Ratio Of Effective Arterial Elastance Research Articles

Development and Clinical Application of Left Ventricular-Arterial Coupling Non-Invasive Assessment Methods.

The constant and dynamic interaction between ventricular function and arterial afterload, known as ventricular-arterial coupling, is key to understanding cardiovascular pathophysiology. Ventricular-arterial coupling has traditionally been assessed invasively as the ratio of effective arterial elastance over end-systolic elastance (Ea/Ees), calculated from information derived from pressure-volume loops. Over the past few decades, numerous invasive and non-invasive simplified methods to estimate the elastance ratio have been developed and applied in clinical investigation and practice. The echocardiographic assessment of left ventricular Ea/Ees, as proposed by Chen and colleagues, is the most widely used method, but novel echocardiographic approaches for ventricular-arterial evaluation such as left ventricle outflow acceleration, pulse-wave velocity, and the global longitudinal strain or global work index have arisen since the former was first published. Moreover, multimodal imaging or artificial intelligence also seems to be useful in this matter. This review depicts the progressive development of these methods along with their academic and clinical application. The left ventricular-arterial coupling assessment may help both identify patients at risk and tailor specific pharmacological or interventional treatments.

Non-invasive global myocardial work index as a new surrogate of ventricular-arterial coupling in hypertensive patients with preserved left ventricular ejection fraction

ObjectiveAs a new method of left ventricular-arterial coupling (VAC), the non-invasive myocardial work index (MWI) may provide more useful information than the classical methods of arterial elastance/left ventricular (LV) elastance index (the ratio of effective arterial elastance (Ea) over end-systolic elastance [Ea/Ees]). This research aims to investigate if MWI might be better associated with hypertension-mediated organ damage (HMOD) and diastolic dysfunction than Ea/Ees in hypertension.MethodsWe prospectively enrolled 104 hypertensives and 69 normotensives. All subjects had speckle-tracking echocardiography for myocardial work, conventional echocardiography, and brachial-ankle pulse wave velocity (baPWV) measurements. The global work index (GWI) is a myocardial work component. The correlation between GWI and HMOD, as well as diastolic dysfunction, was analyzed. The receiver operating characteristic (ROC) curve was utilized for evaluating the GWI predicting efficacy.ResultsThe global work index was significantly higher in hypertensives than in normotensives (2,021.69 ± 348.02 vs. 1,757.45 ± 225.86 mmHg%, respectively, p < 0.001). Higher GWI was a risk factor on its own for increased baPWV, pulse pressure (PP), echocardiographic LV hypertrophy (LVH), and left atrial volume index (LAVI) (p = 0.030, p < 0.001, p = 0.018 p = 0.031, respectively), taking into account the sex, age, mean arterial pressure (MAP), body mass index (BMI), and antihypertensive therapy. However, no considerable associations were found between Ea/Ees and HMOD parameters and the diastolic dysfunction markers. The GWI area under the ROC curve for increased PP and baPWV, echocardiographic LVH, and increased LAVI were 0.799, 0.770, 0.674, and 0.679, respectively (p < 0.05).ConclusionsThe global work index but not traditionally echocardiographic-derived Ea/Ees of VAC is independently related to HMOD and diastolic impairment in hypertensives with preserved LV ejection fraction. The GWI may be a potential marker for evaluating the VAC in hypertension.

Arterial Baroreflex Inhibits Muscle Metaboreflex Induced Increases in Effective Arterial Elastance: Implications for Ventricular-Vascular Coupling.

The ventricular-vascular relationship assesses the efficacy of energy transferred from the left ventricle to the systemic circulation and is quantified as the ratio of effective arterial elastance to maximal left ventricular elastance. This relationship is maintained during exercise via reflex increases in cardiovascular performance raising both arterial and ventricular elastance in parallel. These changes are, in part, due to reflexes engendered by activation of metabosensitive skeletal muscle afferents—termed the muscle metaboreflex. However, in heart failure, ventricular-vascular uncoupling is apparent and muscle metaboreflex activation worsens this relationship through enhanced systemic vasoconstriction markedly increasing effective arterial elastance which is unaccompanied by substantial increases in ventricular function. This enhanced arterial vasoconstriction is, in part, due to significant reductions in cardiac performance induced by heart failure causing over—stimulation of the metaboreflex due to under perfusion of active skeletal muscle, but also as a result of reduced baroreflex buffering of the muscle metaboreflex-induced peripheral sympatho-activation. To what extent the arterial baroreflex modifies the metaboreflex-induced changes in effective arterial elastance is unknown. We investigated in chronically instrumented conscious canines if removal of baroreflex input via sino-aortic baroreceptor denervation (SAD) would significantly enhance effective arterial elastance in normal animals and whether this would be amplified after induction of heart failure. We observed that effective arterial elastance (Ea), was significantly increased during muscle metaboreflex activation after SAD (0.4 ± 0.1 mmHg/mL to 1.4 ± 0.3 mmHg/mL). In heart failure, metaboreflex activation caused exaggerated increases in Ea and in this setting, SAD significantly increased the rise in Ea elicited by muscle metaboreflex activation (1.3 ± 0.3 mmHg/mL to 2.3 ± 0.3 mmHg/mL). Thus, we conclude that the arterial baroreflex does buffer muscle metaboreflex induced increases in Ea and this buffering likely has effects on the ventricular-vascular coupling.

Optimizing left ventricular-arterial coupling during the initial resuscitation in septic shock \u2013 a pilot prospective randomized study

BackgroundLeft ventricular-arterial coupling (VAC), defined as the ratio of effective arterial elastance (Ea) to left ventricular end-systolic elastance (Ees), has been extensively described as a key determinant of cardiovascular work efficacy. Previous studies indicated that left ventricular-arterial uncoupling was associated with worse tissue perfusion and increased mortality in shock patients. Therefore, this study aims to investigate whether a resuscitation algorithm based on optimizing left VAC during the initial resuscitation can improve prognosis in patients with septic shock.MethodsThis pilot study was conducted in an intensive care unit (ICU) of a tertiary teaching hospital in China. A total of 83 septic shock patients with left ventricular-arterial uncoupling (i.e., the Ea/Ees ratio ≥ 1.36) were randomly assigned to receive usual care (usual care group, n = 42) or an algorithm-based resuscitation that attempt to reduce the Ea/Ees ratio to 1 within the first 6 h after randomization (VAC-optimized group, n = 41). The left VAC was evaluated by transthoracic echocardiography every 2 h during the study period. The primary endpoint was 28-days mortality. The secondary endpoints included lactate clearance rate, length of ICU stay, and duration of invasive mechanical ventilation (IMV).ResultsEighty-two patients (98.8%) completed the study and were included in the final analysis. The Ea/Ees ratio was reduced in both groups, and the decrease in Ea/Ees ratio in the VAC-optimized group was significantly greater than that in the usual care group [median (interquartile range), 0.39 (0.26, 0.45) vs. 0.1 (0.06, 0.22); P < 0.001]. Compared with the usual care group, the VAC-optimized group likely exhibited the potential to reduce the 28-days mortality (33% vs. 50%; log-rank hazard ratio = 0.526, 95% confidence interval: 0.268 to 1.033). Moreover, the VAC-optimized group had a higher lactate clearance rate than the usual care group [27.7 (11.9, 45.7) % vs. 18.3 (− 5.7, 32.1) %; P = 0.038]. No significant difference was observed in terms of the length of ICU stay or duration of IMV.ConclusionsDuring the initial resuscitation of septic shock, optimizing left ventricular-arterial coupling was associated with improved lactate clearance, while likely having a beneficial effect on prognosis.Trial registrationChinese Clinical Trial Registry, ChiCTR1900024031. Registered 23 June 2019 - Retrospectively registered.

Data-driven clustering supports adaptive remodeling of athlete's hearts: An echocardiographic study from the Taipei Summer Universiade

Sport-specific adaptations of athlete's hearts are still under investigation. This study sought to 1) identify athlete groups with similar characteristics by clustering echocardiographic data; 2) externally validate the data-driven clusters with sport classifications of various dynamic or static loads to support the conventional hypothesis-driven approach in delineating the athlete's heart. Anthropometric, echocardiographic and electrocardiographic assessments were collected during the 2017 Summer Universiade in Taiwan. Besides standard echocardiography and strain measurements, ventricular-arterial coupling (VAC) was assessed by the ratio of effective arterial elastance (Ea) to left ventricular end-systolic elastance (Ees) as calculated by a modified single-beat algorithm. We grouped 598 elite athletes (348 male, age 23±2.5 years, across 24 disciplines) using Mitchell's classification. The hypothesis-driven analysis showed dynamic training-related adaptations in heart rate and morphology, including ventricular size, mass, and stroke volume. In comparison, the unsupervised approach found two clusters for each sex. Male athletes participating in high dynamic-load exercises had larger chambers, supranormal diastolic functions, depressed Ees, lower Ea and preserved optimal VAC implicating the resting status of a reservoir-rich pump, which affirmed sport-specific adaptation. The female athletes could be clustered with more noticeable functional alterations, such as depressed biventricular strain. However, the imbalanced number between clusters impeded the validation of load-related remodeling. Hierarchical clustering could analyze complicated multiparametric interactions among numerous echocardiography-derived phenotypes to discern the adaptive propensity of the athlete's heart. The endorsement or generation of hypotheses by a data-driven approach can be applied to various domains.

Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure.

Dynamic exercise elicits robust increases in sympathetic activity in part due to muscle metaboreflex activation (MMA), a pressor response triggered by activation of skeletal muscle afferents. MMA during dynamic exercise increases arterial pressure by increasing cardiac output via increases in heart rate, ventricular contractility, and central blood volume mobilization. In heart failure, ventricular function is compromised, and MMA elicits peripheral vasoconstriction. Ventricular-vascular coupling reflects the efficiency of energy transfer from the left ventricle to the systemic circulation and is calculated as the ratio of effective arterial elastance (Ea) to left ventricular maximal elastance (Emax). The effect of MMA on Ea in normal subjects is unknown. Furthermore, whether muscle metaboreflex control of Ea is altered in heart failure has not been investigated. We utilized two previously published methods of evaluating Ea [end-systolic pressure/stroke volume (EaPV)] and [heart rate × vascular resistance (EaZ)] during rest, mild treadmill exercise, and MMA (induced via partial reductions in hindlimb blood flow imposed during exercise) in chronically instrumented conscious canines before and after induction of heart failure via rapid ventricular pacing. In healthy animals, MMA elicits significant increases in effective arterial elastance and stroke work that likely maintains ventricular-vascular coupling. In heart failure, Ea is high, and MMA-induced increases are exaggerated, which further exacerbates the already uncoupled ventricular-vascular relationship, which likely contributes to the impaired ability to raise stroke work and cardiac output during exercise in heart failure.

Evaluation of ventricular-arterial coupling by impedance cardiography in healthy volunteers

Background: The interplay between cardiac function and the arterial system is currently defined as ventricular-arterial coupling (VAC) and it is an expression of global cardiovascular efficiency. VAC involves a variety of complex interactions between the heart and the vasculature. A basic index of VAC is the ratio of effective arterial elastance (Ea)/ end-systolic elastance (Ees). While this is often done with echocardiography, obtaining Ea/Ees using impedance cardiography is feasible, although this possibility has not been explored so far. Objective: The aim of this study was to compare the Ea/Ees values obtained using echocardiography and impedance cardiography. Approach: Two independent operators estimated Ea/Ees in 91 (41 ± 14 years old, women 51%) untreated apparently healthy individuals using (1) Doppler echocardiography with the single-beat method developed by Chen et al (2001 J. Am. Coll. Cardiol. 38 2028–34); and (2) data provided by impedance cardiography. The differences between Ea/Ees values were compared and correlation between both methods was estimated. Main results: Although Ea and Ees values calculated by impedance cardiography were lower than those estimated by echocardiography (−0.201 ± 0.457 mmHg ml−1 and −0.193 ± 0.413 mmHg ml−1), Ea/Ees ratio values were similar. Thus, there was no significant difference between the mean values of Ea/Ees estimated by impedance cardiography or echocardiography (Ea/Ees impedance cardiography − Ea/Ees echocardiography = −0.015 ± 0.096, p = 0.150). Ea/Ees values calculated by both methods were highly correlated (r = 0.85, p < 0.001), as well as the pre-ejection and left ventricular ejection time (r = 0.83 and r = 0.91, respectively). Significance: In healthy individuals, estimation of Ea/Ees by impedance cardiography yielded similar values to those obtained using echocardiography.

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.

Ventricular-Arterial Coupling in Chronic Heart Failure.

Measures of interaction between the left ventricle (LV) and arterial system (ventricular-arterial coupling) are important but under-recognised cardiovascular phenotypes in heart failure. Ventriculo-arterial coupling is commonly assessed in the pressure-volume plane, using the ratio of effective arterial elastance (EA) to LV end-systolic elastance (EES) to provide information on ventricular-arterial system mechanical efficiency and performance when LV ejection fraction is abnormal. These analyses have significant limitations, such as neglecting systolic loading sequence, and are less informative in heart failure with preserved ejection fraction (HFpEF). EA is almost entirely dependent on vascular resistance and heart rate. Assessment of pulsatile arterial haemodynamics and time-resolved myocardial wall stress provide critical incremental physiological information and should be more widely utilised. Pulsatile arterial load represents a promising therapeutic target in HFpEF. Here, we review various approaches to assess ventricular-arterial interactions, and their pathophysiological and clinical implications in heart failure.

Myocardial fibrosis detected with gadolinium delayed enhancement in cardiac magnetic resonance imaging is related with arterioventricular coupling alterations in patients with acute myocarditis

Background Delayed Gandolinium Myocardium Enhancement (DE) extent on Cardiac Magnetic Resonance (CMR) is significantly correlated to biomarkers of myocardial injury in patients with acute viral myocarditis, and is a significant independent predictor of adverse cardiovascular outcome. Arterial Venrticular Coupling (VAC) is related to the efficiency of mechanical energy transfer from the heart to the arteries, and it has been expressed by means of the ratio of effective arterial elastance (Ea) to end-systolic elastance (Ees), which is relatively independent of loading conditions. In this work we aimed to evaluate alterations in Ees, Ea and VAC indices in relation with DE in patients with acute myocarditis.

Non-invasively estimated end-systolic elastance in patients with resistant hypertension and type 2 diabetes mellitus

Ventriculo-arterial coupling (VAC) has been shown to be impaired in patients with type 2 diabetes mellitus (type 2 DM) and hypertension, and to improve with antihypertensive treatment. We examined if VAC in patients with type 2 DM and hypertension improved after a period of intensified antihypertensive treatment. VAC was estimated as the ratio of effective arterial elastance (E A) to end-systolic elastance (E ES) using pressure and flow curves obtained non-invasively (applanation tonometry and echocardiography). Left ventricular (LV) systolic and diastolic functions were evaluated using LV volumes, ejection fraction (EF), mitral inflow pattern, and Doppler tissue mitral annulus velocities. In total, 180 patients were included and for 100 patients the data met the quality criteria. Patients were categorized as having controlled (CH, n = 34), uncontrolled (UH, n = 32) or resistant (RH, n = 34) hypertension. In patients with RH, EF at follow-up was reduced from 48 to 42% (p = 0.005) and E ES from 2.18 mmHg/ml to 1.47 mmHg/ml (p = 0.003). EES, however, was also reduced in patients with CH and UH (CH 2.41-2.26, p = 0.05, UH 2.51-2.04, p = 0.05). In the present study, intensified antihypertensive treatment did not improve VAC or LV function in patients with hypertension and type 2 DM despite better control of BP. We speculate whether this is due to a reduction in myocardial perfusion pressure or to a gradual progression of diabetic cardiomyopathy.

Assessment of left ventricular function by pulse wave analysis in critically ill patients

Left ventricular (LV) performance is often quantified by echocardiography in critically ill patients. Pulse wave analysis (PWA) systems can also monitor cardiac function but in a continuous fashion. We compared echocardiographic and PWA-derived indices of LV function. We enrolled 70 critically ill patients equipped with invasive arterial pressure monitoring who required echocardiography. We simultaneously assessed LV ejection fraction (LVEF), the rate of LV pressure rise during systole (dP/dt MAX) obtained with echocardiography (EC-dP/dt MAX), the ratio of effective arterial elastance to LV end-systolic elastance (E a/E es) determined by echocardiography, the dP/dt MAX estimated from the arterial pressure waveform (AP-dP/dt MAX) and the cardiac cycle efficiency (CCE) using PWA. Mean LVEF was 53 ± 18 % and CCE 0.16 ± 0.26. CCE was correlated linearly with LVEF (r = 0.88, 95 % CI 0.81 to 0.92, P < 0.001), and the dP/dt MAX values from the two techniques were linearly correlated (r = 0.93, 95 % CI 0.87 to 0.96, P < 0.001). There was minimal bias between the techniques for measurement of dP/dt MAX (23.7 mmHg/ms; 95 % CI -23.6 to 71.0). E a/E es and CCE were inversely correlated (r = -0.81, 95 % CI -0.88 to -0.71, P < 0.001). A CCE value of <0.07 predicted LVEF <40 % with a sensitivity of 0.93 and a specificity of 0.96 (AUC 0.98, 95 % CI 0.90 to 1.0, P < 0.001). A CCE value of >0.12 predicted LVEF ≥50 % with a sensitivity of 0.96 and a specificity of 0.82 (AUC 0.94, 95 % CI 0.87 to 1.0, P < 0.001). A CCE value <0.12 predicted E a/E es ≥1.3 with a sensitivity of 0.93 and a specificity of 0.89 (AUC 0.94, 95 % CI 0.83 to 1.0, P < 0.001). PWA-derived variables provide relevant information on cardiac contractility and performance in critically ill patients. PWA provides an easy method for online hemodynamic evaluation in critically ill patients.

Ventricular–arterial coupling: Invasive and non-invasive assessment

Interactions between the left ventricle (LV) and the arterial system, (ventricular–arterial coupling) are key determinants of cardiovascular function. Ventricular–arterial coupling is most frequently assessed in the pressure–volume plane using the ratio of effective arterial elastance (EA) to LV end-systolic elastance (EES). EA (usually interpreted as a lumped index of arterial load) can be computed as end-systolic pressure/stroke volume, whereas EES (a load-independent measure of LV chamber systolic stiffness and contractility) is ideally assessed invasively using data from a family of pressure–volume loops obtained during an acute preload alteration. Single-beat methods have also been proposed, allowing for non-invasive estimations of EES using simple echocardiographic measurements. The EA/EES ratio is useful because it provides information regarding the operating mechanical efficiency and performance of the ventricular–arterial system. However, it should be recognized that analyses in the pressure–volume plane have several limitations and that “ventricular–arterial coupling” encompasses multiple physiologic aspects, many of which are not captured in the pressure–volume plane. Therefore, additional assessments provide important incremental physiologic information about the cardiovascular system and should be more widely used. In particular, it should be recognized that: (1) comprehensive analyses of arterial load are important because EA poorly characterizes pulsatile LV load and does not depend exclusively on arterial properties; (2) The systolic loading sequence, an important aspect of ventricular–arterial coupling, is neglected by pressure–volume analyses, and can profoundly impact LV function, remodeling and progression to heart failure. This brief review summarizes methods for the assessment of ventricular–arterial interactions, as discussed at the Artery 12 meeting (October 2012).

Abstract 89: The Ventriculo-Ventricular Coupling Index: A Novel Approach to Assessing Biventricular Function

Bi-ventricular (Bi-V) function in primary pulmonary hypertension (PPH) or PH secondary to left heart failure (SPH) remains difficult to characterize. As a measure of ventricular efficiency, ventriculo-arterial coupling (VAC) is calculated as the ratio of effective arterial elastance (Ea) to end-systolic elastance (Ees). No measure currently assesses ventriculo-ventricular coupling (VVC). Therefore, we developed a novel catheter-based approach to quantify Bi-V function using pressure-volume loop (PVL) analysis and hypothesized that Bi-V VAC ratios, defined as the VVC index (VVCI), may discriminate PPH and SPH. Methods: Adult male mice (n=6/group) underwent constriction of the pulmonary artery (PAC) or thoracic aorta (TAC) to model PPH and SPH respectively. Sham-operated animals underwent a left thoracotomy. Closed chest simultaneous Bi-V catheterization was performed after 7 days in PPH and 10 weeks in SPH. Conductance catheters were used for right and left ventricular PVL analysis via the right external jugular vein and right common carotid artery under steady-state conditions and with variable preload. Results: Steady-state Bi-V PVL and changes in VAC ratios and the VVCI are shown below. In sham mice VAC ratios and the VVCI reflect optimal ventricular efficiency. In PPH, the VVCI is significantly increased, while in SPH, the VVCI is significantly decreased compared to controls. Conclusion: These results identify a novel method to quantify Bi-V function in mice and further show that the VVCI can distinguish PPH and SPH. These findings have important implications for examining cardiac function in preclinical and clinical studies of left- and right-sided heart failure.

Prenatal nicotine exposure induces gender-associated left ventricular-arterial uncoupling in adult offspring.

Alterations in vascular or myocardial structure and function have been demonstrated in offspring subjected to prenatal nicotine exposure (PNE), however, limited data are available on how these changes interact. The present study assessed the hypothesis that prenatal nicotine exposure induced gender-specific alterations of left ventricular-arterial coupling indices in adult offspring. Female Sprague-Dawley rats were exposed to either nicotine (8 mg/kg/day) or saline via subcutaneous osmotic mini-pumps throughout gestation. Male and female offspring, aged 12 months, underwent non-invasive echocardiography and invasive left ventricular cannulation. Left ventricular-arterial coupling was analysed as the ratio of effective arterial elastance (Ea) to ventricular end-systolic elastance (Ees). The left ventricular myocardium and aorta were stained with hematoxylin and eosin and the myocardial cell cross-sectional area was calculated. Simultaneously, the ratio of medium thickness to internal diameter in the aorta and mesenteric artery was determined. The fibrosis component of left ventricle myocardium was analyzed by Sirius-red staining and further confirmed by hydroxyproline determination. The elastic properties of the aortic wall were analyzed by van Gieson staining. PNE caused significant increases in pulse pressure (56.36 ± 7.41 vs. 50.16 ± 4.94 mmHg; P<0.05) and left ventricular meridional wall stress (78.25 ± 9.12 vs. 69.64 ± 7.58 kdyne/cm(2); P<0.05) in male offspring compared with the control. Conversely, no similar effect was observed in female offspring. An elevated augmentation index was noted in male and female pups. Additionally, Ea/Ees was reduced in PNE males compared with control males, due to a disproportionate increase in Ees vs. Ea whereas in females, Ea/Ees did not differ significantly due to tandem increase in Ea and Ees. In addition, collagen cross-linking was markedly higher in male offspring, whereas it was unaltered in females compared with their respective controls. Fragmentation of the elastic network in the aorta and the increased ratio of medial thickness to internal diameter in the mesenteric artery were more evident in male offspring when compared with female offspring. PNE caused combined ventricular-arterial stiffening in male and female offspring, with lower Ea/Ees in males, while Ea/Ees was preserved in females. Enhanced collagen cross-linking in the myocardium, underdeveloped elastic fibers in the aorta and remodeled resistance vessels were associated with pathological ventricular arterial mismatching. The results of the present study indicated that male offspring were more susceptible to the development of ventricular and arterial dysfunction in response to PNE compared with female offspring.

Arterial-ventricular coupling with aging and disease.

Age is the dominant risk factor for cardiovascular diseases. Understanding the coupling between the left ventricle (LV) and arterial system, termed arterial–ventricular coupling (EA/ELV), provides important mechanistic insights into the complex cardiovascular system and its changes with aging in the absence and presence of disease. EA/ELV can be indexed by the ratio of effective arterial elastance (EA; a measure of the net arterial load exerted on the LV) to left ventricular end-systolic elastance (ELV; a load-independent measure of left ventricular chamber performance). Age-associated alterations in arterial structure and function, including diameter, wall thickness, wall stiffness, and endothelial dysfunction, contribute to a gradual increase in resting EA with age. Remarkably there is a corresponding increase in resting ELV with age, due to alterations to LV remodeling (loss in myocyte number, increased collagen) and function. These age-adaptations at rest likely occur, at least, in response to the age-associated increase in EA and ensure that EA/ELV is closely maintained within a narrow range, allowing for optimal energetic efficiency at the expense of mechanical efficacy. This optimal coupling at rest is also maintained when aging is accompanied by the presence of hypertension, and obesity, despite further increases in EA and ELV in these conditions. In contrast, in heart failure patients with either reduced or preserved ejection fraction, EA/ELV at rest is impaired. During dynamic exercise, EA/ELV decreases, due to an acute mismatch between the arterial and ventricular systems as ELV increases disproportionate compared to EA (≈200 vs. 40%), to ensure that sufficient cardiac performance is achieved to meet the increased energetic requirements of the body. However, with advancing age the reduction in EA/ELV during acute maximal exercise is blunted, due to a blunted increase ELV. This impaired EA/ELV is further amplified in the presence of disease, and may explain, in part, the reduced cardiovascular functional capacity with age and disease. Thus, although increased stiffness of the arteries itself has important physiological and clinical relevance, such changes also have major implications on the heart, and vice versa, and the manner in the way they interact has important ramifications on cardiovascular function both at rest and during exercise. Examination of the alterations in arterial–ventricular coupling with aging and disease can yield mechanistic insights into the pathophysiology of these conditions and increase the effectiveness of current therapeutic interventions.

Arterial-Ventricular Coupling in Preterms with Patent Ductus Arteriosus

Aim of the study: To analyze arterial-ventricular coupling (AV-C) in a cohort of preterms before and after ductal closure. Patients and methods. Inclusion criteria: Gestational age < 33+0, normal intracardiac anatomy, no coarctation, minimum stay in the NICU from day 1 to day 3 of life in the period from 11/2009 - 11/2010. Further criteria were complete M-mode (left atrium, left ventricle) and Doppler recordings (left pulmonary artery, descending aorta and PDA), Patients were stratified into 4 subgroups according to GA. PDA flow patterns were classified according to Skinner (PDA type 1-6). As a measure for AV-C the ratio of effective arterial elastance to left-ventricular endsystolic elastance (EA /ELV ) was calculated based on M-mode derived volumes. Results: The study cohort comprised of 79 patients (subgroup 1 (GA23+0-24+6) n=17, subgroup 2 (GA 25+0-26+6) n=29, subgroup 3 (GA 27+0-28+6) n=21, subgroup 4 GA29+0 -32+6) n=12). PDA types 5 and 6 were found in 41%, 28%, 24% and 8% of patients in subgroups 1,2,3, and 4 respectively. 67/79 patients with a PDA type 3-6 received ibuprofen, in 12 of them ductal clipping was required. Calculation of EA / ELV before and after ductal closure revealed the following ratios: Subgroup 1: 0.28 vs. 0.27, subgroup 2: 0.31 vs.0.35, subgroup 3: 0.45 vs.0.39 and subgroup 4: 0.51 vs. 0.33. Conclusion: Our preliminary data indicate that the effect of ductal closure on either EA or ELV or both depends on gestational age.

Attenuating The Age-associated Deficit In Peak Arterial-ventricular Coupling With Sodium Nitroprusside

Cardiovascular performance is influenced by the interaction of the left ventricle (LV) and the arterial system. This interaction can be indexed by the ratio of effective arterial elastance (EA; a measure of net arterial load), to LV end-systolic elastance (ELV; a measure of LV performance). During exercise, there is an age-associated deficit in the ability to reduce EA/ELV. PURPOSE: We evaluated the effects of unloading the heart with sodium nitroprusside (SN) on EA/ELV and its components at rest and during graded exercise. METHODS: SN and saline placebo were administered to 15 older (70±8years) and 9 younger (31±4years) healthy subjects on separate days. Cardiac volumes were measured at rest and exercise (cycle ergometry) using gated blood pool scans to derive EA=end-systolic pressure (ESP)/SV, ELV=ESP/ESV from which EA/ELV was calculated as end-systolic volume (ESV)/stroke volume(SV). RESULTS: At rest, in the older and younger groups, SN respectively lowered EA by 10% (p<0.05) and 4% (p=NS), increased ELV by 47%(p<0.01) and 27%(p<0.01), and thus reduced EA/ELV by 31%(p<0.01) and 27% (p<0.01) compared to placebo. At peak exercise, SN did not significantly influence EA in either age group. However, SN increased ELV by 68% (p<0.01) and 46% (p<0.07) in the older and younger groups respectively, and thus reduced EA/ELV by 36%(p<0.01) and 22% (p<0.01) compared to placebo. Importantly, the age-associated deficit in peak EA/ELV was attenuated from 23% to 13% by SN. CONCLUSION: Our results suggest that the age-associated deficits in peak EA/ELV are acutely reversible with SN. Thus, examining EA/ELV and its components can provide useful mechanistic insights into cardiovascular performance both at rest and during exercise.

Usefulness of systolic time intervals in the identification of abnormal ventriculo‐arterial coupling in stable heart failure patients*

The ratio of effective arterial elastance (Ea) to ventricular end-systolic elastance (Ees) indicates the status of ventriculo-arterial coupling. We investigated if systolic time intervals (pre-ejection period, PEP; ejection time, ET; and their ratio, PEP/ET) can be used to identify heart failure patients with abnormal ventriculo-arterial coupling. Age and sex-matched study subjects included 54 apparently healthy subjects with normal left ventricular (LV) function, and stable patients with LV diastolic (n=54) and systolic dysfunction (n=54). Ees and Ea were estimated non-invasively by echocardiography, and abnormal ventriculo-arterial coupling was defined as Ea/Ees>1.2. PEP, ET, and PEP/ET were measured automatically using electrocardiography, phonocardiography, and brachial pulse volume recording. Ea/Ees>1.2 was present in 48.1% of subjects with systolic dysfunction. The PEP/ET was significantly associated with most parameters of LV structure and function, and Ea/Ees (r=0.67, p<0.001). Using PEP/ET> or =0.423 as cut point, the sensitivity and specificity to identify patients with Ea/Ees>1.2 were 85.7% and 84.3%, respectively for the whole population, and 84.6% and 78.6%, for patients with systolic dysfunction. Abnormal ventriculo-arterial coupling was present in almost half of stable patients with systolic dysfunction. PEP/ET was useful in identifying such patients.

Arterial-ventricular coupling: mechanistic insights into cardiovascular performance at rest and during exercise.

Understanding the performance of the left ventricle (LV) requires not only examining the properties of the LV itself, but also investigating the modulating effects of the arterial system on left ventricular performance. The interaction of the LV with the arterial system, termed arterial-ventricular coupling (E(A)/E(LV)), is a central determinant of cardiovascular performance and cardiac energetics. E(A)/E(LV) can be indexed by the ratio of effective arterial elastance (E(A); a measure of the net arterial load exerted on the left ventricle) to left ventricular end-systolic elastance (E(LV); a load-independent measure of left ventricular chamber performance). At rest, in healthy individuals, E(A)/E(LV) is maintained within a narrow range, which allows the cardiovascular system to optimize energetic efficiency at the expense of mechanical efficacy. During exercise, an acute mismatch between the arterial and ventricular systems occurs, due to a disproportionate increase in E(LV) (from an average of 4.3 to 13.2, and 4.7 to 15.5 mmHg.ml(-1).m(-2) in men and women, respectively) vs. E(A) (from an average of 2.3 to 3.2, and 2.3 to 2.9 mmHg.ml(-1).m(-2) in men and women, respectively), to ensure that sufficient cardiac performance is achieved to meet the increased energetic requirements of the body. As a result E(A)/E(LV) decreases from an average of 0.58 to 0.34, and 0.52 to 0.27 in men and women, respectively. In this review, we provide an overview of the concept of E(A)/E(LV), and examine the effects of age, hypertension, and heart failure on E(A)/E(LV) and its components (E(A) and E(LV)) in men and women. We discuss these effects both at rest and during exercise and highlight the mechanistic insights that can be derived from studying E(A)/E(LV).