scholarly journals Directional Representations of 4D Echocardiography for Temporal Quantification of LV Volume

Author(s):  
Elsa Angelini ◽  
Andrew Laine ◽  
Shin Takuma ◽  
Shunichi Homma
1997 ◽  
Vol 36 (08) ◽  
pp. 259-264
Author(s):  
N. Topuzović

Summary Aim: The purpose of this study was to investigate the changes in blood activity during rest, exercise and recovery, and to assess its influence on left ventricular (LV) volume determination using the count-based method requiring blood sampling. Methods: Forty-four patients underwent rest-stress radionuclide ventriculography; Tc-99m-human serum albumin was used in 13 patients (Group I), red blood cells was labeled using Tc-99m in 17 patients (Group II) in vivo, and in 14 patients (Group III) by modified in vivo/in vitro method. LV volumes were determined by a count-based method using corrected count rate in blood samples obtained during rest, peak exercise and after recovery. Results: In group I at stress, the blood activity decreased by 12.6 ± 5.4%, p <0.05, as compared to the rest level, and increased by 25.1 ± 6.4%, p <0.001, and 12.8 ± 4.5%, p <0.05, above the resting level in group II and III, respectively. This had profound effects on LV volume determinations if only one rest blood aliquot was used: during exercise, the LV volumes significantly decreased by 22.1 ± 9.6%, p <0.05, in group I, whereas in groups II and III it was significantly overestimated by 32.1 ± 10.3%, p <0.001, and 10.7 ± 6.4%, p <0.05, respectively. The changes in blood activity between stress and recovery were not significantly different for any of the groups. Conclusion: The use of only a single blood sample as volume aliquot at rest in rest-stress studies leads to erroneous estimation of cardiac volumes due to significant changes in blood radioactivity during exercise and recovery.


Author(s):  
Hannah Sjögren ◽  
Barbro Kjellström ◽  
Anna Bredfelt ◽  
Katarina Steding-Ehrenborg ◽  
Göran Rådegran ◽  
...  

AbstractTo evaluate the association between impaired left ventricular (LV) longitudinal function and LV underfilling in patients with pulmonary arterial hypertension (PAH). Thirty-nine patients with PAH and 18 age and sex-matched healthy controls were included. LV volume and left atrial volume (LAV) were delineated in short-axis cardiac magnetic resonance (CMR) cine images. LV longitudinal function was assessed from atrio-ventricular plane displacement (AVPD) and global longitudinal strain (GLS) was assessed using feature tracking in three long-axis views. LV filling was assessed by LAV and by pulmonary artery wedge pressure (PAWP) using right heart catheterisation. Patients had a smaller LAV, LV volume and stroke volume as well as a lower LV-AVPD and LV-GLS than controls. PAWP was 6 [IQR 5––9] mmHg in patients. LV ejection fraction did not differ between groups. LV stroke volume correlated with LV-AVPD (r = 0.445, p = .001), LV-GLS (r = − 0.549, p < 0.0001) and LAVmax (r = .585, p < 0.0001). Furthermore, LV-AVPD (r = .598) and LV-GLS (r = − 0.675) correlated with LAVmax (p < 0.0001 for both). Neither LV-AVPD, LV-GLS, LAVmax nor stroke volume correlated with PAWP. Impaired LV longitudinal function was associated with low stroke volume, low PAWP and a small LAV in PAH. Small stroke volumes and LAV, together with normal LA pressure, implies that the mechanism causing reduced LV longitudinal function is underfilling rather than an intrinsic LV dysfunction in PAH.


1988 ◽  
Vol 64 (6) ◽  
pp. 2552-2557 ◽  
Author(s):  
A. Roy ◽  
M. Doyon ◽  
J. G. Dumesnil ◽  
J. Jobin ◽  
F. Landry

There are still disagreements concerning the adaptation of cardiac structures in relation to different training stimuli. To eliminate some of the variance due to individual differences in body surface area, we utilized a new approach based on the calculation of the percentages of each individual's normal predicted values (%NPV). We studied 46 strength (S, bodybuilders) and 57 endurance (E, runners) athletes. Left ventricular (LV) mass was 143.8 +/- 21.9 %NPV (mean +/- SD) in E vs. 134.3 +/- 23.4 %NPV in S (P less than 0.05), and LV volume was 131.0 +/- 24.0 %NPV in E vs. 120.0 +/- 25.5 %NPV in S (P less than 0.05). Moreover, the LV wall thickness-to-radius ratio did not differ from normal values in either group. From these data we conclude that 1) cardiac modifications are greater in E than S, 2) the predominant stimulus is a volume overload type in both groups, and 3) concentric LV hypertrophy may not be as prevalent in S as previously suggested.


2001 ◽  
Vol 280 (2) ◽  
pp. H674-H683 ◽  
Author(s):  
Gregory L. Brower ◽  
Joseph S. Janicki

We previously reported an approximately 50% incidence of rats with symptoms of congestive heart failure (CHF) at 8 wk postinfrarenal aorto-caval fistula. However, it was not clear whether compensatory ventricular remodeling could continue beyond 8 wk or whether the remaining animals would have developed CHF or died. Therefore, the intent of this study was to complete the characterization of this model of sustained volume overload by determining the morbidity and mortality and the temporal response of left ventricular (LV) remodeling and function beyond 8 wk. The findings demonstrate an upper limit to LV hypertrophy and substantial increases in LV volume and compliance, matrix metalloproteinase activity, and collagen volume fraction associated with the development of CHF. There was an 80% incidence of morbidity and mortality following 21 wk of chronic volume overload. These findings indicate that the development of CHF is triggered by marked ventricular dilatation and increased compliance occurring once the myocardial hypertrophic response is exhausted.


1998 ◽  
Vol 275 (3) ◽  
pp. H1062-H1069 ◽  
Author(s):  
Otto A. Smiseth ◽  
Kjetil Steine ◽  
Gunnar Sandbæk ◽  
Marie Stugaard ◽  
Tor Ø. Gjølberg

This study investigates mechanisms of left ventricular (LV) intracavitary flow during early, rapid filling. In eight coronary artery disease patients with normal LV ejection fraction we recorded simultaneous LV apical and outflow tract pressures and intraventricular flow velocities by color M-mode Doppler echocardiography. In five anesthetized dogs we also recorded left atrial pressure and LV volume by sonomicrometry. In patients, as the early diastolic mitral-to-apical filling wave arrived at the apex, we observed an apex-outflow tract pressure gradient of 3.5 ± 0.3 mmHg (mean ± SE). This pressure gradient correlated with peak early apex-to-outflow tract flow velocity ( r = 0.75, P < 0.05). The gradient was reproduced in the dog model and decreased from 3.1 ± 0.3 to 1.7 ± 0.5 mmHg ( P < 0.05) with caval constriction and increased to 4.2 ± 0.5 mmHg ( P < 0.001) with volume loading. The pressure gradient correlated with peak early transmitral flow (expressed as time derivative of LV volume; r = 0.95) and stroke volume ( r = 0.97). In conclusion, arrival of the early LV filling wave at the apex was associated with a substantial pressure gradient between apex and outflow tract. The pressure gradient was sensitive to changes in preload and correlated strongly with peak early transmitral flow. The significance of this gradient for intraventricular flow propagation in the normal and the diseased heart remains to be determined.


2015 ◽  
Vol 137 (8) ◽  
Author(s):  
Longling Fan ◽  
Jing Yao ◽  
Chun Yang ◽  
Dalin Tang ◽  
Di Xu

Methods to quantify ventricle material properties noninvasively using in vivo data are of great important in clinical applications. An ultrasound echo-based computational modeling approach was proposed to quantify left ventricle (LV) material properties, curvature, and stress/strain conditions and find differences between normal LV and LV with infarct. Echo image data were acquired from five patients with myocardial infarction (I-Group) and five healthy volunteers as control (H-Group). Finite element models were constructed to obtain ventricle stress and strain conditions. Material stiffening and softening were used to model ventricle active contraction and relaxation. Systolic and diastolic material parameter values were obtained by adjusting the models to match echo volume data. Young's modulus (YM) value was obtained for each material stress–strain curve for easy comparison. LV wall thickness, circumferential and longitudinal curvatures (C- and L-curvature), material parameter values, and stress/strain values were recorded for analysis. Using the mean value of H-Group as the base value, at end-diastole, I-Group mean YM value for the fiber direction stress–strain curve was 54% stiffer than that of H-Group (136.24 kPa versus 88.68 kPa). At end-systole, the mean YM values from the two groups were similar (175.84 kPa versus 200.2 kPa). More interestingly, H-Group end-systole mean YM was 126% higher that its end-diastole value, while I-Group end-systole mean YM was only 29% higher that its end-diastole value. This indicated that H-Group had much greater systole–diastole material stiffness variations. At beginning-of-ejection (BE), LV ejection fraction (LVEF) showed positive correlation with C-curvature, stress, and strain, and negative correlation with LV volume, respectively. At beginning-of-filling (BF), LVEF showed positive correlation with C-curvature and strain, but negative correlation with stress and LV volume, respectively. Using averaged values of two groups at BE, I-Group stress, strain, and wall thickness were 32%, 29%, and 18% lower (thinner), respectively, compared to those of H-Group. L-curvature from I-Group was 61% higher than that from H-Group. Difference in C-curvature between the two groups was not statistically significant. Our results indicated that our modeling approach has the potential to determine in vivo ventricle material properties, which in turn could lead to methods to infer presence of infarct from LV contractibility and material stiffness variations. Quantitative differences in LV volume, curvatures, stress, strain, and wall thickness between the two groups were provided.


2011 ◽  
Vol 301 (5) ◽  
pp. H2154-H2160 ◽  
Author(s):  
Munetaka Shibata ◽  
Daisuke Takeshita ◽  
Koji Obata ◽  
Shinichi Mitsuyama ◽  
Haruo Ito ◽  
...  

Impaired Ca2+ handling is one of the main characteristics in heart failure patients. Recently, we reported abnormal expressions of Ca2+-handling proteins in isoproterenol (ISO)-induced hypertrophied rat hearts. On the other hand, Na+/H+ exchanger (NHE)-1 inhibitor has been demonstrated to exert beneficial effects in ischemic-reperfusion injury and in the development of cardiac remodeling. The aims of the present study are to investigate the role of NHE-1 on Ca2+ handling and development of cardiac hypertrophy in ISO-infused rats. Male Wistar rats were randomly divided into vehicle [control (CTL)] and ISO groups without or with pretreatment with a selective NHE-1 inhibitor, BIIB-723. ISO infusion for 1 wk significantly increased the ratios of heart to body weight and left ventricle (LV) to body weight and collagen accumulation. All of these increases were antagonized by coadministration with BIIB-723. The ISO-induced significant increase in LV wall thickness was suppressed significantly ( P < 0.05) by BIIB-723. ISO-induced decreases in cardiac stroke volume and a total mechanical energy per beat index, systolic pressure-volume area at midrange LV volume, were normalized by BIIB-723. The markedly higher expression of NHE-1 protein in the ISO group than that in CTL group was suppressed ( P < 0.05) by BIIB-723. Surprisingly, ISO induced downregulation of the important Ca2+-handling protein sarcoplasmic reticulum Ca2+-ATPase 2a, the expression of which was also normalized by BIIB-723 without changes in phosphorylated phospholamban (PLB)/PLB expression. We conclude that NHE-1 contributes to ISO-induced abnormal Ca2+ handling associated with cardiac hypertrophy. Inhibition of NHE-1 ameliorates cardiac Ca2+-handling impairment and prevents the development of cardiac dysfunction in ISO-infused rats.


2020 ◽  
Vol 35 (2) ◽  
pp. 98-105
Author(s):  
A. I. Chernyavina ◽  
N. A. Koziolova

Objective. To determine the risk of developing chronic heart failure (CHF) in patients with hypertension (HTN) depending on the actual arterial stiffness.Material and Methods. The study included 175 patients with HTN without a verified diagnosis of heart failure. The average age was 48.5 ± 6.8 years. Patients underwent general clinical examination, volume sphygmoplethysmography assessments of cardio-ankle vascular index (CAVI), echocardiography study (left ventricular (LV) ejection fraction, LV diastolic function, LV myocardial mass index, indexed LV volume by echocardiography), and tests for serum N-terminal pro-B-type natriuretic peptide (NT-proBNP). Patients were divided into two groups depending on CAVI. Group 1 included 141 (80.6%) patients with CAVI < 9; group 2 included 34 (19.4%) patients with CAVI > 9.Results. In patients of group 1, the level of NT-proBNP was 0.008 [0.006; 5.770], which was significantly lower than the corresponding value in group 2, where the level of NT-proBNP was 13.08 [0.01; 350.65] ng/mL (p = 0.041). Indicators of odds ratio (OR) and relative risk (RR) were also significant. The chance of developing CHF with CAVI > 9 increased by almost 7 times (OR = 6.9; 95% CI = 2.8–16.8), and OR of CHF onset was 4.1 (95% CI = 2.2–7.6). Sensitivity and specificity rates were 55.9% and 84.4%, respectively. Correlation analysis revealed a medium degree of dependence and direct relationships between NT-proBNP level and CAVI values (r = 0.35; p <0.05).Conclusion. Serum level of NT-proBNP depended on the actual arterial stiffness. Patients with CAVI > 9 indicative of an increase in true arterial stiffness had a greater risk of developing heart failure assessed based on the level of NT-proBNP in the blood. Further studies are required to assess the effects of arterial stiffness, registered within the intermediate values of CAVI index, on the risk of heart failure onset. 


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 26-27
Author(s):  
Alessia Pepe ◽  
Nicola Martini ◽  
Antonio De Luca ◽  
Vincenzo Positano ◽  
Laura Pistoia ◽  
...  

Background.Cardiovascular magnetic resonance (CMR) is the only available technique for the non-invasive quantification of MIO. The native T1 mapping has recently been proposed as an alternative to the universally adopted T2* technique, due to the higher sensitivity for detection of changes associated with mild or early iron overload. Objective.To study the association between T1 values and left ventricular (LV) function in thalassemia major (TM) and to evaluate for the first time if T1 measurements quantifying MIO are influenced by macroscopic myocardial fibrosis. Methods.146 TM patients (87 females, 38.7±11.1 years) consecutively enrolled in the Extension-Myocardial Iron Overload in Thalassemia Network underwent CMR. Native T1 values were obtained by Modified Look-Locker Inversion recovery (MOLLI) sequence in all 16 myocardial segments and the global value was the mean. LV function parameters were quantified by cine images. Late gadolinium enhancement (LGE) technique was used to detect macroscopic myocardial fibrosis. Results.No correlation was detected between global heart T1 values and LV volume indexes, LV mass index, or LV ejection fraction. Foourteen (9.6%) patients had an abnormal LV motion (13 hypokinesia and 1 dyskinesia) and they showed significantly lower global heart T1 values than patients without LV motion abnormalities (883.8±139.7 ms vs 959.0±91.3 ms; P=0.049). LGE images were acquired in 88 patients (60.3%) and macroscopic myocardial fibrosis was detected in 36 patients (40.9%). The 72.2% of patients had two or more foci of fibrosis. Patients with macroscopic myocardial fibrosis had significantly lower global heart T1 values (921.3±100.3 ms vs 974.5±72.7 ms; P=0.027) (Figure 1A). Data about the LGE was present for 1408 segments (88 patients x 16 segments) and 105 (7.5%) were positive. Segments with LGE had significantly lower T1 values than segments LGE-negative (905.6±110.6 ms vs 956.9±103.8 ms; P&lt;0.0001) (Figure 1B). Conclusion.No correlation between T1 values and LV function parameters was detected, probably because the majority of the patients had normal or mild abnormal LV parameters. TM patients with macroscopic myocardial fibrosis showed significantly lower T1 values suggesting that T1 measurements for quantifying MIO are not influenced by macroscopic myocardial fibrosis and an association between myocardial iron and macroscopic fibrosis, previously detected only in pediatric TM patients. Figure Disclosures Pepe: Chiesi Farmaceutici S.p.A.:Other: no profit support and speakers' honoraria;Bayer:Other: no profit support;ApoPharma Inc.:Other: no profit support.Pistoia:Chiesi Farmaceutici S.p.A.:Other: speakers' honoraria.Meloni:Chiesi Farmaceutici S.p.A.:Other: speakers' honoraria.


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