Ventricular-arterial Coupling Ratio Research Articles

Angiotensin receptor-neprilysin inhibition and improved ventricular-arterial coupling in heart failure with reduced ejection fraction.

Sacubitril/valsartan improves outcome in chronic heart failure (HF) with reduced ejection fraction (EF). The underlying mechanisms on left ventricular (LV) myocardial function are incompletely understood. In this study, 117 patients with symptomatic HF and LV-EF ≤ 40% were enrolled prospectively. Non-invasive pressure-volume analysis was calculated from transthoracic echocardiography with simultaneous arm-cuff blood pressure measurements. Primary outcome parameters were LV end-systolic elastance (Ees; a measure of LV contractility), effective arterial elastance (Ea; a measure of afterload), and the ventricular-arterial coupling ratio (Ea/Ees). Mean age was 65±13 years, 30% were female, and 54.7% had ischemic heart disease. During six months of follow-up, eight patients died, three withdrew their consent, and four were lost to follow-up. 102 patients were included in pressure-volume analyses. After six months of sacubitril/valsartan treatment, Ees increased (0.66mmHg/ml [IQR 0.45-0.94] vs. 0.78mmHg/ml [IQR 0.57-1.10], p=0.001), Ea decreased (1.76mmHg/ml [IQR 1.48-2.13] vs. 1.62mmHg/ml [IQR 1.36-1.96], p=0.014), and the Ea/Ees ratio improved (2.52 [IQR 1.88-4.05] vs. 1.93 [IQR 1.50-2.63], p<0.001). LV end-diastolic pressure and LV volumes were reduced, and LVEF increased from 33% to 43% (both p<0.001). Clinical improvement occurred in NYHA functional class, NT-proBNP level, and 6-minute walking distance. Change in LVEF correlated with change in Ees (r=0.33, p=0.0008), while change in NT-proBNP was associated with change in LVEDP (r=0.42, p<0.0001). In conclusion, sacubitril/valsartan is associated with improved ventricular-arterial coupling by enhancing LV contractility and reducing afterload. Beyond LV reverse remodeling, optimized ventricular-arterial interaction may contribute to the favorable outcome of sacubitril/valsartan treatment in HF with reduced EF.

Analysis of ventricular-vascular properties during preeclampsia: an echocardiography study.

The aim of the study is to analyze ventricular-vascular properties with different ventricular-arterial coupling (VAC) ratio in the preeclamptic women. Seventy-seven pregnant women with preeclampsia and eighty-nine with normal pregnancy were performed echocardiography. VAC was defined as the ratio between aortic elastance (Ea) and left ventricular (LV) end-systolic elastance (Ees). Using the VAC value of 0.8 as the cut-off near uncoupling, the preeclampsia cases were divided into two subgroups: VAC ratio ≥ 0.8 and <0.8. Cardiac structure and function, VAC properties, as well as four components of the LV pressure-strain loop, including global myocardial work index (GWI), constructive work (GCW), wasted work (GWW), and work efficiency (GWE) were determined. The preeclampsia with VAC ≥ 0.8 had an enlarger indexed ventricular volume and a thicker relative ventricular wall than the VAC < 0.8. The Ees significantly increased in the subgroup with VAC < 0.8 and decreased in the VAC ≥ 0.8, while the Ea increased in both of them. The preeclampsia with VAC ≥ 0.8 showed an obvious augmentation in GWI, GCW and GWE, along with a similar GWW compared to those with VAC < 0.8. There were variable relationships between the LV pressure-strain components and VAC properties. Thus, the preeclampsia with VAC ≥ 0.8 undergoes a more adverse remodeling and a greater impact on cardiac contractility. The increased stiffness of the heart and arterial system, and increased resistance of peripheral vessels net lead to the deteriorative ventricular efficiency with elevated myocardial oxygen consumption during a preeclampsia pregnancy.

Treatment with sacubitril/valsartan and improvement of ventricular-arterial coupling in heart failure with reduced ejection fraction

Abstract Background Treatment with the angiotensin receptor-neprilysin inhibitor sacubitril/valsartan (S/V) in patients with heart failure and reduced ejection fraction (HFrEF) reduces mortality and heart failure (HF) hospitalizations. The specific hemodynamic mechanisms underlying these beneficial effects are currently unclear. Purpose This study aimed to assess the effects of S/V treatment on left ventricular (LV) end-systolic elastance (Ees), effective arterial elastance (Ea), and the ventricular-arterial coupling ratio (Ea/Ees) in patients with HFrEF using non-invasive pressure-volume analysis. Methods 117 patients with symptomatic HF and LVEF &amp;lt;40% in whom treatment with S/V was initiated were enrolled in this multicenter German prospective study. We used transthoracic echocardiography with simultaneous arm-cuff blood pressure measurements for non-invasive pressure-volume loop analyses. Primary endpoints were changes in Ees, Ea, and Ea/Ees ratio after six months of S/V treatment. Results The mean age was 65 (±13) years and 30% were female. In 54.7% of the patients, the etiology of HF was ischemic, and 45.3% was non-ischemic. 58.4% had first HF diagnosis at baseline. 102 patients with complete clinical and echocardiographic data at baseline and after six months of follow-up were analyzed. Among those, 62% were on target dose of S/V. Six months of S/V treatment resulted in a significant increase of Ees (0.66 mmHg/ml, IQR [0.45;0.94] vs. 0.78 mmHg/ml [0.57;1.10], p=0.001) and decrease of Ea (1.76 mmHg/ml [1.48;2.13] vs. 1.62 mmHg/ml [1.36;1.96], p=0.014). Hence, the Ea/Ees ratio significantly improved (2.52 [1.88;4.05] vs. 1.93 [1.50;2.63], p&amp;lt;0.001). In addition, LV volumes and pressure improved significantly with a regression of the LV end-systolic volume (LVESV: 142 ml [115;180] vs. 96 ml [65;124]), end-diastolic volume (LVEDV: 216 ml [179;247] vs. 165 ml [132;200]) and LV end-diastolic pressure (LVEDP: 19.6 mmHg [18.2;22.4] vs. 17.8 mmHg [16.6;19.9]), p&amp;lt;0.001 respectively. The LVEF increased from a median of 33% (27;37) to 43% (36;49), p&amp;lt;0.001. NT-proBNP level decreased from (median) 1771 pg/ml [838;5211] to 724 pg/ml [300;1575] and mean 6-minute walking distance increased from 371m (±125) to 423 m (±122), p&amp;lt;0.001 respectively. The percentage of patients with NYHA class III changed from 25.6% to 5.9%. Conclusion In a 6-months treatment period, initiation of sacubitril/valsartan in patients with heart failure and reduced ejection fraction was associated with reduction of LV volumes, improved LV function, reduction in afterload and fewer heart failure symptoms. These new data indicate that beyond reverse LV remodeling, improvement of LV contractility and ventricular-arterial coupling may contribute to the favorable clinical outcomes on treatment with sacubitril/valsartan in chronic heart failure.

A method for calculating left ventricular ejection fraction noninvasively from left ventricular arterial coupling (Ees/Ea)

BackgroundEjection fraction (EF), which is assessed using ultrasonography, is a standard parameter for evaluating cardiac function in clinical cardiology and for cardiovascular management during general anesthesia. However, it is impossible to continuously and non-invasively assess EF using ultrasonography. The aim of our study was to develop a method for estimating EF non-invasively using the left ventricular arterial coupling ratio (Ees/Ea).MethodsEes/Ea was estimated non-invasively using the parameters pre-ejection period (PEP), ejection time (ET), end-systolic pressure (Pes) and diastolic pressure (Pad), which were calculated from a vascular screening system, VeSera 1000/1500 (Fukuda Denshi Co., Ltd., Tokyo, Japan). Then, left ventricular efficiency (Eff) as a pump, defined as the ratio of external work (EW) to myocardial oxygen consumption, which strongly correlates with the pressure-volume area (PVA), was calculated by a new formula using Ees/Ea, and was used to approximate EF (EFeff). Simultaneously, we measured EF using transthoracic echocardiography (EFecho), and compared it with EFeff.ResultsThe study included 44 healthy adults (36 males, 8 females), in whom mean EFecho was 66 ± 5% and EFeff was 57 ± 9%. We found a positive correlation between EFecho and EFeff (R2 = 0.219, p < 0.05) on Bland-Altman analysis, with limits of agreement of – 7.5 to 24.4%, and percentage error of 24%.ConclusionThe results suggest that EF can be measured non-invasively using left ventricular arterial coupling.

Effects of Sacubitril/Valsartan on left ventricular pressure-volume relationship in heart failure

Abstract Background In patients with heart failure (HF) and reduced ejection fraction, Sacubitril/Valsartan (S/V) reduces the risk for death and hospitalisations. However, the underlying mechanism for these beneficial effects of S/V, is still lacking. Methods Consecutive patients with symptomatic HF and LV ejection fraction (EF) ≤40% who were assigned to S/V were prospectively included in this study (n=117). Non-invasive pressure volume loops were obtained from echocardiography with simultaneous arm-cuff blood pressure measurement. By this method, LV end-systolic elastance (Ees), effective arterial elastance (Ea) and ventricular-arterial coupling (Ea/Ees) were calculated. LV end-diastolic pressure was derived from the E/e' ratio. This is a prespecified interim analysis of 50 patients with completed 6 months of follow-up. The study is registered with ClinicalTrials.gov, NCT04498780. Results Mean age was 61.8±18.6 years and 12 (24%) patients were females. Ischaemic heart failure was present in 22 (44%), non-ischaemic aetiology in 24 (48%), and myocarditis in 4 (8%) patients. 34 (68%) patients were on the target dose of S/V after 6 months of treatment. At 6 months, LV end-diastolic volume (110±28 ml/m2 vs. 87±31 ml/m2, p&amp;lt;0.0001) and end-systolic volume (78±26 ml/m2 vs. 52±26 ml/m2, p&amp;lt;0.0001) were reduced, hence mean LVEF increased (30±7% vs. 42±11%, p&amp;lt;0.0001). LV end-diastolic pressure was significantly reduced (21±3.9 mmHg vs. 18±2.7 mmHg, p&amp;lt;0.0001). These hemodynamic changes were associated with improved NYHA functional class (8% class III vs. 20% at baseline), reduced median NT-proBNP level (2398 pg/ml, interquartile range [IQR]: 1185–6034 to 813 pg/ml, IQR: 299–1971, p&amp;lt;0.001) and increased mean six-minute walk test (6MWT) distance (356.8m (±150.5) at baseline to 415.0m (±397.0) at six months, p=0.003). LV end-systolic elastance (Ees), arterial elastance (Ea) and the ventricular-arterial coupling ratio Ea/Ees remained similar at 6 months of follow-up compared to baseline (p=ns). Conclusion After 6 months of treatment with Sacubitril/Valsartan, LV remodelling and reduced LV filling pressures were observed. These changes were associated with improvements in functional capacity, natriuretic peptide levels and NYHA functional class. Thus, the study provides important mechanistic insides into the hemodynamics of angiotensin–neprilysin inhibition in heart failure which might help to individualize therapy. Funding Acknowledgement Type of funding sources: None.

Abstract 12995: Sex and Race Differences in Ventricular-Arterial Coupling in the Coronary Artery Risk Development in Young Adults (CARDIA) Study

Background: Coupling between the left ventricle and arterial system can be quantified as the ventricular-arterial coupling (VAC) ratio with 1.00 reflecting optimal physiology. VAC has been most studied in heart failure, with higher values associating with worse prognosis, but its correlates among individuals without heart failure are less characterized. Thus, in the Coronary Artery Risk Development in Young Adults (CARDIA) study we tested the hypothesis that VAC ratio differs by sex and race. Methods: We studied VAC in 2,812 (42% male, 47% black, median age 50 years) CARDIA year 25 exam participants with transthoracic echocardiogram data available and no history of heart failure, myocardial infarction, peripheral vascular disease, or valvular disease. VAC was calculated as arterial elastance (Ea) divided by LV end systolic elastance (Ees). Ea and Ees were calculated as end systolic pressure/stroke volume and by the modified Chen single beat method, respectively. Associations between sex and race with VAC were tested in multivariable-adjusted linear regression. Results: VAC ratio differed by both sex and race with higher unadjusted values in men (median 1.14 [25 th -75 th percentile 1.08-1.20]) compared with women (1.11 [1.05-1.17]), p &lt; 0.001, and white (1.12 [1.07-1.18]) compared with black (1.11 [1.06-1.18]) individuals, p = 0.004. In adjusted models, male sex (beta 0.027 [95% CI 0.021 to 0.037], p &lt;0.001) and white race (0.007 [0.002 to 0.012], p = 0.009) remained associated with higher VAC ratio (Figure 1). Sex, LV ejection fraction (beta -0.096 [95% CI -0.099 to -0.093], and total arterial compliance (-0.045 [-0.049 to -0.041]) were the most strongly associated correlates of VAC. Systolic blood pressure, creatinine, heart rate, LDL, and triglycerides inversely associated with VAC. Age and LV remodeling index positively associated with VAC. Conclusions: In community dwelling middle-aged adults, male sex and white race independently associated with higher VAC.

Phosphodiesterase 9a Inhibition in Mouse Models of Diastolic Dysfunction.

Low myocardial cGMP-PKG (cyclic guanosine monophosphate-protein kinase G) activity has been associated with increased cardiomyocyte diastolic stiffness in heart failure with preserved ejection fraction. Cyclic guanosine monophosphate is mainly hydrolyzed by PDE (phosphodiesterases) 5a and 9a. Importantly, PDE9a expression has been reported to be upregulated in human heart failure with preserved ejection fraction myocardium and chronic administration of a PDE9a inhibitor reverses preestablished cardiac hypertrophy and systolic dysfunction in mice subjected to transverse aortic constriction (TAC). We hypothesized that inhibiting PDE9a activity ameliorates diastolic dysfunction. To examine the effect of chronic PDE9a inhibition, 2 diastolic dysfunction mouse models were studied: (1) TAC-deoxycorticosterone acetate and (2) Leprdb/db. PDE9a inhibitor (5 and 8 mg/kg per day) was administered to the mice via subcutaneously implanted osmotic minipumps for 28 days. The effect of acute PDE9a inhibition was investigated in intact cardiomyocytes isolated from TAC-deoxycorticosterone acetate mice. Atrial natriuretic peptide together with PDE9a inhibitor were administered to the isolated intact cardiomyocytes through the cell perfusate. For acute inhibition, no cellular stiffness reduction was found, whereas chronic PDE9a inhibition resulted in reduced left ventricular chamber stiffness in TAC-deoxycorticosterone acetate, but not in Leprdb/db mice. Passive cardiomyocyte stiffness was reduced by chronic PDE9a inhibition, with no differences in myocardial fibrosis or cardiac morphometry. PDE9a inhibition increased the ventricular-arterial coupling ratio, reflecting impaired systolic function. Chronic PDE9a inhibition lowers left ventricular chamber stiffness in TAC-deoxycorticosterone acetate mice. However, the usefulness of PDE9a inhibition to treat high-diastolic stiffness may be limited as the required PDE9a inhibitor dose also impairs systolic function, observed as a decline in ventricular-arterial coordination, in this model.

Right Ventricular-Arterial Coupling Ratio Derived From 3-Dimensional Echocardiography Predicts Outcomes in Pediatric Pulmonary Hypertension.

Right ventricular (RV) function is an important determinant of outcomes in pulmonary hypertension (PH). RV-arterial coupling ratio using stroke volume (SV) to end-systolic volume (ESV) has been shown to be an independent predictor of outcome in adults with PH. SV/ESV has not been used in pediatrics to predict outcomes. We compared SV/ESV between pediatric patients with PH, controls, and among groups based on disease severity. We correlated SV/ESV to RV strain and evaluated SV/ESV as a predictor of outcomes in pediatric PH. One hundred and twenty-five children with PH (8 years [3-12 years]) underwent 3-dimensional echocardiography from 2014 to 2017 and compared with 65 controls (9 years [7-13 years]). Offline analysis generated 3-dimensional end-diastolic volume, ESV, SV, and free-wall RV longitudinal strain. SV/ESV ratios were compared between patients with PH, controls, and disease severity. Correlations between SV/ESV to free-wall RV longitudinal strain were assessed using general linear mixed models. Cox proportional hazards analysis assessed the predictive ability of SV/ESV. Patients with PH had lower SV/ESV compared with controls (0.88±0.18 versus 1.24±0.23; P<0.0001). There were significant associations between SV/ESV to free-wall RV longitudinal strain (r=-0.53; P<0.001). SV/ESV emerged as a strong predictor of adverse clinical event (hazard ratio [CI], 0.52 [0.38-0.69] per 0.1 increase in SV/ESV; P<0.0001). SV/ESV as a volume estimate of RV-arterial coupling ratio correlates with RV strain and is a strong predictor of adverse clinical events in pediatric PH.

The influence of esmolol on right ventricular function in early experimental endotoxic shock.

The mechanism by which heart rate (HR) control with esmolol improves hemodynamics during septic shock remains unclear. Improved right ventricular (RV) function, thereby reducing venous congestion, may play a role. We assessed the effect of HR control with esmolol during sepsis on RV function, macrocirculation, microcirculation, end‐organ‐perfusion, and ventricular‐arterial coupling. Sepsis was induced in 10 healthy anesthetized and mechanically ventilated sheep by continuous IV administration of lipopolysaccharide (LPS). Esmolol was infused after successful resuscitation of the septic shock, to reduce HR and stopped 30‐min after reaching targeted HR reduction of 30%. Venous and arterial blood gases were sampled and the small intestines’ microcirculation was assessed by using a hand‐held video microscope (CytoCam‐IDF). Arterial and venous pressures, and cardiac output (CO) were recorded continuously. An intraventricular micromanometer was used to assess the RV function. Ventricular–arterial coupling ratio (VACR) was estimated by catheterization‐derived single beat estimation. The targeted HR reduction of >30% by esmolol infusion, after controlled resuscitation of the LPS induced septic shock, led to a deteriorated RV‐function and macrocirculation, while the microcirculation remained depressed. Esmolol improved VACR by decreasing the RV end‐systolic pressure. Stopping esmolol showed the reversibility of these effects on the RV and the macrocirculation. In this animal model of acute severe endotoxic septic shock, early administration of esmolol decreased RV‐function resulting in venous congestion and an unimproved poor microcirculation despite improved cardiac mechanical efficiency.

Altered Metabolic Profile With Sodium-Restricted Dietary Approaches to Stop Hypertension Diet in Hypertensive Heart Failure With Preserved Ejection Fraction

BackgroundHeart failure with preserved ejection fraction (HFpEF) is increasingly recognized as a distinct entity with unique pathophysiology. In the Dietary Approaches to Stop Hypertension in Diastolic Heart Failure (DASH-DHF) study, the sodium-restricted Dietary Approaches to Stop Hypertension diet (DASH/SRD) was associated with improved blood pressure and cardiovascular function in 13 hypertensive patients with HFpEF. With the use of targeted metabolomics, we explored metabolite changes and their relationship with energy-dependent measures of cardiac function in DASH-DHF. Methods and ResultsWith the use of chromatography and mass spectrometry, 152 metabolites including amino acids, free fatty acids, phospholipids, diglycerides, triglycerides, cholesterol esters, and acyl carnitines were measured. Comparison of baseline and post–DASH/SRD samples revealed increases in short-chain acetyl, butryl, and propionyl carnitines (P values .02, .03, .03, respectively). Increases in propionyl carnitine correlated with ventricular–arterial coupling ratio (Ees:Ea; r = 0.78; P = .005) and ventricular contractility (maximum rate of change of pressure-normalized stress [dσ*/dtmax]; r = 0.66; P = .03). Changes in L-carnitine also correlated with Ees:Ea (r = 0.62; P = .04) and dσ*/dtmax (r = 0.60; P = .05) and inversely with ventricular stiffness (r = −0.63; P = .03). ConclusionsMetabolite profile changes of patients with HFpEF during dietary modification with the use of DASH/SRD suggest improved energy substrate utilization. Additional studies are needed to clarify connections between diet, metabolic changes, and myocardial function in HFpEF.

Galectin-3: A Link between Myocardial and Arterial Stiffening in Patients with Acute Decompensated Heart Failure?

BackgroundHeart failure is accompanied by abnormalities in ventricular-vascular interaction due to increased myocardial and arterial stiffness. Galectin-3 is a recently discovered biomarker that plays an important role in myocardial and vascular fibrosis and heart failure progression.ObjectivesThe aim of this study was to determine whether galectin-3 is correlated with arterial stiffening markers and impaired ventricular-arterial coupling in decompensated heart failure patients.MethodsA total of 79 inpatients with acute decompensated heart failure were evaluated. Serum galectin-3 was determined at baseline, and during admission, transthoracic echocardiography and measurements of vascular indices by Doppler ultrasonography were performed.ResultsElevated pulse wave velocity and low arterial carotid distensibility are associated with heart failure in patients with preserved ejection fraction (p = 0.04, p = 0.009). Pulse wave velocity, carotid distensibility and Young’s modulus did not correlate with serum galectin-3 levels. Conversely, raised galectin-3 levels correlated with an increased ventricular-arterial coupling ratio (Ea/Elv) p = 0.047, OR = 1.9, 95% CI (1.0‑3.6). Increased galectin-3 levels were associated with lower rates of left ventricular pressure rise in early systole (dp/dt) (p=0.018) and raised pulmonary artery pressure (p = 0.046). High galectin-3 levels (p = 0.038, HR = 3.07) and arterial pulmonary pressure (p = 0.007, HR = 1.06) were found to be independent risk factors for all-cause mortality and readmissions.ConclusionsThis study showed no significant correlation between serum galectin-3 levels and arterial stiffening markers. Instead, high galectin-3 levels predicted impaired ventricular-arterial coupling. Galectin-3 may be predictive of raised pulmonary artery pressures. Elevated galectin-3 levels correlate with severe systolic dysfunction and together with pulmonary hypertension are independent markers of outcome.

Changes of ventricular and peripheral performance in patients with heart failure and normal ejection fraction: insights from ergometry stress echocardiography.

We assessed the left ventricular (LV) and peripheral performance at rest and during exercise in healthy and heart failure subjects with normal ejection fraction (HFNEF) or with reduced ejection fraction (HFREF). All subjects received echocardiography at rest and with bicycle Ergometer exercise. The exercise images for two-dimensional speckle tracking were acquired with submaximal heart rate of 90-100 beats/min, while images for M-mode and tissue Doppler imaging were stored with attainment of >85% of predicted heart rate. A total of 80 HFNEF, 50 HFREF and 50 controls were studied. There was progressive decrease of two-dimensional global circumferential, radial and longitudinal strains (GCS, GRS and GLS), M-mode and tissue Doppler imaging long-axis parameters from controls, HFNEF to HFREF patients (all P < 0.05) at rest and on exercise. The degree of exercise-induced, long-axis augmentation (GLS and M-mode long axis excursion) decreased progressively from controls, HFNEF to HFREF subjects (all P < 0.05), while the increase in GCS and GRS was similar in all groups. The ventricular-arterial coupling ratio did not change in HFREF but reduced in HFNEF and controls during exercise (P < 0.01). All subjects had a similar resting heart rate, but patients exhibited chronotropic non-competence during exercise (P < 0.001). Ventricular and peripheral dysfunction was evident in HFNEF at rest and deteriorated during exercise. The HFNEF patients had significantly impaired long-axis augmentation at stress that was intermediate between HFREF patients and controls. These findings have relevance to generation of symptoms on exercise in both HFNEF and HFREF.

Peak Systolic Mitral Annulus Velocity Reflects the Status of Ventricular-Arterial Coupling—Theoretical and Experimental Analyses

Peak systolic mitral annular velocity (S(m)) measured by tissue Doppler echocardiography has been recognized as an independent predictor of mortality in patients with heart failure and in the general population. However, the mechanical determinants of S(m) remain poorly defined. A theoretical model of S(m) was derived, which indicates that S(m) is affected positively by left ventricular (LV) contractility and preload and inversely by LV afterload and ejection time (EJT). In 16 anesthetized dogs, S(m), LV volume, and LV pressure were measured using sonomicrometry and catheter-tip micromanometry. LV contractility, preload, and afterload were indexed by the end-systolic pressure/volume ratio (E(es)'), end-diastolic volume (V(ed)), and effective arterial elastance (E(a)), respectively. LV contractility, loading conditions, and heart rate were varied over wide ranges, and a total of 76 data sets were obtained for S(m) (1.2-9.1 cm/sec), E(es)' (1.5-17.6 mm Hg/mL), V(ed) (11-99 mL), E(a) (3.6-58.4 mm Hg/mL), EJT (100-246 msec), heart rate (66-192 beats/min), and the ventricular-arterial coupling ratio (E(es)'/E(a); 0.2-3.0). The theoretical model accurately predicted S(m) (R(2)= 0.79, P < .0001). By univariate analysis, S(m) was correlated significantly with E(es)' (R(2)= 0.64, P < .0001) and with the reciprocal of E(a) (R(2)= 0.49, P < .01). V(ed) and EJT did not affect S(m). E(es)'/E(a) was correlated strongly with S(m) (R(2)= 0.73, P < .0001). E(es)' and the reciprocal of E(a) were not correlated with each other. LV contractility and afterload independently determine S(m). The effects of LV preload and EJT on S(m) might be small, even though they are theoretically associated with S(m). S(m) strongly reflects the status of ventricular-arterial coupling.

Resting global and regional left ventricular contractility in patients with heart failure and normal ejection fraction: insights from speckle-tracking echocardiography

ObejctiveTo compare left ventricular (LV) systolic performance and contractility in patients with heart failure and normal ejection fraction (HFNEF), compared with patients with heart failure and reduced ejection fraction (HFREF)...

Impact of vascular adaptation to chronic aortic regurgitation on left ventricular performance.

This investigation was designed to test the hypothesis that vascular adaptation occurs in patients with chronic aortic regurgitation to maintain left ventricular (LV) performance. Forty-five patients with chronic aortic regurgitation (mean age 50+/-14 years) were studied using a micromanometer LV catheter to obtain LV pressures and radionuclide ventriculography to obtain LV volumes during multiple loading conditions and right atrial pacing. These 45 patients were subgrouped according to their LV contractility (Ees) and ejection fraction values. Group I consisted of 24 patients with a normal Ees. Group IIa consisted of 10 patients with impaired Ees values (Ees <1.00 mm Hg/mL) but normal LV ejection fractions; Group IIb consisted of 11 patients with impaired contractility and reduced LV ejection fractions. The left ventricular-arterial coupling ratio, Ees/Ea, where Ea was calculated by dividing the LV end-systolic pressure by LV stroke volume, averaged 1.60+/-0.91 in Group I. It decreased to 0.91+/-0.27 in Group IIa (P<0.05 versus Group I), and it decreased further in Group IIb to 0.43+/-0.24 (P<0.001 versus Groups I and IIa). The LV ejection fractions were inversely related to the Ea values in both the normal and impaired contractility groups (r=-0.48, P<0.05 and r=-0.56, P<0.01, respectively), although the slopes of these relationships differed (P<0.05). The average LV work was maximal in Group IIa when the left ventricular-arterial coupling ratio was near 1.0 because of a significant decrease in total arterial elastance (P<0.01 versus Group I). In contrast, the decrease in the left ventricular-arterial coupling ratio in Group IIb was caused by an increase in total arterial elastance, effectively double loading the LV, contributing to a decrease in LV pump efficiency (P<0.01 versus Group IIa and P<0.001 versus Group I). Vascular adaptation may be heterogeneous in patients with chronic aortic regurgitation. In some, total arterial elastance decreases to maximize LV work and maintain LV performance, whereas in others, it increases, thereby double loading the LV, contributing to afterload excess and a deterioration in LV performance that is most prominent in those with impaired contractility.

Left ventricular pump efficiency in long-term mitral regurgitation assessed by means of left ventricular-arterial coupling relations

The left ventricular-arterial coupling relationship was used in patients with long-term mitral regurgitation to test the hypothesis that the low impedance left atrial contribution to left ventricular ejection obscures an impairment in left ventricular-arterial coupling and forward left ventricular pump efficiency. Twenty-two control patients and 26 patients with long-term mitral regurgitation were studied. Micromanometer left ventricular pressures and radionuclide angiograms for left ventricular volumes were acquired over a range of loading conditions. Left ventricular-arterial coupling was assessed by the ratio of left ventricular chamber elastance, E es, to total arterial elastance, E a. Forward left ventricular pump efficiency was calculated as the ratio of forward left ventricular stroke work to the corresponding pressure-volume area. There was a progressive decrease in E es in the patients with long-term mitral regurgitation ( p < 0.001), but there was no significant difference in E a in comparison to the control patients. Consequently, E es E a demonstrated a progressive decrease ( p < 0.001). Although the efficiency of performing total left ventricular stroke work was only reduced when left ventricular contractile function was severely impaired ( p < 0.001), there was a progressive reduction in left ventricular pump efficiency for performing forward left ventricular stroke work in the patients with long-term mitral regurgitation ( p < 0.001). Further, normalized left ventricular stroke work was reduced for any left ventricular-arterial coupling ratio in the patients with long-term mitral regurgitation compared with the control patients. These data indicate that despite the outward evidence for normal left ventricular ejection in patients with long-term mitral regurgitation, a progressive deterioration in left ventricular contractile state leads to impaired left ventricular-arterial coupling and to an impairment in the efficiency of performing forward left ventricular stroke work. Once the left ventricle begins to dilate in patients with long-term mitral regurgitation, the progressive deterioration in left ventricular-arterial coupling and pump efficiency suggests that an earlier consideration of mitral valve surgery may be warranted to preserve left ventricular contractile function.

Annuloplasty with flexible or rigid ring does not alter left ventricular systolic performance, energetics, or ventricular-arterial coupling in conscious, closed-chest dogs

Eighteen dogs were randomly chosen to undergo mitral annuloplasty with either a Carpentier-Edwards rigid ring (n = 6 in each group) or a Duran-Medtronic flexible ring or to undergo a sham procedure with an operation, but no ring. Tantalum markers were inserted to measure left ventricular volume and geometry. After 1 and 6 weeks, biplane videofluoroscopic images were obtained during steady-state conditions and during vena caval occlusion. Global and regional systolic function was assessed with load-insensitive indexes. Comparison of all three groups and both times (1 and 6 weeks) showed no significant differences among the three groups in global or regional (basal, equatorial, and apical) left ventricular systolic performance. Furthermore, neither type of annuloplasty ring significantly affected left ventricular pump efficiency, ventricular-arterial coupling ratio, or systolic circumferential contraction and rotation of the basal left ventricular sites.