 0.293), with an area under the receiver operating characteristic curve of 0.816 (95% CI: 0.646 to 0.927).ConclusionsThe left VAC has the ability to predict SV response to NE infusion in septic shock patients.Trial registrationChinese Clinical Trial Registry, ChiCTR1900024031, Registered 23 June 2019 - Retrospectively registered, http://www.chictr.org.cn/edit.aspx?pid=40359&htm=4.

ECMO Assistance during Mechanical Ventilation: Effects Induced on Energetic and Haemodynamic Variables

Background and ObjectiveSimulation in cardiovascular medicine may help clinicians understand the important events occurring during mechanical ventilation and circulatory support. During the COVID-19 pandemic, a significant number of patients have required hospital admission to tertiary referral centres for concomitant mechanical ventilation and extracorporeal membrane oxygenation (ECMO). Nevertheless, the management of ventilated patients on circulatory support can be quite challenging. Therefore, we sought to review the management of these patients based on the analysis of haemodynamic and energetic parameters using numerical simulations generated by a software package named CARDIOSIM©. MethodsNew modules of the systemic circulation and ECMO were implemented in CARDIOSIM© platform. This is a modular software simulator of the cardiovascular system used in research, clinical and e-learning environment. The new structure of the developed modules is based on the concept of lumped (0-D) numerical modelling. Different ECMO configurations have been connected to the cardiovascular network to reproduce Veno-Arterial (VA) and Veno-Venous (VV) ECMO assistance. The advantages and limitations of different ECMO cannulation strategies have been considered. We have used literature data to validate the effects of a combined ventilation and ECMO support strategy. ResultsThe results have shown that our simulations reproduced the typical effects induced during mechanical ventilation and ECMO assistance. We focused our attention on ECMO with triple cannulation such as Veno-Ventricular-Arterial (VV-A) and Veno-Atrial-Arterial (VA-A) configurations to improve the hemodynamic and energetic conditions of a virtual patient. Simulations of VV-A and VA-A assistance with and without mechanical ventilation have generated specific effects on cardiac output, coupling of arterial and ventricular elastance for both ventricles, mean pulmonary pressure, external work and pressure volume area. ConclusionThe new modules of the systemic circulation and ECMO support allowed the study of the effects induced by concomitant mechanical ventilation and circulatory support. Based on our clinical experience during the COVID-19 pandemic, numerical simulations may help clinicians with data analysis and treatment optimisation of patients requiring both mechanical ventilation and circulatory support.

Force-based left ventricular contractile reserve predicts outcome in patients with exercise stress echocardiography without regional wall motion abnormalities

Abstract Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): Investigaciones Médicas, Cardiodiagnostic Introduction. The behavior of the ejection fraction (EF) during exercise stress echocardiography (ESE) is used to measure the left ventricular (LV) contractile reserve (CR). Ventricular Elastance or Force defined as the ratio between systolic blood pressure (SBP) and LV end-systolic volume (ESV) could be better as it is less dependent of heart rate, preload, and afterload conditions. Objective. To establish the relative prognostic value of EF-based and novel Force-based LVCR in patients (pts) without ischemia during ESE. Materials and methods. In a retrospective analysis of prospectively enrolled pts, we enrolled 904 pts, (61.92 ± 12.59 years, 509 men, 56.3%) with negative ESE for RWMA. LV volumes were measured with biplane Simpson’s rule. LVCR was assessed based on EF ≥5 points increase at peak over rest and based on Force peak/rest ratio &amp;gt; 2. The average follow-up was 17.7 ± 5.44 months. Major cardiovascular event was defined as: death, acute myocardial infarction, cerebrovascular accident and/or need for hospitalization due to cardiovascular causes. Results. LVCR by EF was present in 536 (59.3%) and absent in 368 (40.7%) pts. LVCR by Force was present in 200 pts (22.1%) and absent in 704 pts (77.9%) pts. The overall concordance between LVCR assessed by EF and Force was 538 pts (89.6%) with presence of CR by EF and not by Force being the most frequent source of discrepant result in 336 pts. In the long-term follow up, 52 pts experienced events: 0 all-cause death, 3 acute myocardial infarctions, 5 cerebrovascular accidents and 44 for hospitalization due to cardiovascular causes. Lack of LVCR based on EF identified patients at higher risk (see Figure) but Force-based LVCR allowed to further separate patients with EF-based LVCR (n = 536) into a lower risk with (n = 200, event rate 2%) and higher risk subgroup without Force-based LVCR (n= 336, event rate 5.3 %, p&amp;lt;.01 vs subgroup with Force-based LVCR) Cox Regression model identified Force-based LVCR was the only predictor of events (HR: 3.22, 95% CI 1.83-5.6, p &amp;lt; 0.001). Conclusions. In patients with negative SE for RWMA, the evaluation of LVCR based on EF allows a better stratification of outcome, which is further refined by addition of Force-based LVCR, especially useful in the subset with LVCR by EF not confirmed by Force. Force-based LVCR allowed to identify a subgroup of worse long-term prognosis outperforming EF-based LVCR. Abstract Figure. LVCR by EF and Event Free Survival

Intermittent outpatient administration of levosimendan improves right ventricular-pulmonary arterial coupling in ambulatory patients with advanced heart failure

Abstract Funding Acknowledgements Type of funding sources: None. Background Intermittent infusions of levosimendan in an outpatient setting have been associated with improved symptoms and reduced hospitalizations in patients with advanced heart failure (HF). Little is known on the potential effect of intermittent levosimendan infusions on right ventricle (RV)-pulmonary arterial (PA) coupling in ambulatory patients with advanced HF. Purpose Aim of the present study was to explore the effects of intermittent levosimendan infusions on the ratio between tricuspid annular plane systolic excursion (TAPSE) and pulmonary artery systolic pressure (PAPs), an echocardiographic measure of RV/PA coupling, in ambulatory patients with advanced HF, and on left ventricular arterial coupling (VAC), expressed as the relationship between arterial elastance (Ea) and ventricular elastance (Ees). Methods 17 ambulatory patients with advanced HF treated with intermittent levosimendan (6-hour intravenous infusion, 0.2 ug/kg/min without bolus) received baseline clinical, biochemical and echocardiographic evaluation and changes in TAPSE/PAPs ratio were assessed from baseline to 48 hours after the infusion, based on the pharmacokinetic profile of levosimendan. VAC, expressed as Ea/Ees ratio, was obtained by a calculator (iElastance) designed for non-invasive single beat measure of end-systolic Ees and Ea according to Chen"s method. Results After 48 hours from levosimendan infusion, there was a significant improvement of TAPSE/PAPs ratio (p = 0.04), stroke voume (SV) (p = 0.05) and cardiac output (CO)(p = 0.04). We observed a significant reduction of Ea (p = 0.007) and of Ees (p = 0.01) and a non significant improvement of VAC (p = 0.4)(Tab.1). Conclusion. Our results show that an intermittent 6-hour levosimendan infusion at 0.2 ug/kg/min improves after 48 hours RV-PA coupling, SV, CO, Ea and Ees in ambulatory patients with advanced HF. Further studies including more patients are necessary to confirm these preliminary findings. Tab.1 Baseline 48h afterlevosimendan infusion p value NT-proBNP (pg/mL) 5607 ± 4300 3868 ± 3856 &amp;lt;0.001 LVEF (%) 24.1 ± 7.7 25.7 ± 7.3 0.5 SV (mL) 36.8 ± 12.4 46.1 ± 14.8 0.05 CO (L/min)36.8 ± 12.4 2.6 ± 0.7 3.2 ± 0.9 0.05 TAPSE/PAPs (mm/mmHg) 0.38 ± 0.13 0.49 ± 0.16 0.04 Ea (mmHg/mL/m2) 2.9 ± 0.9 2.1 ± 0.6 0.007 Ees (mmHg/mL/m2) 1.3 ± 0.4 1.0 ± 0.2 0.01 VAC 2.2 ± 0.6 2.0 ± 0.4 0.4

Echocardiographic estimation of left ventricular-arterial coupling in dogs with myxomatous mitral valve disease.

BackgroundThe effective arterial elastance (Ea) to left ventricular (LV) end‐systolic elastance (Ees) ratio (Ea/Ees) is an index of the interaction between LV and systemic arterial systems, left ventricular‐arterial coupling (VAC). The Ea is an index of total arterial load of the LV, whereas Ees is an index of LV systolic function. In humans, inappropriate VAC based on increased Ea/Ees estimated using echocardiography is associated with more advanced heart disease severity.HypothesisLeft ventricular‐arterial coupling assessed by echocardiographic estimation of Ea/Ees is associated with disease severity in dogs with myxomatous mitral valve disease (MMVD).AnimalsNinety MMVD dogs and 61 healthy dogs.MethodsProspective cross‐sectional study. The MMVD dogs were classified into stages B1, B2, or C according to American College of Veterinary Internal Medicine guidelines. Effective arterial elastance was echocardiographically estimated using the formula: mean blood pressure/(forward stroke volume/body weight). End‐systolic elastance was echocardiographically estimated using the formula: mean blood pressure/(LV end‐systolic volume/body weight). The ratio Ea/Ees was calculated.ResultsThe ratio Ea/Ees was higher in stage B2 dogs than in healthy dogs and dogs stage B1 (both P < .0001), and higher in stage C dogs than in healthy dogs and dogs in the other 2 stages (healthy vs C and B1 vs C, P < .0001; B2 vs C, P = .0005). Multivariable logistic regression analysis showed that Ea/Ees and the peak velocity of early diastolic transmitral flow to isovolumic relaxation time ratio were independent predictors of stage C among echocardiographic indices in MMVD dogs.Conclusions and Clinical ImportanceInappropriate VAC assessed by echocardiographically estimated Ea/Ees is associated with advanced disease severity in dogs with MMVD.

Maternal hemodynamics, arterial stiffness and elastic aortic properties in twin pregnancy

Objective: There is scant information about maternal cardiovascular hemodynamic change during twin pregnancies. Aim of the study is to investigate longitudinal changes in maternal arterial stiffness, elastic aortic properties and ventricular-arterial coupling (VAC) in uncomplicated twin pregnancies compared to singleton ones. Approach: In this prospective longitudinal study, we performed applanation tonometry and transthoracic echocardiography in the first (T1; 10–15 weeks’ gestation (w)), second (T2; 19–26 w) and third trimesters (T3; 30–38 w) in women with uncomplicated twin pregnancies, both monochorionic and dichorionic. Heart-rate-corrected augmentation index (AIx@75) was studied as indicator of arterial stiffness. Aortic diameters and elastic properties were calculated. VAC was defined as the ratio between aortic elastance (Ea) and left ventricular end-systolic elastance (Ees). Finally, stroke volume (SV), cardiac output (CO) and total vascular resistance (TVR) were evaluated. The findings were compared to those of women with uncomplicated singleton pregnancies. Main results: Thirty women with twin gestations (11 monochorionic) and 30 singleton controls were obtained for analysis. Blood pressure and TVR significantly decreased from T1 to T2 and then rose in T3, with higher values in twins than in singletons. AIx@75 showed the same trend in both groups with lower values at T2 in twins. SV and CO linearly increased throughout gestation with no significant intergroup difference. Aortic diameters and elastic properties remained stable throughout gestation, with no significant intergroup differences. Both Ea and Ees were greater (i.e. worse) in twins than in singletons at T1 and T3, showing a significant linear trend towards reduction in the two groups, meaning lower vascular and ventricular loads. Using longitudinal analysis blood pressure, TVR, Ea and Ees depended from both multiple gestation and gestational age. Significance: In twins, maternal hemodynamics does not seem to undergo more significant changes than in singletons being characterized by higher blood pressures and TVR with no differences in CO, SV, aortic dimensions and elastic properties. Despite VAC is maintained within its normal range, total vascular load (i.e., Ea) resulted higher in twin than singleton pregnancies throughout gestation. It is conceivable that these findings may represent one of the underlying cause for the increased risk of adverse obstetric outcomes described in multiple gestations.

Single-Beat Measurement of Left Ventricular Contractility in Normothermic Ex Situ Perfused Porcine Hearts.

For heart transplantation, donor heart status needs to be evaluated during normothermic ex situ perfusion (ESHP). Left ventricular end-systolic elastance (E es) measures the left ventricular contractile function, but its estimation requires the occlusion of the left atrium line in the ESHP, which may cause unnecessary damage to the donor heart. We present a novel method to quantify E es based on hemodynamic parameters obtained from only one steady-state PV loop in ESHP. E es was obtained by the end-systolic point (P es, V es) and the volume axis intercept point of E es (V 0). V 0 was estimated through the support vector machine regression (SVR) method using parameters derived from the measured steady-state PV loop. To achieve high V 0 estimation accuracy, a filter-based support vector machine recursive feature elimination method (SVM-RFE) algorithm selected the parameters for V 0 estimation. Hemodynamic parameter samples (n = 101) obtained from ESHP experiments with pig's hearts were used to train the E es calculation model. Early post-transplantation outcomes in six heart transplantation experiments were then estimated from the trained E es calculation model. E es calculated by the proposed method agreed well with conventional multi-beat estimates obtained by the occlusion process (r = 0.88, p <0.001, n = 101) and was capable of predicting the early post-transplant cardiac index (r = 0.84, p <0.05, n = 6). This method effectively assesses left ventricular contractility during ESHP and predicts early post-transplant outcomes in the porcine model. Our approach is the first to quantify E es by estimating V 0 from steady-state beats in ESHP for accurately predicting early post-transplantation outcomes.

Abstract 13421: Ventricular and Arterial Elastance During Isometric Handgrip Exercise and Post-exercise Circulatory Arrest in Heart Failure With and Without Preserved Ejection Fraction

Introduction: Isometric handgrip (IHG) training at 30% maximal voluntary contraction (MVC) lowers blood pressure in hypertensive patients. Impacts of IHG exercise and post-exercise circulatory arrest (PECA), which isolates metaboreflex control, have been unclear in heart failure (HF). Purpose: To investigate the impacts of IHG exercise and PECA on ventricular-arterial stiffness and left ventricular (LV) relaxation in HF with preserved (HFpEF) and reduced ejection fraction (HFrEF). Methods: We invasively obtained LV pressure-volume (PV) loops in 20 patients (10 HFpEF, 10 HFrEF) using conductance catheter with microtip-manometer during 3 minutes of IHG at 30%MVC and 3 minutes of PECA. Hemodynamics and LV-arterial function including LV end-systolic elastance (Ees) by the single-beat method, effective arterial elastance (Ea), and time constant of LV relaxation (Tau) were evaluated every minute. Results: At rest, HFpEF had higher LV end-systolic pressure (ESP) and lower heart rate than HFrEF with similar LV end-diastolic pressure (EDP). The coupling ratio (Ees/Ea) was greater in HFpEF than HFrEF (1.0±0.3 vs. 0.6±0.3, p&lt;0.01). IHG for 3minutes similarly increased heart rate in HFpEF (by 10±8 bpm) and HFrEF (by 14±6 bpm). IHG also increased end-diastolic and LVESP (134±21 vs. 158±30 mmHg and 113±25 vs. 139±25 mmHg) in both groups (groupхtime effect p≥0.25). In HFpEF, Ees, Ea and Ees/Ea (1.0±0.3 vs. 1.1±0.4) were unaffected during IHG. In HFrEF, IHG induced variable increases in Ea. LV end-systolic volume and the ESPV volume-axis intercept were larger, and Ees at IHG 3 rd min was greater (1.30±0.7 vs. 3.1±2.1 mmHg/ml, p&lt;0.01) than baseline, resulting in unchanged Ees/Ea at IHG 3 rd min (0.6±0.3 vs. 0.8±0.4, p≥0.37). Tau was prolonged only in HFrEF during IHG and was returned to the baseline value during PECA. During the first 2 minutes of PECA, LVESP was lower than that at IHG 3 rd min only in HFpEF, suggesting less metaboreflex control of blood pressure in HFpEF during IHG. Conclusions: IHG exercise at 30%MVC induced modest increases in LV end-systolic and end-diastolic pressures in HFpEF and HFrEF. Although the prolongation of LV relaxation was observed only in HFrEF, the ventricular and arterial coupling was maintained throughout the IHG exercise in both groups.

Abstract 16138: Validation of a Non-invasive Approach for the Assessment of Left Ventricular-arterial Coupling Following Transcatheter Aortic Valve Replacement

Introduction: Transcatheter aortic valve replacement (TAVR) is an established treatment for patients with severe, symptomatic aortic stenosis (AS). Ventriculoarterial (LV-arterial) coupling defined as the ratio of total arterial elastance (Ea) to left ventricular end-systolic elastance (Ees) reflects effective cardiac energetics and is a well-accepted index for quantification of LV-arterial coupling. Despite its usefulness, estimating Ees/Ea has technical difficulties. Intrinsic Frequency (IF) method is a noninvasive and single waveform system-based approach for quantification of LV-arterial coupling. The objective of this study was to compare IF variables with Ea/Ees in predicting optimum LV-arterial energetics following TAVR. Method: Twenty-eight patients with severe AS, undergoing TAVR were included. Mean age was 85±4, 53% male with mean ejection fraction 59±6.4. IFs during systole (ω1), diastole (ω2), and total IF variation (Δω=ω1-ω2) were computed from the ascending aortic pressure waveforms at baseline and following TAVR. Ea/Ees was computed using single-beat technique proposed by Takeuchi et al. ( Circulation . 1991;83(1):202-212). Results: There was a significant decrease in Ea/Ees (p&lt;0.001) toward optimum coupling immediately after TAVR (Figure 1a). There was a statistically significant correlation between Ea/Ees and Δω (r= 0.68, p&lt;0.01) (Figure 1b). Conclusion: IF appears to be an accurate and reliable index for quantification of LV-arterial coupling given significant concordance with Ea/Ees. The management of patients with acutely altered hemodynamic states post TAVR can benefit from the assessment of LV-arterial coupling. Since IFs can be measured noninvasively using hand-held devices (e.g. an iPhone), this approach should broaden the clinical applicability of this useful parameter for assessing systolic function, therapeutic response and ventricular-arterial interaction post TAVR.

Is 24 hour central aortic pressure superior to single measurement of central aortic pressure in well controlled hypertensive patients

Abstract Background Non-invasive measurements of 24 h ambulatory central aortic systolic pressure (24hCASP) is now feasible method than single measurement of CASP. There is growing interest in CASP as cardiovascular risk marker beyond conventional brachial blood pressure (BP). Pulse wave velocity estimates arterial stiffness, whereas CASP is representative of the BP in major organs. Purpose To evaluate non- invasive parameters for arterial stiffness using oscillometric method and to compare 24hCASP with single measurement of CASP in well-controlled hypertensive patients to detect target organ damage (TOD). Methods A total 95 patients (57±14 years) with hypertension, were separated in two groups: 22 patients with normal EA/Ees ratio (Arterial elastance (EA) and ventricular elastance (Ees)) and 73 hypertensive patients with decrease EA/Ees ratio, marker for ventriculo-arterial coupling. EA and Ees were calculated as and – systolic pressure/stroke volume and end-systolic pressure/end-systolic volume. Parameters for arterial stiffness – 24hCASP, ambulatory central systolic pressure (CASP), 24-hour pulse wave velocity (PWV24h) and ambulatory PWV were measured non-invasively with oscillometric method by Mobil-O-graph PWA. Results Statistically significant differences in parameters of vascular stiffness were found in patients with normal ventriculo-arterial coupling in comparison with disturbed EA/Ees: 24hCASP (107.64±9.19 vs. 116.64±16.7 mm Hg, p=0.02), CAP (117.45±9.26 vs. 128.42±16.15 mm Hg, p&amp;lt;0.0001). There were no statistically significant differences in PWV and PWV24h. Multiple regression analysis demonstrated that CAP (B=−0.264 p=0.003; 95% CI: −0.003–0.014) is independent predictor of TOD in hypertensive patients, than 24 hour central aortic pressure. Conclusion There is no superiority of 24hCASP than single measurment of CASP. CASP could predict preclinical damage and cardiovascular outcome. Funding Acknowledgement Type of funding source: None

A closer look at physiological indicators of cardiovascular function post‐transplantation

A closer look at physiological indicators of cardiovascular function post‐transplantation

Right Ventricular Arterial Elastance is Associated with Prognostic Value in one Year Mortality Following Left Ventricular Assist Device Placement

Background In patients with end-stage heart failure (HF), acute right heart failure (RHF) after left ventricular assist device (LVAD) implantation is known to be a source of significant morbidity and mortality. Previous data identified RV pulsatility load using pulmonary arterial compliance as a marker for 6-month mortality in LVAD patients. We aimed to test whether the right ventricular arterial elastance (RVEa) was associated with increased risk of 1 year mortality after LVAD implantation. Hypothesis Patients with higher RVEa at preimplantation have a higher risk of dying at 1 year. Methods We retrospectively identified 381 patients with complete pre-implant hemodynamics obtained Results The majority of patients (65%) had RVEa≥1 (Fig. 1). When comparing baseline demographics, those with RVEa ≥1 were younger, had a lower proportion of hypertension, coronary artery disease, and more likely to be on inotropes pre-implantation. Those with RVEa ≥1 had lower SV, and pulmonary artery pressure index; and higher mean pulmonary artery pressure, pulmonary wedge capillary pressure and transpulmonary gradient. Multivariate survival analysis adjusted for heart rate, BMI, age, and gender demonstrated the only independent predictor of mortality was RVEa ≥1 (hazard ratio 1.80, [95% CI 1.07 - 3.05], p= 0.028). Conclusions Our multi-institutional study demonstrates that higher RVEa is associated with increased 1 year mortality post-VAD implantation. These data may be generalizable to other academic institutions and warrants further investigation in larger cohorts.

Implementation and Calibration of a Deep Neural Network to Predict Parameters of Left Ventricular Systolic Function Based on Pulmonary and Systemic Arterial Pressure Signals.

The evaluation of cardiac contractility by the assessment of the ventricular systolic elastance function is clinically challenging and cannot be easily obtained at the bedside. In this work, we present a framework characterizing left ventricular systolic function from clinically readily available data, including systemic and pulmonary arterial pressure signals. We implemented and calibrated a deep neural network (DNN) consisting of a multi-layer perceptron with 4 fully connected hidden layers and with 16 neurons per layer, which was trained with data obtained from a lumped model of the cardiovascular system modeling different levels of cardiac function. The lumped model included a function of circulatory autoregulation from carotid baroreceptors in pulsatile conditions. Inputs for the DNN were systemic and pulmonary arterial pressure curves. Outputs from the DNN were parameters of the lumped model characterizing left ventricular systolic function, especially end-systolic elastance. The DNN adequately performed and accurately recovered the relevant hemodynamic parameters with a mean relative error of less than 2%. Therefore, our framework can easily provide complex physiological parameters of cardiac contractility, which could lead to the development of invaluable tools for the clinical evaluation of patients with severe cardiac dysfunction.

Levosimendan and Global Longitudinal Strain Assessment in Sepsis (GLASSES 1): a study protocol for an observational study

IntroductionCardiogenic shock is a condition of low cardiac output that represents the end stage of a progressive deterioration of cardiac function. The main cause is ischaemic heart disease, but there...

Fluid expansion improve ventriculo-arterial coupling in preload-dependent patients: a prospective observational study

BackgroundThe objectives of the present study was to evaluate the effect of fluid challenge (FC) on ventriculo-arterial (V-A) coupling, its determinants: arterial elastance and ventricular elastance, and ability to predict fluid responsiveness.MethodsThirty patients admitted to cardio-thoracic ICU in whom the physician decided to perform FC were included. Arterial pressure, cardiac output, arterial elastance, and ventricular elastance, were measured before and after FC with 500 ml of lactated Ringer’s solution. Fluid responders were defined as patients with more than a 15% increase in stroke volume. V-A coupling was evaluated by the arterial elastance to ventricular elastance ratio.ResultsTwenty-three (77%) of the 30 patients included in the study were fluid responders. Before FC, responders had higher arterial elastance and arterial elastance to ventricular elastance ratio. FC significantly increased mean arterial pressure, stroke volume and cardiac output, and significantly decreased systemic vascular resistance, arterial elastance and consequently the arterial elastance to ventricular elastance ratio. Changes in arterial elastance were correlated with changes in stroke volume, systemic vascular resistance, and arterial compliance. Baseline arterial elastance to ventricular elastance ratio over 1.4 predicted fluid responsiveness (area under the curve [95% confidence interval]: 0.84 [0.66–1]; p < 0.0001).ConclusionsFluid responsiveness patients had V-A coupling characterized by increase arterial elastance to ventricular elastance ratio, in relation to an increase arterial elastance. Fc improved the V-A coupling ratio by decreasing arterial elastance without altering ventricular elastance. Arterial elastance changes were related to those of systemic vascular resistance (continue component) and of arterial compliance (pulsatile component).

Inhaled nitric oxide has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute pulmonary embolism.

Inhaled nitric oxide (iNO) effectively reduces right ventricular afterload when administered in the immediate phase of acute pulmonary embolism (PE) in preclinical animal models. In a porcine model of intermediate-risk PE, we aimed to investigate whether iNO has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute PE. Anesthetized pigs (n = 18) were randomized into three subgroups. An acute PE iNO-group (n = 6) received iNO at 40 ppm at one, three, six, nine and 12 hours after onset of PE. Vehicle animals (n = 6) received PE, but no active treatment. A third group of sham animals (n = 6) received neither PE nor treatment. Animals were evaluated using intravascular pressures, respiratory parameters, biochemistry and intracardiac pressure-volume measurements. The administration of PE increased mean pulmonary artery pressure (mPAP) (vehicle vs sham; 33.3 vs 17.7 mmHg, p < 0.0001), pulmonary vascular resistance (vehicle vs sham; 847.5 vs 82.0 dynes, p < 0.0001) and right ventricular arterial elastance (vehicle vs sham; 1.2 vs 0.2 mmHg/ml, p < 0.0001). Significant mPAP reduction by iNO was preserved at 12 hours after the onset of acute PE (vehicle vs iNO; 0.5 vs -3.5 mmHg, p < 0.0001). However, this response was attenuated over time (p = 0.0313). iNO did not affect the systemic circulation. iNO is a safe and effective pulmonary vasodilator both in the immediate and prolonged phase of acute PE in an in-vivo porcine model of intermediate-risk PE.

Arterial-Ventricular Coupling Evaluation in Individuals with Stress-Evidenced Diastolic Dysfunction: A Pilot Study.

Arterial-ventricular coupling (AVC) has been recognized as a key determinant of global cardiovascular performance. Diastolic dysfunction (DD) occurs when inadequate filling of the ventricles is related to an abnormal elevation of intracardiac filling pressures. In some cases, DD is evidenced during cardiac stress, provoked by exercise. To evaluate AVC in individuals with stress evidenced DD, in relation to controls. Stress echocardiography was applied to assess cardiac function during exercise. Arterial-ventricular coupling was evaluated, based on the assessment of left ventricular and arterial elastances. AVC showed a significant difference at peak exercise compared to controls, basically due to a loss of cardiac contractility. The manifestation of AVC coupling imbalance could act as a complementary parameter to support the diagnosis of DD.

Right ventriculo-pulmonary arterial uncoupling and poor outcomes in pulmonary arterial hypertension.

Right ventricular function critically affects the prognosis of patients with pulmonary arterial hypertension. We aimed to analyze the prognostic value of right ventricular indices calculated using magnetic resonance imaging and right heart catheterization metrics in pulmonary arterial hypertension. We retrospectively collected data from 57 Japanese patients with pulmonary arterial hypertension and 18 controls and calculated six indices of right ventricular function: two indices of contractility (end-systolic elastance calculated with right ventricular maximum pressure and with magnetic resonance imaging metrics); two indices of right ventricular–pulmonary arterial coupling (end-systolic elastance/arterial elastance calculated with the pressure method (end-systolic elastance/arterial elastance (P)) and with the volume method (end-systolic elastance/arterial elastance (V)); and two indices of right ventricular diastolic function (stiffness (β) and end-diastolic elastance). We compared the indices between controls and patients with pulmonary arterial hypertension and examined their prognostic role. In patients with pulmonary arterial hypertension, end-systolic elastance (right ventricular maximum pressure) was higher (pulmonary arterial hypertension 0.94 (median) vs control 0.42 (mmHg/mL), p < 0.001), end-systolic elastance/arterial elastance (V) was lower (pulmonary arterial hypertension 0.72 vs control 1.69, p < 0.001), and β and end-diastolic elastance were significantly higher than those in the controls. According to the log-rank test, end-systolic elastance/arterial elastance (P) and end-diastolic elastance were significantly associated with the composite event rate. According to the multivariate Cox regression analysis, decreased end-systolic elastance/arterial elastance (P) was associated with a higher composite event rate (hazard ratio 11.510, 95% confidence interval: 1.954–67.808). In conclusion, an increased right ventricular contractility, diastolic dysfunction, and a trend of impaired right ventricular–pulmonary arterial coupling were observed in our pulmonary arterial hypertension cohort. According to the multivariate outcome analysis, a decreased end-systolic elastance/arterial elastance (P), suggestive of impaired right ventricular–pulmonary arterial coupling, best predicted the pulmonary arterial hypertension-related event.

Cardiovascular Outcomes in Young Adulthood in a Population-Based Very Low Birth Weight Cohort

To assess differences in left heart structure and function, and endothelial function in a national cohort of very low birth weight (VLBW) young adults and term-born controls. The New Zealand VLBW study is a prospective, population-based, longitudinal cohort study which included all infants born <1500g in 1986. The VLBW cohort (n=229; 71% of survivors) and term-born controls (n=100), were assessed at age 26-30years. Measures of left heart structure and function were evaluated by echocardiography, vascular function was assessed using blood pressure, reactive hyperemia index, and arterioventricular coupling by calculating left ventricular (LV) and arterial elastance. Compared with controls, those born VLBW had smaller LVs, even when indexed for body surface area (mean LV mass, 89.7±19.3g/m2 vs 95.0±22.3g/m2 [P=.03]; LV end-diastolic volume, 58.3±10.9mL/m2 vs 62.4±12.4mL/m2 [P=.002]; and LV end-systolic volume, 20.8±4.9mL/m2 vs 22.6±5.8mL/m2 [P=.004]). VLBW participants had lower stroke volume (median, 37.2mL/m2 [IQR, 33-42mL/m2] vs median, 40.1mL/m2 [IQR, 34-45mL/m2]; P=.0059) and cardiac output (mean, 4.8±1.2 L/min vs 5.1±1.4 L/min; P=.03), but there was no difference in ejection fraction. The VLBW group had higher LV elastance (3.37±0.88mm Hg/mL vs 2.86±0.75mm Hg/mL; P<.0001) and arterial elastance (1.84±0.4 vs 1.6±0.4; P<.0001) and lower reactive hyperemia index (0.605±0.28 vs 0.688±0.31; P=.041). These measures were influenced by birth weight and sex, but we found limited associations with other perinatal factors. Being born preterm and VLBW is associated with differences in cardiovascular structure and function in adulthood. This population may be more vulnerable to cardiovascular pathology as they age. Australian Clinical Trials Registry ACTRN12612000995875.

Radiation-induced myocardial fibrosis: Mechanisms underlying its pathogenesis and therapeutic strategies.

Radiation‐induced myocardial fibrosis (RIMF) is a potentially lethal clinical complication of chest radiotherapy (RT) and a final stage of radiation‐induced heart disease (RIHD). RIMF is characterized by decreased ventricular elasticity and distensibility, which can result in decreased ejection fraction, heart failure and even sudden cardiac death. Together, these conditions impair the long‐term health of post‐RT survivors and limit the dose and intensity of RT required to effectively kill tumour cells. Although the exact mechanisms involving in RIMF are unclear, increasing evidence indicates that the occurrence of RIMF is related to various cells, regulatory molecules and cytokines. However, accurately diagnosing and identifying patients who may progress to RIMF has been challenging. Despite the urgent need for an effective treatment, there is currently no medical therapy for RIMF approved for routine clinical application. In this review, we investigated the underlying pathophysiology involved in the initiation and progression of RIMF before outlining potential preventative and therapeutic strategies to counter this toxicity.