Ventricular End-systolic Elastance Research Articles

415 Comparison between two methods for assessing ventricular-arterial coupling: the Chen single-beat method and carotid artery wave intensity

Abstract Background Ventricular arterial coupling (VAC) can be defined as the ratio of the arterial elastance (Ea) to the ventricular elastance (Ees). . The Ea/Ees ratio has been consistently demonstrated to be a reliable and effective measure of cardiovascular performance. The Chen single-beat method is the most used non-invasive method for this measurement. Carotid artery wave intensity (WI) is also considered a index of VAC, as the first peak (W1) represents the forward compression wave, reflecting left ventricle (LV) contractile function. However, data about the relationship between the two methods are nowadays scarce. Purpose Aim of the study was to compare carotid WI and Ventricular-Arterial Coupling (VAC) in a population of patient with heart failure. Methods We examined 50 consecutive patients with heart failure (9 females, 41 males, mean age 67 + 12 years, range 29-97 years, 34 ischemic, 16 not ischemic). Carotid artery wave intensity was achieved merging the echo-tracking of the vessel with its doppler signal. Simultaneous not-invasive oscillometric blood pressure was obtained. The VAC was assessed by the ratio between the arterial elastance (Ea) and the end-systolic ventricular elastance (Ees). Ea was calculated from stroke volume (SV) and end-systolic pressure (Ea=(Systolic BP x 0.9)/SV) and Ees was calculated by the modified single-beat Chen method, using an estimated normalized ventricular elastance at arterial end-diastole (ENd) Ees = [Diastolic BP-(ENd(est) x Systolic BP x 0.9)]/(ENd(est) x SV). Three subgroups were created according to the left ventricle ejection fraction values (LVEF ≤ 35%, LVEF >35% <50%, LVEF ≥ 50%, with 26, 14, 10 patients respectively). Results The correlation between Ea/Ees and W1 was significant (Pearson’s correlation r= -0.35, p 0.01). The W1 and VAC values of the three LVEF-sorted subgroups were processed with ANOVA test (p 0.054 and p 0.0002 respectively). W1 values resulted to be, as expected, reduced especially in the group of severe ventricular dysfunction (mean 4,97+- 3,29), as well as the ventricular-arterial coupling was increased (mean 2.04 +- 1.04). Interestingly W1 shows to be correlated with the Left atrial volume index (Pearson’s correlation r= -0,30 p = 0,037). Conclusions Carotid WI technique seems to be a reliable method to estimate the ventricular-arterial interplay. Larger studies are needed to evaluate the respective role of W1 and Ea/Ees in the prognostic evaluation. Results EF ≤ 35 (n = 10) 35 < EF < 50 (n = 14) EF≥ 50 (n = 26) p value W1 4.97 ± 3.29 8.05 ± 3.79 7.85 ± 3.12 0.054 Ea/Ees 2.04 ± 1.04 1.39 ± 0.31 1.16 ± 0.3 0.0002 Abstract 415 Figure.

Reduced Coronary Flow Reserve Is Associated with Impaired Ventricular-vascular Interaction in Patients with Obstructive Sleep Apnea.

Background and ObjectivesObstructive sleep apnea (OSA) is associated with cardiac and arterial damage and adverse cardiovascular outcomes. We aimed to determine whether coronary flow reserve (CFR), which represents microvascular dysfunction, might be associated with the ventricular-vascular coupling index (VVI), which represents the afterload-adjusted contractility in patients with OSA.MethodsWe enrolled 281 patients (257 males; mean age, 43±11 years) with newly diagnosed OSA. Transthoracic echocardiography was performed, and adenosine-associated CFR was measured in the left anterior descending coronary artery. We evaluated the differences between the patients with normal CFR ≥2.5 and reduced CFR <2.5. VVI was calculated using the effective arterial elastance (Ea) and left ventricular (LV) end-systolic elastance (Ees) as follows: 10×Ea/Ees.ResultsThe normal CFR group (n=214) showed increased Ees (7.28±2.31 vs. 8.14±2.33 mmHg/mL, p=0.016) and preserved VVI (3.17±1.53 vs. 2.78±1.20, p=0.044) compared with the reduced CFR group (n=67). There were no differences in LV dimension, LV ejection fraction, left atrial-volume index, E/e′, left atrial strain and LV global longitudinal strain between the 2 groups (all p>0.05). CFR was significantly correlated to Ees (r=0.139; p=0.023) and VVI (r=−0.137; p=0.025).ConclusionsReduced CFR is associated with decreased Ees and impaired VVI in OSA patients. It suggests the necessity of more intensive observation in OSA patients with reduced CFR to improve cardiovascular outcomes.

P744Ventriculo-arterial interplay in acute pulmonary edema: relationship with the ejection fraction and the clinical outcome

Abstract Ventriculo-arterial coupling (VAC) represents a comprehensive expression of the mechanical efficiency and performance of the ventriculo-vascular system. It is defined as the ratio between the arterial elastance (Ea) and the end-systolic ventricular elastance (EES) and it has potential clinical applicability in different settings. The interaction between the ventricle and the aorta in the setting of acute heart failure has been insufficiently investigated. We sought to assess the VAC in patients with acute pulmonary edema (PE) and to establish its relationship with the ejection fraction (EF) and clinical outcome. We included 120 consecutive patients (mean age 74±12 years, 61 men) admitted for acute PE, with either preserved or reduced EF. The control group consisted of 50 subjects (mean age 40±13 years, 35 men) with no previous cardiac history. All patients underwent standard echocardiography on admission and we assessed the VAC non-invasively. We followed the patients for a composite endpoint of death, recurrent PE and acute coronary syndrome (ACS) for a month after hospitalisation. The VAC was significantly impaired in the acute PE group: 1.05±0.49 vs. 0.84±0.16 (p&lt;0.001). In the study group, 59 patients (49%) had preserved EF (mean EF 55±8%) and 61 patients (51%) had reduced EF (mean EF 28±7%, p&lt;0.001). Subgroup analysis in the study group showed that the VAC was more impaired in patients with low EF (1.29±0.56) vs. preserved EF (0.79±0.20, p&lt;0.001). VAC had a moderate negative correlation with the EF in the study group, both for low EF patients (r=−0.31, p=0.01) and preserved EF patients (r=−0.30, p=0.02). 14 patients (12%) in the study group had at least one in-hospital major cardiovascular event (MACE): in the low EF subgroup, there were 7 recurrent PE (11.5%) and 1 death (1.6%), while in the preserved EF subgroup, there were 5 recurrent PE (8.5%) and 1 ACS (1.7%). There was no significant difference in VAC between patients with in-hospital MACE and MACE-free patients (p=0.55 for low EF subgroup, p=0.59 for preserved EF subgroup). 10 patients (8.3%) in the study group had at least one MACE in the first month after discharge: in the low EF subgroup, there were 4 recurrent PE (6.6%) and 1 death (1.6%), while in the preserved EF subgroup, there were 2 deaths (3.4%) and 3 recurrent PE (5.1%). VAC was more impaired in low EF patients with MACE at 1 month (2.27±0.85) vs. low EF patients MACE-free at 1 month (1.21±0.44, p=0.04). No differences in VAC were noticed for the preserved EF subgroup (p=0.97). Ventriculo-vascular interaction is decoupled in acute PE, with VAC being more impaired when the EF is reduced. Furthermore, for patients with acute PE and low EF, VAC was worse in those who suffered a MACE at 30 days. This suggests the prognostic value of VAC in acute PE and it highlights the importance of integrating this easy-to-obtain parameter in the echocardiographic evaluation of acute heart failure patients. Acknowledgement/Funding This work was supported by CREDO Project - ID: 49182, financed through the SOP IEC-A2-0.2.2.1-2013-1 cofinanced by the ERDF

P6470Ventriculo-arterial coupling in severe aortic stenosis: does the flow-gradient pattern play a role?

Abstract Background Ventriculo-arterial coupling (VAC) assesses the interplay between ventricular contractility and afterload and it is calculated as the ratio between arterial elastance (Ea) and end-systolic left ventricular elastance (EES). Severe aortic stenosis (AS) carries different configurations according to transvalvular flow rates and pressure gradients and each of these entities has its particularities in terms of physiology and clinical outcome. Little has been studied so far regarding the changes of VAC in severe AS. Purpose We sought to assess the VAC non-invasively in patients (pts) with severe AS and to characterize it according to the flow-gradient pattern. Methods We included 61 consecutive pts with severe AS (78±13 years, 30 men, indexed aortic valve area &lt;0.6 cm2/m2), for whom we performed a comprehensive echocardiography. VAC was determined as the ratio between Ea and EES. Patients were divided in 4 groups, depending on stroke volume index (low-flow [LF] vs. normal-flow [NF]: 35 ml/m2) and mean transaortic pressure gradient (low-gradient [LG] vs. normal gradient [NG]: 40 mm Hg). This resulted in the following flow-gradient patterns: LFLG, LFNG, NFLG, NFNG. Data were compared between groups with one-way analysis of variance and then with a Tukey test. Results There were 11 pts (18%) in the LFLG group, 20 pts (32.8%) in the LFNG group, 8 pts (13.2%) in the NFLG group and 22 pts (36%) in the NGNG group. The arterial elastance was highest in the LFLG group: 3.37±1.49 vs. 2.79±0.92 in the LFNG, 2.05±0.57 in the NFLG and 1.54±0.49 in the NFNG group (p&lt;0.001). The ventricular elastance was also highest in the LFLG group (4.03±2.46) vs. 3.16±1.33 in the LFNG, 2.21±1.22 in the NFLG and 2.29±0.78 in the NFNG group (p=0.007). VAC was most impaired in the NFLG group (1.35±1.08), followed by LFNG group (1.00±0.47), LFLG group (0.93±0.27) and NFNG group (0.70±0.14) (p=0.01). Valvulo-arterial impedance (ZVA) was highest in the LFNG group: 7.78±2.15, followed by 7.38±2.17 in the LFLG group, 4.93±1.17 in the NFLG group and 4.33±1.23 in the NFNG group (p&lt;0.001). VAC and ZVA showed no significant correlation (p=0.27), with VAC being significantly more impaired in patients with abnormal ZVA (&gt;4.5 mm Hg/ml/m2): 0.99±0.60 vs. 0.73±0.20 (p=0.02). Conclusion The ventriculo-vascular interaction in severe AS varies noticeably according to the flow-gradient pattern. Low-gradient states, particularly NFLG, have the most impaired VAC. This study supports the idea that these 4 configurations are different clinical entities and it highlights the importance of integrating the flow-gradient pattern for a comprehensive evaluation of AS severity. Acknowledgement/Funding This work was supported by CREDO Project - ID: 49182, financed through the SOP IEC -A2-0.2.2.1-2013-1 cofinanced by the ERDF

P1499Data-driven clustering unveils the adaptive remodeling of athlete heart: an echocardiographic study from 2017 Taipei summer universiade

Abstract Background Sport-specific adaptations of the athlete's heart are still under investigation. This study sought to provide a proof-of-concept for hierarchical clustering of echocardiography-derived parameters in unfolding the adaptations and to make a comparison between hypothesis-driven and data-driven approaches for characterizing the athlete's heart. Methods Anthropometric, echocardiographic and electrocardiographic assessments were collected during the peri-participation cardiovascular examination of 2017 Summer Universiade. Besides standard echocardiography and strain measurements, ventricular-arterial coupling was assessed by the ratio of effective arterial elastance (Ea) to left ventricular end-systolic elastance (Ees), using a modified single-beat algorithm to calculate Ees. Results A total of 598 elite athletes (348 male, mean age 23±2.5 years) engaged 24 disciplines were grouped by Mitchell's classification. The hypothesis-driven approach showed significant differences in heart rate, ventricular size, and stroke volume when classified by dynamic levels. Adaptations of ventricular function were not found. Contrarily, the data-driven approach not only hierarchically clustered athletes with more manifest morphologic remodeling, more proportions playing high dynamic sports but also showed a functional propensity of lower Ea and Ees, supranormal diastolic function and preserved ventricular-arterial coupling with ample pumping reserve. Phenotype heatmaps of athletes Conclusions The hierarchical clustering can analyze numerous echocardiography-derived phenotypes pertaining to an individual athlete as well as discern an adaptive propensity of the athlete's heart to be the resting status of a reservoir-rich pump. This pilot demonstration of the data-driven approach in figuring out integrated physiologic adaptations with remodeling-relevant geometry and function leads to a fundamentally improved understanding of the athlete's heart and then will be applicable to various domains.

Assessment of the Left Ventricular-Arterial Coupling: A More Reasonable Method.

To the Editor: We read with great interest the article by Li et al. recently published in Shock(1) which investigated the performance of left ventricular–arterial coupling (VAC) in septic shock patients who are unresponsive to fluid administration. As described in the article (1), the formula for calculating the effective arterial elastance (Ea), left ventricular (LV) end-systolic elastance (Ees), and VAC (defined as Ea/Ees) is shown as follows: Ea = ESP/SV, Ees = ESP/(ESV-V0), and VAC = (ESV-V0)/SV, where V0 was defined as the volume axis intercept of the end-systolic pressure–volume relationship (see the Figure 1 in the article (1), ESP represents end-systolic pressure of ventricular, ESV represents end-systolic volume of ventricular, and SV represents stroke volume). We respectfully disagreed with the method applied in this study for evaluating the VAC because the abovementioned approximated calculations are unreliable and may overestimate the actual value measured by the invasive method. First, to simplify the formula for calculation, the authors made a simple assumption that the V0 is negligible. Indeed, the parameter V0 is, theoretically, near to 0 when the heart load is in the physiologic range (2, 3). However, in some case, particularly in cardiac dysfunction, the V0 is not equal to 0 and should not be neglected. A study by Ky et al. (4) revealed a median V0 of 43 mL (interquartile range: −2.6 mL to 113 mL) for patients with chronic systolic heart failure, and the V0 was positively associated with the New York Heart Association (NYHA) functional class (ρ = 0.31; P < 0.001), indicating that the worse the cardiac function, the greater the V0. In the study by Li et al. (1), we can guess that the patients included in this study had a cardiac dysfunction according to the data regarding the global end-diastolic ventricular volume index (GEDVI) and stroke volume index (SVI), despite a normal cardiac index. Hence, roughly neglecting the V0 in this study would, inevitably, result in an overestimation of the true VAC. Second, the ratio ESP/ESV was used to calculate Ees by Li et al (1); however, this formula was proven as a suboptimal method for estimating Ees in the study by Chen et al. (5). Chen et al. found that the approximately calculated Ees (ESP/ESV) was not well correlated with the invasively measured Ees (y = 0.18x + 0.69; r = 0.56, P < 0.001), and the residuals of the calculated Ees to the invasively measured Ees were significantly different from 0, averaging 2.2 mmHg/mL (5). Meanwhile, a novel method, named the “single-beat” method, was proposed by Chen et al. (5) to estimate Ees; this method was validated as more well correlated with the invasively measured Ees (y = 0.78x + 0.55; r = 0.81, P < 0.0001) compared with the ratio ESP/ESV. Importantly, the “single-beat” method just requires several parameters that can be noninvasively measured by echocardiography; it thus seems to be more reasonable and suitable for evaluating Ees and VAC in critically ill patients. Lastly, the authors (1) used the arterial systolic pressure (ASP) of the femoral artery to represent the LV ESP; this method for assessing LV ESP is also not reasonable. The invasive method using LV catheterization is the “gold-standard” for the assessment of LV ESP; however, it is an unrealistic practice in the intensive care unit at present. Alternatively, the researchers have commonly used the mean aortic pressure (MAP) (3, 6) and 90% of the ASP (7, 8) as surrogate for LV ESP, and the ratio of MAP/SV was confirmed as a robust surrogate for Ea and is interchangeably in any peripheral artery (9). Therefore, this unreasonable approximation for LV ESP used in this study (1) may also lead to an overestimation of Ea and VAC. Overall, the inappropriate method for assessing the Ea, Ees, and VAC will downgrade the credibility of their evidence to some extent.

Acute Change in Ventricular Contractility-Load Coupling After Corrective Surgery for Congenital Heart Defect: A Retrospective Cohort Study

Ventricular performance and its loading condition change drastically after surgical correction of congenital heart defect. Pressure–volume loops analysis can provide quantitative information about ventriculo-arterial coupling (VAC) indicating the interaction between ventricular contractility and loading condition. Therefore, we investigated changes in VAC after corrective surgery for ventricular septal defect (VSD)/tetralogy of Fallot (TOF), and implication of ventriculo-arterial decoupling as a prognostic factor of post-operative outcomes. In children with VSD/TOF, pre- and post-operative arterial elastance (Ea), end-systolic ventricular elastance (Ees) and VAC (Ea/Ees) were non-invasively estimated using echocardiographic parameters. Post-operative outcomes included maximum vasoactive-inotropic score, the duration of mechanical ventilation and hospital stay. Preoperatively, patients with VSD had significantly lower Ea and Ees than patients with TOF; however, VAC were preserved in both. In patients with VSD, post-operative Ea increased disproportionately to change in Ees, resulting in increased VAC. Post-operative higher VAC in patients with VSD was independently associated with maximum vasoactive-inotropic score (odds ratio [OR] 63.9; 95% Confidence Interval [CI] 4.0–553.0; P = 0.003), prolonged mechanical ventilation (OR 6.3; 95% CI 1.1–37.8; P = 0.044) and longer hospitalization (OR 17.6; 95% CI 1.6–187.0; P = 0.018). In patients with TOF, Ea and Ees reduced post-operatively; however, VAC remained unchanged and was not associated with post-operative outcomes. Despite of different loading condition, preoperative VAC maintained in both of VSD and TOF. However, particularly in VSD patients, abrupt increase in post-operative loading state induces contractility-load decoupling, which leads to worse post-operative outcomes.

Ventricular-Arterial Coupling in Children and Infants With Congenital Heart Disease After Cardiopulmonary Bypass Surgery: Observational Study.

Ventricular-arterial coupling represents the interaction between the left ventricle and the arterial system. Ventricular-arterial coupling is measured as the ratio between arterial elastance and ventricular end-systolic elastance. Scant information is available in critically ill children about these variables. The aim of this study was to prospectively assess ventricular-arterial coupling after pediatric cardiac surgery and evaluate its association with other commonly recorded hemodynamic parameters. Single-center retrospective observational study. Pediatric cardiac surgery operating room. Children undergoing corrective cardiac surgery. Hemodynamic monitoring with transesophageal echocardiography. Twenty-seven patients with biventricular congenital heart disease, who underwent elective cardiac surgery with cardiopulmonary bypass, were enrolled before operating room discharge. Chen single-beat modified method was applied to calculate ventricular-arterial coupling. The median arterial elastance and end-systolic elastance values were 5.9 mm Hg/mL (2.2-9.3 mm Hg/mL) and 4.3 mm Hg/mL (1.9-8.3 mm Hg/mL), respectively. The median ventricular- arterial coupling was 1.2 (1.1-1.6). End-systolic elastance differences between patients with a ventricular-arterial coupling below (low ventricular-arterial coupling) and above (high ventricular-arterial coupling) the median value were -5.2 (95% CI, -6.28 to -0.7; p = 0.008). Differently, arterial elastance differences were -2.1 (95% CI, -5.7 to 1.6; p = 0.19). Ventricular-arterial coupling showed a significant association with pre-ejection time (r, 0.44; p = 0.02), total ejection time (r, -0.41; p = 0.003), cardiac cycle efficiency (r, -0.46; p = 0.02), maximal delta pressure over delta time (r, -0.44; p = 0.02), ejection fraction (r, -0.57; p = 0.01), and systemic vascular resistances indexed (0.56; p = 0.003). After adjustment, total ejection time (p = 0.001), pre-ejection time (p = 0.02), and ejection fraction (p = 0.001) remained independently associated with ventricular-arterial coupling. Median ventricular-arterial coupling values in children after cardiac surgery appear high (above 1). Uncoupling was particularly evident in high ventricular-arterial coupling patients who showed the lowest end-systolic elastance values (but not significantly different arterial elastance values) compared with low ventricular-arterial coupling. Ventricular-arterial coupling appears to be inversely proportional to pre-ejection time, total ejection time, and ejection fraction.

Vascular-ventricular coupling during exercise is not affected by exaggerated blood pressures in endurance-trained athletes.

This study sought to examine whether cardiovascular performance during exercise, assessed using the vascular-ventricular coupling index (VVC), was affected by exaggerated blood pressure (EBP) responses in endurance-trained athletes. Subjects were middle-aged endurance-trained men and women. Blood pressure measurements and left ventricular echocardiography were performed in a semiupright position at rest and during steady-state cycling at workloads that elicited 100-110 beats/min (stage 1) and 130-140 beats/min (stage 2). These data were used to calculate effective arterial elastance index (EaI), left ventricular end-systolic elastance index (ELVI), and their ratio (VVC). Additional measurements of left ventricular volumes and function (i.e., stroke volume, cardiac output, and longitudinal strain) and indirect assessments of peripheral vascular function (i.e., total arterial compliance and peripheral vascular resistance) were examined. Fourteen subjects with EBP (EBP+, 50% men) and 14 sex-matched subjects without EBP (EBP-) participated, with results presented as EBP+ versus EBP-. EaI and ELVI increased from rest to exercise while VVC decreased, but only ELVI was different between groups at stage 1 [7.6 (1.8) vs. 6.4 (1.0) mmHg·ml-1·m-2, P = 0.045] and stage 2 [10.3 (1.6) vs. 8.0 (1.7) mmHg·ml-1·m-2, P < 0.001]. Additional comparisons revealed no group difference in the contribution of the Frank-Starling mechanism or left ventricular and peripheral vascular function during exercise. The cardiovascular adjustment to exercise in athletes with EBP is achieved through a matched increase in both EaI and ELVI, and the absence of between-group differences in left ventricular or peripheral vascular function suggests that other factors may contribute to the EBP response.NEW & NOTEWORTHY Cardiovascular performance during submaximal exercise, assessed using vascular-ventricular coupling, is unaffected by exaggerated blood pressure (EBP) responses in endurance-trained athletes. The underlying mechanisms of EBP in athletes remain unknown as changes in left ventricular and peripheral vascular function during exercise were similar in athletes with and without EBP.

Rolipram, a PDE4 Inhibitor, Enhances the Inotropic Effect of Rat Heart by Activating SERCA2a.

This study was designed to investigate the hemodynamic effect of rolipram, a phosphodiesterase type 4 (PDE4) inhibitor, in normal rat hearts both in vivo and in vitro and its underlying mechanism. The pressure-volume loop, isolated heart, and Ca2+ transients triggered by field stimulation or caffeine were used to analyze the hemodynamic mechanism of rolipram. The results demonstrated that rolipram (3 mg/kg, ip) significantly increased the in vivo rat heart contractility by enhancing stroke work, cardiac output, stroke volume, end-systolic volume, end-diastolic volume, end-systolic pressure, heart rate, ejection fraction, peak rate of rise of left pressure (+dp/dtmax), the slopes of end-systolic pressure-volume relationship (slope of ESPVR) named as left ventricular end-systolic elastance, and reduced the slopes of end-diastolic pressure-volume relationship (slope of EDPVR). Meanwhile, the systolic blood pressure, diastolic blood pressure, and pulse pressure were significantly enhanced by rolipram. Also, rolipram deviated normal ventricular-arterial coupling without changing the arterial elastance. Furthermore, rolipram (0.1, 1, 10 μM) also exerted positive inotropic effect in isolated rat hearts by increasing the left ventricular development pressure, and +dp/dtmax in non-paced and paced modes. Rolipram (10 μM) increased the SERCA2a activity, Ca2+ content, and Ca2+ leak rate without changing diastolic Ca2+ level. Rolipram had significant positive inotropic effect with less effect on peripheral vascular elastance and its underlying mechanism was mediated by increasing SERCA2a activity. PDE4 inhibition by rolipram resulted in a positive inotropic effect and might serve as a target for developing agents for the treatment of heart failure in clinical settings.

Right Ventricular - Pulmonary Vascular Coupling at Rest and Exercise in Patients with Dyspnea and/or Suspected Pulmonary Hypertension

Purpose Exercise during right heart catheterization (RHC) is employed in select centers to demonstrate the extent to which pulmonary artery (PA) hemodynamics and/or left heart filling pressures may be abnormal. We examined right ventricular (RV) end-systolic elastance (Ees), effective PA elastance (Ea), and their coupling (Ees:Ea) at rest and during exercise in patients with dyspnea and/or suspected pulmonary hypertension. Methods Patients referred for an exercise hemodynamic study performed submaximal cycle-ergometry during RHC. We transduced RV and PA pressures simultaneously, and measured thermodilution cardiac output. We determined Ees using the single-beat method and calculated Ea from the ratio of PA pressure to stroke volume. Exercise hemodynamic classifications defined a priori include: 1) left heart disease ( Ex-LHD ) based on an increased slope of the PA wedge pressure/cardiac output relationship; 2) pulmonary vascular disease ( Ex-PVD ) based on an elevated end-diastolic pressure gradient; 3) combined ( Ex-CPH) if both criteria are met; 4) hemodynamically Ex-Normal if neither criteria are met. Results Preliminary data were available for 54 patients (50% male; Age = 59 ± 14); exercise hemodynamic classifications comprised 23 Ex-Normal, 14 Ex-LHD, 12 Ex-PVD, and 5 Ex-CPH. At rest, Ees was similar in Ex-Normal, Ex-LHD, and Ex-PVD; Ea was higher in Ex-LHD and Ex-PVD compared to Ex-Normal (p Conclusion In patients with pulmonary vascular and/or left heart disease, ventricular-vascular coupling is less favorable than in patients with normal hemodynamics, and abnormalities persist during exercise.

Elastic properties of ascending aorta and ventricular–arterial coupling in women with previous pregnancy complicated by HELLP syndrome

To compare the elastic properties of the ascending aorta and ventricular-arterial coupling (VAC) in women with a previous pregnancy complicated by hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome, women who experienced preeclampsia, and healthy controls. Women with a history of preeclampsia (n = 60) or HELLP syndrome (n = 49) and matched healthy controls (n = 60) underwent transthoracic echocardiography at 6 months to 4 years after delivery. Aortic M-mode and tissue Doppler imaging (TDI) parameters were measured. Aortic diameters were assessed at end-diastole at four levels: Valsalva sinuses, sinotubular junction, tubular tract, and aortic arch. Aortic compliance, distensibility, stiffness index, Peterson's elastic modulus, pulse-wave velocity, and M-mode strain were calculated using standard formulae. Aortic expansion velocity, early and late diastolic retraction velocities, and peak systolic tissue strain (TDI-ε) were determined. VAC was defined as the ratio between aortic elastance (Ea) and left ventricular end-systolic elastance (Ees). All women were free from cardiovascular risk factors. Women with a history of HELLP syndrome showed larger aortas than those with previous preeclampsia or controls, probably related to a higher blood pressure. Aortic elastic properties, including Ea, were similar between HELLP and preeclampsia groups, even comparing cases with early-onset preeclampsia and HELLP. In contrast, Ees was more impaired in the HELLP group than in the other two. Consequently, about one-quarter of women who experienced HELLP syndrome had a pathological VAC, whereas only 5% of previously preeclamptic patients did. Multivariate analysis confirmed the association between HELLP syndrome and VAC, whereas other parameters including aortic compliance, distensibility, stiffness index, and elastic modulus are linked only to gestational age at preeclampsia onset, ad also Ea and Ees did. We found a significant overlap between the aortic elastic properties in women with a history of preeclampsia and those with a previous HELLP syndrome, suggesting a common pathophysiologic pathway. However, women who experienced HELLP syndrome showed a higher blood pressure than other cases and controls, probably determining larger aortas. In addition, VAC was more altered in the HELLP group than in the others because of a higher Ea and a lower Ees.

A13994 Blood pressure variability and hypertensive target organ damage

Objectives: to investigate an impact of blood pressure variability (BPV) on heart and brain hypertensive damage in the middle-aged untreated patients with grade 1–2 essential arterial hypertension (EAH) without concomitant cardiovascular diseases. Methods: we examined 60 naive hypertensive patients (HP) with EAH and 44 sex- and age-matched healthy individuals. Comprehensive transthoracic echocardiography (Vivid 7 Dimension, GE) with 2D speckle tracking analysis and ambulatory blood pressure monitoring were performed in all participants. BPV was estimated as standard deviation. 41 HP underwent brain magnetic resonance imaging (MAGNETOM Skyra 3.0T, Siemens AG). Fazekas scale was used to quantify the amount of white matter hyperintensities (WMH). Results: nighttime systolic BPV (sBPV) and nighttime diastolic BPV (dBPV) were significantly (p < 0,001 for all) higher in HP (12,1 ± 0,1 vs. 9,3 ± 0,4 mmHg in controls and 9,8 ± 0,4 vs. 6,9 ± 0,3 mmHg in controls, respectively). Correlation analyses in HP revealed significant association of nighttime sBPV with left ventricular (LV) end-systolic elastance (r = −0,375; p < 0,01) and LV end-diastolic stiffness (r = −0,429; p < 0,01). Daytime dBPV significantly correlated with LV diastolic elastance (r = 0,265; p < 0,05), nighttime dBPV - with left atrial expansion index (r = −0,282; p < 0,05). WMH (Fazekas 1 and 2) were found in 53,7% HP patients. In HP with WMH 24 hours sBPV (19,7 ± 3,9 mmHg) and daytime sBPV (18,0 ± 4,5 mmHg) were significantly (p < 0,05 for all) higher compared to same parameters in HP without WMH (17,2 ± 3,3 and 15,7 ± 3,1 mmHg, respectively). Conclusion: middle-aged untreated patients with grade 1–2 uncomplicated EAH are different from the sex- and age-matched healthy individuals by higher nighttime BPV. BPV associated with heart and brain hypertensive organ damage.

Ventricular-Vascular Coupling at Rest and after Exercise Is Associated with Heart Failure Hospitalizations in Patients With Coronary Artery Disease

The ventricular-vascular coupling ratio, defined as the ratio of arterial elastance (Ea) to left ventricular end-systolic elastance (Ees), has not been examined in populations with coronary artery disease (CAD), and its association with heart failure (HF) in this population is unknown. Ventricular-vascular coupling was measured at rest and after exercise using echocardiography and cuff blood pressure in 815 patients with stable CAD enrolled in the Heart and Soul Study. Adjusted Cox proportional-hazard models were used to evaluate the association between ventricular-vascular coupling and future HF hospitalizations. After a median of 8.9years, 144 patients (18%) were hospitalized for HF. After multivariate adjustment, patients in the highest tertile of Ees (rest: hazard ratio [HR], 0.31 [95% CI, 0.17-0.57; P<.001]; exercise: HR, 0.26 [95% CI, 0.13-0.50; P<.001]) were at decreased risk for HF hospitalization, while patients in the highest tertile of the Ea/Ees ratio (rest: HR, 3.36 [95% CI, 1.91-5.93; P<.001]; exercise: HR, 4.09; [95% CI, 2.22-7.51; P<.001]) were at increased risk, compared with the lowest tertiles. Ea and the relative change observed in Ees and the Ea/Ees ratio with exercise were not associated with HF hospitalizations. The Ea/Ees ratio and Ees, at rest and after exercise, are strongly associated with future HF hospitalizations in patients with stable CAD and low rates of baseline HF. Ventricular-vascular coupling obtained from echocardiography shows promise as a risk assessment tool for HF in patients with CAD.

Left ventricular torsion rate and the relation to right ventricular function in pediatric pulmonary arterial hypertension.

The right ventricle and left ventricle are physically coupled through the interventricular septum. Therefore, changes in the geometry and mechanics of one ventricle can directly affect the function of the other. In treatment of pediatric pulmonary arterial hypertension, the left ventricle is often overlooked, with clinical focus primarily on improving right ventricular function. Pediatric pulmonary arterial hypertension represents a disease distinct from adult pulmonary arterial hypertension based on etiology and survival rates. We aimed to assess left ventricular torsion rate in pediatric pulmonary arterial hypertension and its role in right ventricular dysfunction. Cardiac magnetic resonance images with tissue tagging were prospectively acquired for 18 pediatric pulmonary arterial hypertension (WHO class I) patients and 17 control subjects with no known cardiopulmonary disease. The pulmonary arterial hypertension cohort underwent cardiac magnetic resonance within 48 hours of clinically indicated right heart catheterization. Using right heart catheterization data, we computed single beat estimation of right ventricular end-systolic elastance (as a measure of right ventricular contractility) and ventricular vascular coupling ratio (end-systolic elastance/arterial afterload). Left ventricular torsion rate was quantified from harmonic phase analysis of tagged cardiac magnetic resonance images. Ventricular and pulmonary pressures and pulmonary vascular resistance were derived from right heart catheterization data. Right ventricular ejection fraction and interventricular septum curvature were derived from cardiac magnetic resonance. Left ventricular torsion rate was significantly reduced in pulmonary arterial hypertension patients compared to control subjects (1.40 ± 0.61° vs. 3.02 ± 1.47°, P < 0.001). A decrease in left ventricular torsion rate was significantly correlated with a decrease in right ventricular contractility (end-systolic elastance) (r = 0.61, P = 0.007), and an increase in right ventricular systolic pressure in pulmonary arterial hypertension kids (r = –0.54, P = 0.021). In both pulmonary arterial hypertension and control subjects, left ventricular torsion rate correlated with right ventricular ejection fraction (controls r = 0.45, P = 0.034) (pulmonary arterial hypertension r = 0.57, P = 0.032). In the pulmonary arterial hypertension group, interventricular septum curvature demonstrated a strong direct relationship with right ventricular systolic pressure (r = 0.7, P = 0.001) and inversely with left ventricular torsion rate (r = –0.57, P = 0.013). Left ventricular torsion rate showed a direct relationship with ventricular vascular coupling ratio (r = 0.54, P = 0.021), and an inverse relationship with mean pulmonary arterial pressure (r = –0.60, P = 0.008), and pulmonary vascular resistance (r = –0.47, P = 0.049). We conclude that in pediatric pulmonary arterial hypertension, reduced right ventricular contractility is associated with decreased left ventricular torsion rate.

Estimating Left Ventricular Elastance from Aortic Flow Waveform, Ventricular Ejection Fraction, and Brachial Pressure: An In Silico Study.

Although left ventricular end-systolic elastance (Ees) serves as a major index of cardiac contractility, a widely-accepted noninvasive estimation of Ees does not exist. To overcome this limitation, we developed a two-step inverse method that allows for its noninvasive estimation from measurements of aortic flow and brachial pressure using a previously validated one-dimensional model of the cardiovascular system. In a first step, aortic flow is set as the model input and the output brachial pressure is compared with the "real" values. Subsequently, the basic properties of the arterial tree are tuned according to an optimization algorithm. In a second step, the same optimization method is used to estimate the elastance parameters that produce an aortic flow waveform that matches the "real" one. Additional knowledge of the ejection fraction can allow for the accurate estimation of the entire P-V loop, including end-diastolic elastance. The method was tested on a database of 50 different in silico hemodynamic cases generated after varying cardiac and arterial model parameters. Implementation of the method yielded good agreement (r = 0.99) and accuracy (n-RMSE = 4%) between "real" and estimated values of Ees. Furthermore, a sensitivity analysis revealed that errors due to poor arterial adjustment and measurements are small (≤ 8% for Ees).

Adiposity, body composition and ventricular-arterial stiffness in the elderly: the Atherosclerosis Risk in Communities Study.

Weight gain appears to accelerate age-related ventricular-arterial stiffening, which has been implicated in the development of heart failure (HF), but it is unclear whether body fat accumulation underpins this association. We evaluated the relationship of adiposity, using measures of body composition, with ventricular-arterial stiffness among the elderly in the community. Adiposity was accessed through body mass index (BMI), waist circumference, and body fat percentage. We studied the association of these measures with carotid-femoral pulse wave velocity (cfPWV), arterial elastance index (EaI), left ventricular (LV) end-systolic elastance index (EesI) and LV end-diastolic elastance index (EedI) in 5520 community-based, elderly Atherosclerosis Risk in Communities (ARIC) Study participants, who underwent echocardiography between 2011 and 2013. BMI and waist circumference were directly associated with EaI, EedI and EesI even after adjusting for age, sex, race, hypertension, diabetes mellitus, heart rate, prevalent coronary heart disease and HF. After further adjustment for BMI, body fat percentage demonstrated significant independent linear relationships with EaI [standardized beta coefficient (β)=0.17, P<0.001], EesI (β=0.08, P=0.003) and EedI (β=0.20, P<0.001), and significant non-linear relationships with cfPWV (P=0.033). In this biracial community-based cohort, increased adiposity was associated with increased ventricular-arterial stiffness among the elderly and suggests a potential mechanism by which obesity might contribute to the development of HF.

What the Current Arterial‐Ventricular Coupling Index Fails to Tell Us

BACKGROUNDThe arterial‐ventricular (AV) coupling index (k) is often employed to evaluate ventricular performance in relation to arterial properties. The index k is defined as the ratio of end‐systolic (ES) ventricular elastance (Emax) and effective arterial elastance (Ea). Emax describes the nonlinear trajectory of ventricular pressure (P) and volume (V) at end‐systole. Within a sufficiently small range Emax may be approximated by ESP/(ESV − Vo), where Vo is the extrapolated volume axis intercept. Likewise Ea is defined as ESP/SV, where SV is stroke volume. It may be convenient to index (i) volumes for body surface area (BSA). However, in the formula for k, both ESP and BSA cancel out, resulting in a dimensionless index. Unfortunately, the term Vo is neglected in most studies.AIMSThis investigation addresses the question if AV coupling can be described completely by k, or if an additional cofactor (kc) may be necessary, regardless of inclusion of Vo or not.METHODSSince k concerns a ratio, information is lost compared to the constitutive details available, namely SV and (ESV‐Vo). Plotting SV vs (ESV‐Vo) shows k as the tangent, while the missing companion of k (here termed kc) can be identified as the distance from the origin. The Pythagorean theorem states that kc equals the root of the sum of SV and (ESV‐Vo) each squared. We calculated the possible association between k and kc for published data (Asanoi et al., Circ Res 1989;65: 483–493) on 12 healthy individuals and 16 patients with cardiac dysfunction including heart failure. In their study Emax and Vo were obtained via linear regression analysis on more than 5 data points obtained by combined 2D echocardiography and variation of ESP as induced by phenylephrine and sodium nitroprusside i.v., respectively. While omitting Vo (indicated by the prime for k and kc), we also calculated k′ and kc′.RESULTSAlthough there is an association k′ = 0.486 k + 0.4861, R2 = 0.3928 (P&lt;0.001), N=28, the connection strongly diverges for k&gt;1, where a value between 1 and 2 is supposed to correspond with optimal matching. The kc relates to k via kc = −17.22 ln (k) + 71.57, R2 = 0.384, N=28, and likewise kc′ to k′ as kc′ = −31.81 ln (k′) + 77.96, R2 = 0.624, N=28.CONCLUSIONSThe dimensionless metric k is only characterized by SV, ESV and Vo, not by end‐systolic pressure level. The companion kc depends on the same variables, and has the dimension of volume (index). AV‐coupling is more completely characterized by the combination of k and kc. Consideration of the value of k in isolation provides an incomplete description of AV‐coupling characteristics, regardless of the fact whether Vo is included.Support or Funding InformationnoneThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Ventricular‐arterial Coupling in Prostate Cancer Patients Treated with Androgen Deprivation Therapy at Rest and During Exercise

IntroductionAndrogen‐deprivation therapy (ADT) in prostate cancer has been suggested to promote an unfavorable cardiovascular disease risk profile and long‐term cardiovascular mortality. Impairments in vascular structure (increased arterial stiffness) and function (decreased endothelial‐dependent dilation) are known to occur with ADT, however, it remains unknown if the changes in structure‐function relationship adversely impacts the interaction between ventricular and arterial systems. Ventricular‐arterial coupling is a measure of effective arterial elastance (Ea) and left ventricular end‐systolic elastance (Ees) and is a central determinant of cardiovascular performance and cardiac energetics. Therefore, this study sought to evaluate ventricular‐arterial coupling at rest and during submaximal exercise in prostate cancer patients with and without a history of ADT.MethodsTo date, 7 prostate cancer patients with (n=3) and without (n=4) a history of androgen‐deprivation therapy treatment have completed the study. Ea, Ees, and ventricular‐arterial coupling (Ea/Ees) were measured at rest and during supine submaximal exercise. A high Ea/Ees is reflective of a compromised interaction between ventricular and arterial systems. To minimize the effect of heart rate on each parameter submaximal exercise was performed at a work rate corresponding to a heart rate of 100 beats/min.ResultsAt rest Ea (ADT: 2.9±0.2 mmHg/mL; non‐ADT: 3.4±0.8 mmHg/mL; P=0.2), Ees (ADT: 3.2±1.9 mmHg/mL; non‐ADT: 3.6±0.6 mmHg/mL; P=0.2), and Ea/Ees (ADT: 0.79±0.39; non‐ADT: 0.97±0.30; P=0.5) were similar between ADT and non‐ADT groups. Ea was not different between groups during exercise (ADT: 7.0±1.1 mmHg/mL; non‐ADT: 6.6±0.6 mmHg/mL; P=0.3). Moderate‐intensity exercise‐induced increases in Ees trended to be decreased in the ADT group (ADT: 3.5±1.2 mmHg/mL; non‐ADT: 4.7±0.5 mmHg/mL; P=0.05). Ea/Ees was also higher in the ADT group during exercise compared to the non‐ADT group, but did not reach statistical significance (ADT: 0.93±0.16; non‐ADT: 0.77±0.16; P=0.1).ConclusionsThe findings from this study provide preliminary data that indicates ADT in prostate cancer patients may adversely alter left ventricular end‐systolic elastance during exercise, but does not significantly alter ventricular‐arterial coupling. Additional data will contribute to the evaluation of the interaction between ventricular and arterial systems in patients receiving ADT.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Inefficient Ventriculoarterial Coupling in Fontan Patients: A Cardiac Magnetic Resonance Study.

The ventriculoarterial coupling (VAC) ratio, the ratio of arterial elastance (Ea) to ventricular end-systolic elastance (Ees), reflects cardiovascular efficiency. Little is known about this ratio in patients who have undergone the Fontan procedure. Our aim was to assess the VAC ratio in a cohort of Fontan patients using a cardiac magnetic resonance (CMR) method, and to examine its relation to outcomes. We retrospectively assessed VAC from CMR data on 195 Fontan patients (age 19.6 ± 10.7years) and 42 controls (age 15.2 ± 2.2years). The VAC ratio was calculated as Ea/Ees (Ea = mean arterial blood pressure (MBP)/ventricular stroke volume; Ees = MBP/end-systolic volume). Compared with controls, Fontan patients had lower body surface area-adjusted median Ees (1.54 vs. 2.4, p < 0.001) and Ea (1.35 vs. 1.48, p = 0.01), and a higher median VAC ratio (0.88 vs. 0.62, p < 0.001). After a median follow-up of 4years (range 1-10), 20 patients reached a composite endpoint of death or heart transplant listing. On multivariable modeling, being in the lowest tertile of the VAC ratio was independently associated with the composite endpoint (odds ratio 11.39, p = 0.02), and inclusion of the VAC ratio in the model improved prediction compared to traditional risk factors. In patients without ventricular dilation, the VAC ratio was the only factor predictive of the composite endpoint (p = 0.02). In conclusion, we found evidence for inefficient ventriculoarterial coupling in Fontan patients. The VAC ratio improved prediction of outcomes and was especially useful in patients without ventricular dilation. Further investigation into the clinical significance of ventriculoarterial coupling in this patient population is warranted.