scholarly journals Characterization of Left Ventricle Main Flow Axis Line Using Echodynamography

2021 ◽  
Vol 11 (2) ◽  
pp. 153
Author(s):  
Sri Oktamuliani ◽  
Kaoru Hasegawa ◽  
Tadanori Minagawa ◽  
Yoshifumi Saijo

<span>Left ventricular (LV) blood flow analysis may play an essential role in evaluating cardiac function besides the classical analysis of wall motion. Echodynamography is an imaging method in which two-dimensional (2D) blood flow vectors are deduced by blood flow information obtained by color Doppler echocardiography. Echodynamography has provided useful information on the blood flow pattern in healthy and abnormal LV. The main flow axis line (MFAL) is defined as a maximum velocity magnitude of blood flow from the LV's apex to LV's outflow, which is a new hemodynamic parameter for cardiac assessment. The present study's objective is to compare blood flow patterns between healthy and abnormal LV by investigating the MFAL and its correlation to vorticity and velocity distribution on MFAL. This study enrolled 12 participants, four healthy volunteers, and eight abnormal patients. Echodynamography analyzed frame by frame Doppler image of apical three-chamber views. The results showed MFAL superimposed on vorticity mapping during ventricular ejection and MFAL path coincide with the irrotational flow of zero vorticity path, ω = 0. A significant difference was observed in the velocity distribution curve (VDC) on the MFAL during early, mid, and late systoles compared to healthy and abnormal LV. VDC showed the linear upward curve and the highest velocity magnitude during the early systole phase in healthy LV. In contrast with abnormal LV, VDC showed the downward convex curve and the highest velocity magnitude during mid systole phase. Furthermore, the gradient and slope angle of the VDC on the MFAL was compared. The result showed that the maximum gradient and slope angle were not significantly different between healthy and abnormal LV. In conclusion, the study of MFAL and the correlation to vorticity based on the Echodynamography computational program provides additional insights for representing a cardiac function, and thus, the clinical implications of MFAL warrant further investigation.</span>

2013 ◽  
Vol 118 (4) ◽  
pp. 796-808 ◽  
Author(s):  
Pornswan Ngamprasertwong ◽  
Erik C. Michelfelder ◽  
Shahriar Arbabi ◽  
Yun Suk Choi ◽  
Christopher Statile ◽  
...  

Abstract Background: Use of high-dose inhalational anesthesia during open fetal surgery may induce maternal–fetal hemodynamic instability and fetal myocardial depression. The authors’ preliminary human retrospective study demonstrated less fetal bradycardia and left ventricular systolic dysfunction with lower dose desflurane supplemented with propofol and remifentanil IV anesthesia (SIVA). In this animal study, the authors compare maternal–fetal effects of high-dose desflurane anesthesia (HD-DES) and SIVA. Methods: Of 26 instrumented midgestational ewes, data from 11 animals exposed to both SIVA and HD-DES in random sequences and six animals exposed to HD-DES while maternal normotension was maintained were analyzed. Maternal electroencephalography was used to guide comparable depths of anesthesia in both techniques. Hemodynamic parameters, blood gas, and fetal cardiac function from echocardiography were recorded. Results: Compared with SIVA, HD-DES resulted in significant maternal hypotension (mean arterial pressure difference, 19.53 mmHg; 95% CI, 17.6–21.4; P &lt; 0.0001), fetal acidosis (pH 7.11 vs. 7.24 at 150 min, P &lt; 0.001), and decreased uterine blood flow. In the HD-DES group with maternal normotension, uterine blood flow still declined and fetal acidosis persisted, with no statistically significant difference from the group exposed to HD-DES that had maternal hypotension. There was no statistically significant difference in fetal cardiac function. Conclusion: In sheep, SIVA affects maternal hemodynamics less and provides better fetal acid/base status than high-dose desflurane. Fetal echocardiography did not reflect myocardial dysfunction in this model.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
N Landler ◽  
S Bro ◽  
B Feldt-Rasmussen ◽  
D Hansen ◽  
A.L Kamper ◽  
...  

Abstract Background The cardiovascular mortality of patients with chronic kidney disease (CKD) is 2–10 times higher than in the average population. Purpose To estimate the prevalence of abnormal cardiac function or structure across the stages CKD 1 to 5nonD. Method Prospective cohort study. Patients with CKD stage 1 to 5 not on dialysis, aged 30 to 75 (n=875) and age-/sex-matched controls (n=173) were enrolled consecutively. All participants underwent a health questionnaire, ECG, morphometric and blood pressure measurements. Blood and urine were analyzed. Echocardiography was performed. Left ventricle (LV) hypertrophy, dilatation, diastolic and systolic dysfunction were defined according to current ESC guidelines. Results 63% of participants were men. Mean age was 58 years (SD 12.6 years). Mean eGFR was 46.7 mL/min/1,73 m (SD 25.8) for patients and 82.3 mL/min/1,73 m (SD 13.4) for controls. The prevalence of elevated blood pressure at physical exam was 89% in patients vs. 53% in controls. Patients were more often smokers and obese. Left ventricular mass index (LVMI) was slightly, albeit insignificantly elevated at CKD stages 1 & 2 vs. in kontrols: 3.1 g/m2, CI: −0.4 to 6.75, p-value 0.08. There was no significant difference in LV-dilatation between patients and controls. Decreasing diastolic and systolic function was observed at CKD stage 3a and later: LVEF decreased 0.95% (CI: −1.5 to −0.2), GLS increased 0.5 (CI: 0.3 to 0.8), and OR for diastolic dysfunction increased 3.2 (CI 1.4 to 7.3) pr. increment CKD stage group. Conclusion In accordance to previous studies, we observe in the CPHCKD cohort study signs of early increase of LVMI in patients with CKD stage 1 & 2. Significant decline in systolic and diastolic cardiac function is apparent already at stage 3 CKD. Figure 1. Estimated GFR vs. GLS & histogram of GLS Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): The Capital Region of Denmark


2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Toshinori Aoyagi ◽  
Takashi Matsui

The risk of heart failure following myocardial infarction is higher in diabetic patients than nondiabetic patients. The mammalian target of rapamycin (mTOR), a key downstream molecule of insulin-phosphoinositide 3-kinase (PI3K)-Akt signaling pathway, plays an important role in cardioprotection. However, the role of cardiac mTOR in ischemic injury in metabolic syndrome has not been well defined. To address this question, we studied the effect of overexpressing cardiac mTOR on cardiac function following ischemia/reperfusion (I/R) in mice with high-fat diet (HFD)-induced obesity. In this study, we used transgenic mice with cardiac-specific overexpression of mTOR (mTOR-Tg) as reported previously. mTOR-Tg and WT mice at 6 weeks old were fed HFD (60% fat by calories) ad libitum for 14 weeks. Control mTOR-Tg and WT mice were fed a normal chow diet (NCD). At 14 weeks after HFD, glucose and insulin tolerance tests demonstrated that HFD generated glucose intolerance and insulin resistance in both mTOR-Tg (n=20) and WT (n=24) mice. Body weight (BW) and heart weight (HW) were significantly higher in HFD mice than SCD mice (p<0.001 for BW in both strains; p<0.001 and p<0.01 for HW/tibia length, WT and mTOR-Tg, respectively) but there was no difference in BW or HW between HFD-mTOR-Tg and HFD-WT mice. Hearts from all four groups were subjected to global I/R (20 min ischemia, 40 min reperfusion) in the ex vivo Langendorff perfusion model. Baseline left ventricular developed pressure (LVDP) was higher in HFD mice than NCD mice in both strains [185.8 ± 10.7 vs. 143.6 ± 5.0 mmHg, HFD-WT (n=11) vs. NCD-WT (n=10) mice, p<0.01; 178.6 ± 10.1 vs. 135.0 ± 6.3, HFD-mTOR-Tg (n=8) vs. NCD-mTOR-Tg (n=11) mice, p<0.01]. Functional recovery after I/R was significantly lower in HFD-WT mice than NCD-WT mice (percent recovery of LVDP, 15.3 ± 5.4 vs. 44.6 ± 6.3 %, HFD-WT vs. NCD-WT mice, p<0.01). Intriguingly, there was no significant difference in LVDP recovery between HFD-mTOR-Tg and NCD-mTOR-Tg mice (36.5±10.8 vs. 58.8±6.0 %, HFD-mTOR-Tg vs. NCD-mTOR-Tg mice, n.s.). These findings suggest that cardiac mTOR is sufficient to substantially limit the metabolic syndrome-induced cardiac dysfunction following I/R in a mouse model of obesity with glucose intolerance and insulin resistance.


1980 ◽  
Vol 49 (3) ◽  
pp. 444-449 ◽  
Author(s):  
R. J. Barnard ◽  
H. W. Duncan ◽  
K. M. Baldwin ◽  
G. Grimditch ◽  
G. D. Buckberg

Five instrumented and eight noninstrumented dogs were progressively trained for 12-18 wk on a motor-driven treadmill. Data were compared with 14 instrumented and 8 noninstrumented control dogs. Gastrocnemius malate dehydrogenase activity was significantly increased in the trained dogs (887 +/- 75 vs. 667 +/- 68 mumol . g-1 . min-1). The trained dogs also showed significant increases in maximum work capacity, cardiac output (7.1 +/- 0.5 vs. 9.1 +/- 0.7 1/min), stroke volume (25.9 +/- 2.0 vs. 32.0 +/- 2.0 ml/beat), and left ventricular (LV) positive dP/dtmax (9,242 +/- 405 vs. 11,125 +/- 550 Torr/s). Negative dP/dtmax was not significantly different. Peak LV systolic pressure increased with exercise, but there was no significant difference between the trained and control dogs. LV end-diastolic pressure did not change with exercise and was the same in both groups. Tension-time index was lower in the trained dogs at rest and submaximum exercise (9.7 km/h, 10%) but was not different at maximum exercise. Diastolic pressure-time index was significantly higher in the trained dogs at rest and during submaximum exercise but was not different at maximum exercise. LV coronary blood flow was significantly reduced at rest (84 +/- 4 vs. 67 +/- 6 mo . min-1 . 100 g-1) and during submaximum exercise (288 +/- 24 vs. 252 +/- 8 ml . min-1 . 100 g-1). During maximum exercise flow was not significantly different (401 +/- 22 vs. 432 +/- 11 ml . min-1 . 100 g-1) between the control and trained groups. The maximum potential for subendocardial flow was unchanged with training despite the development of mild hypertrophy.


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 2034-2034
Author(s):  
Min-Hui Cui ◽  
Craig A Branch ◽  
Rhoda Elison Hirsch

Abstract Hemoglobin E (HbE) is the most common hemoglobin mutation world-wide. EE individuals exhibit a mild anemia as do those with β-thalassemia trait. A paradox arises with the combination of two relatively benign genes in HbE/β-thalassemia (HbE/β-thal) giving rise to highly morbid symptoms, anemia, growth retardation, developmental retardation, thalassemic bone type development, chronic leg ulcers (for a review, S Fucharoen and DJ Weatherall 2012) and often early mortality arising from cardiac failure (N Olivieri, Z Pakbaz et al. 2011). One approach to understanding the characteristics of HbE and this paradox was to generate a transgenic mouse model, expressing solely human HbE. This HbE mouse model exhibits a mild oxidative stress that parallels that observed in human EE individuals (QY Chen, EE Bouhassira et al. 2004, QY Chen, ME Fabry et al. 2012). These transgenic mice also exhibit mild cardiac dysfunction with depressed left ventricular contraction. We present here the first evidence of a significant increase in cerebral blood flow in the full knockout HbE (HbEKO) transgenic mouse model expressing solely human HbE compared to both the HbE+HbF (γ, gamma)-globin transgenic mouse, and the normal background C57 mouse. Cerebral blood flow is assessed non-invasively by MRI imaging. All protocols were approved by the Albert Einstein Institutional Animal Care and Use Committee. Comparing the HbEKO mouse (without human γ globin) to the C57 normal background mouse, a significant increase of over 20% in thalamus cerebral blood flow at baseline is observed (p=0.008). There is also an approximate 18% reduction in thalamus cerebral blood flow comparing HbE low γ mice to the full HbEKO (no γ) (p=0.011). Concomitant with these observations, no significant difference is observed comparing these low gamma HbE mice to the normal C57 background mouse (p=0.384). The goodness of the data is also seen in the relatively small variation in cerebral blood flow amongst the individual mice in each subset. These findings are of particular relevance to reports of neurologic symptoms, intracerebral hemorrhage, and brain infarct in HbE/β-thal patients (V Wong, YL Yu et al. 1990, S Das, S Dubey et al. 2019). In conclusion, these results suggest a direct role of HbE RBC initiating altered cerebral blood flow that when further complexed with β-thal could lead to intracerebral hemorrhage and other cerebral pathophysiology. The finding that the HbEKO mice with high HbF are not significantly different in cerebral blood flow from C57 mice may lend further support to therapeutic approaches enhancing the production of HbF in severe hemoglobinopathies, such as in sickle cell anemia, HbE/β-thal, and β-thal individuals. Disclosures No relevant conflicts of interest to declare.


2021 ◽  
Vol 5 (2) ◽  
Author(s):  
Huailing Su ◽  
Bin Li ◽  
Zhisheng Jia

Objective: To investigate the effect of metoprolol on cardiac function and prognosis in patients with dilated cardiomyopathy. Methods: 100 patients with dilated cardiomyopathy treated in our hospital from January 2018 to December 2019 were randomly divided into control group (n = 50) and observation group (n = 50). The control group was treated with conventional methods, and the observation group was treated with conventional methods and metoprolol for 6 months. The cardiac function [left ventricular ejection fraction (LVEF), stroke volume (SV), cardiac output (CO)] and prognosis [Glasgow Outcome Scale (GOS) score] of the two groups before and at the end of 6 months of intervention were compared, and the incidence of adverse reactions of the two groups were compared. Results: After 6 months of treatment, the levels of LVEF, SV and CO in the two groups were higher than before treatment, and the comparison level between the observation group and the control group was higher, the difference was statistically significant (P  < 0.05);After 6 months of treatment, the GOS score of the observation group was higher than that of the control group, and the difference was statistically significant (P < 0.05);There was no significant difference in the total incidence of adverse reactions between the two groups (P > 0.05). Conclusion:  Metoprolol can improve the cardiac function and prognosis of patients with dilated cardiomyopathy, without increasing the incidence of adverse reactions.


2021 ◽  
Vol 10 (5) ◽  
Author(s):  
Tassia S. R. da Costa ◽  
Ursula Urias ◽  
Marcelo V. Negrao ◽  
Camila P. Jordão ◽  
Clévia S. Passos ◽  
...  

Background Patients treated for breast cancer have a high incidence of cardiovascular complications. In this study, we evaluated the impact of breast cancer on cardiac function and cardiomyocyte Ca 2+ ‐handling protein expression. We also investigated whether exercise training (ET) would prevent these potential alterations. Methods and Results Transgenic mice with spontaneous breast cancer (mouse mammary tumor virus–polyomavirus middle T antigen [MMTV‐PyMT+], n=15) and littermate mice with no cancer (MMTV‐PyMT−, n=14) were studied. For the ET analysis, MMTV‐PyMT+ were divided into sedentary (n=10) and exercise‐trained (n=12) groups. Cardiac function was evaluated by echocardiography with speckle‐tracking imaging. Exercise tolerance test was conducted on a treadmill. Both studies were performed when the tumor became palpable and when it reached 1 cm 3 . After euthanasia, Ca 2+ ‐handling protein expression (Western blot) was evaluated. Exercise capacity was reduced in MMTV‐PyMT+ compared with MMTV‐PyMT− ( P interaction =0.031). Longitudinal strain ( P group <0.001) and strain rate ( P group =0.030) were impaired. Cardiomyocyte phospholamban was increased ( P =0.011), whereas phospho‐phospholamban and sodium/calcium exchanger were decreased ( P =0.038 and P =0.017, respectively) in MMTV‐PyMT+. No significant difference in sarcoplasmic or endoplasmic reticulum calcium 2 ATPase (SERCA2a) was found. SERCA2a/phospholamban ratio was reduced ( P =0.007). ET was not associated with increased exercise capacity. ET decreased left ventricular end‐systolic diameter ( P group =0.038) and end‐diastolic volume ( P group =0.026). Other morphological and functional cardiac parameters were not improved by ET in MMTV‐PyMT+. ET did not improve cardiomyocyte Ca 2+ ‐handling protein expression. Conclusions Breast cancer is associated with decreased exercise capacity and subclinical left ventricular dysfunction in MMTV‐PyMT+, which is at least partly associated with dysregulation of cardiomyocyte Ca 2+ handling. ET did not prevent or reverse these changes.


1983 ◽  
Vol 64 (6) ◽  
pp. 573-580 ◽  
Author(s):  
Allen I. Arieff ◽  
Edward W. Gertz ◽  
Robert Park ◽  
Will Leach ◽  
Virginia C. Lazarowitz

1. Lactic acidosis is a clinical syndrome characterized by metabolic acidaemia (pH < 7.25) and hyperlactaemia (lactate >5 mmol/l). Many patients with type B lactic acidosis have no evidence of tissue hypoxia or myocardial dysfunction when first evaluated. Although it is considered that cardiac dysfunction is secondary to the systemic effects of lactic acidosis, the reverse may sometimes be true. To evaluate this possibility, studies were carried out in 43 dogs consisting of a control group and three groups which had hyperlactataemia and metabolic acidaemia related to either: (1) phenformin infusion; (2) hepatectomy; (3) lactic acid infusion. Serial studies of cardiac function, as well as measurements of GFR (glomerular filtration rate) and hepatic portal vein (HPV) blood flow, were carried out. 2. in dogs infused with phenformin for 99 min, the arterial pH, lactate, bicarbonate, heart rate and mean blood pressure (BP) were normal. However, there was significant deterioration (P < 0.01) in several indices of cardiac function, including the peak positive dP/dt, cardiac output, LVEDP (left ventricular end-diastolic pressure) and percentage extraction of oxygen and lactate by the heart. After 3 h of phenformin, the blood lactate exceeded 5 mmol/l and there were further significant decrements (P < 0.01) in cardiac output, LVEDP and dP/dt, as well as BP and heart rate. in dogs subjected to hepatectomy, the decrement in cardiac output was similar to that with phenformin infusion. However, in animals infused with lactic acid, despite a similar blood pH and lactate, cardiac output was unaffected. Although percentage myocardial oxygen extraction declined in phenformin-infused animals, there was a concomitant increase in coronary sinus blood flow such that myocardial oxygen utilization was probably unaltered. 3. Thus, in certain types of experimental type B lactic acidosis, myocardial dysfunction may be a primary event, with other associated systemic manifestations being secondary.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dong-Hua Liu ◽  
Yi-Le Ning ◽  
Yan-Yan Lei ◽  
Jing Chen ◽  
Yan-Yan Liu ◽  
...  

AbstractLevosimendan and dobutamine are extensively used to treat sepsis-associated cardiovascular failure in ICU. Nevertheless, the role and mechanism of levosimendan in patients with sepsis-induced cardiomyopathy remains unclear. Moreover, previous studies on whether levosimendan is superior to dobutamine are still controversial. More importantly, these studies did not take changes (before-after comparison to the baseline) in quantitative parameters such as ejection fraction into account with the baseline level. Here, we aimed to determine the pros and cons of the two medicines by assessing the changes in cardiac function and blood lactate, mortality, with the standardized mean difference used as a summary statistic. Relevant studies were obtained by a thorough and disciplined literature search in several notable academic databases, including Google Scholar, PubMed, Cochrane Library and Embase until November 2020. Outcomes included changes in cardiac function, lactic acid, mortality and length of hospital stay. A total of 6 randomized controlled trials were included in this study, including 192 patients. Compared with dobutamine, patients treated with levosimendan had a greater improvement of cardiac index (ΔCI) (random effects, SMD = 0.90 [0.20,1.60]; I2 = 76%, P < 0.01) and left ventricular stroke work index (ΔLVSWI) (random effects, SMD = 1.56 [0.90,2.21]; I2 = 65%, P = 0.04), a significant decrease of blood lactate (Δblood lactate) (random effects, MD =  − 0.79 [− 1.33, − 0.25]; I2 = 68%, P < 0.01) at 24-h after drug intervention, respectively. There was no significant difference between levosimendan and dobutamine on all-cause mortality in ICU (fixed effect, OR = 0.72 [0.39,1.33]; I2 = 0%, P = 0.99). We combine effect sizes related to different measurement parameters to evaluate cardiac function, which implied that septic patients with myocardial dysfunction might have a better improvement of cardiac function by levosimendan than dobutamine (random effects, SMD = 1.05 [0.69,1.41]; I2 = 67%, P < 0.01). This study suggested a significant improvement of CI, LVSWI, and decrease of blood lactate in septic patients with myocardial dysfunction in ICU after 24-h administration of levosimendan than dobutamine. However, the administration of levosimendan has neither an impact on mortality nor LVEF. Septic patients with myocardial dysfunction may partly benefit from levosimendan than dobutamine, mainly embodied in cardiac function improvement.


Author(s):  
Hannah Northrup ◽  
Maheshika Somarathna ◽  
Savanna Corless ◽  
Isabelle Falzon ◽  
John Totenhagen ◽  
...  

Arteriovenous fistula (AVF) is essential for chronic kidney disease (CKD) patients on hemodialysis, but treatment for AVF maturation failure remains an unmet clinical need. Successful AVF remodeling occurs through sufficient lumen expansion to increase AVF blood flow and lumen area. Aberrant blood flow is thought to impair AVF remodeling, but previous literature has largely focused on hemodynamics averaged over the entire AVF or at a single location. We hypothesized that hemodynamics is heterogeneous, and thus any treatment’s effect size is heterogeneous in the AVF. To test our hypothesis, we used the PDE5A inhibitor sildenafil to treat AVFs in a rat model and performed magnetic resonance imaging (MRI) based computational fluid dynamics (CFD) to generate a detailed spatial profile of hemodynamics in AVFs. 90 mg/kg of sildenafil was administered to rats in their drinking water for 14 days. On day 14 femoral AVFs were created in rats and sildenafil treatment continued for another 21 days. 21 days post-AVF creation, rats underwent non-contrast MRI for CFD and geometrical analysis. Lumen cross-sectional area (CSA) and flow rate were used to quantify AVF remodeling. Parameters used to describe aberrant blood flow include velocity magnitude, wall shear stress (WSS), oscillatory shear index (OSI), and vorticity. Geometrical parameters include arterial-venous (A-V) distance, anastomosis angle, tortuosity, and nonplanarity angle magnitude. When averaged across the entire AVF, sildenafil treated rats had significantly higher CSA, flow rate, velocity, WSS, OSI, and vorticity than control rats. To analyze heterogeneity, the vein was separated into zones: 0–5, 5–10, 10–15, and 15–20 mm from the anastomosis. In both groups: 1) CSA increased from the 0–5 to 15–20 zone; 2) velocity, WSS, and vorticity were highest in the 0–5 zone and dropped significantly thereafter; and 3) OSI increased at the 5–10 zone and then decreased gradually. Thus, the effect size of sildenafil on AVF remodeling and the relationship between hemodynamics and AVF remodeling depend on location. There was no significant difference between control and sildenafil groups for the other geometric parameters. Rats tolerated sildenafil treatment well, and our results suggest that sildenafil may be a safe and effective therapy for AVF maturation.


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