Assessment of cardiac function, blood flow and myocardial tissue relaxation parameters at 0.35 T

2020 ◽  
Vol 33 (7) ◽  
Author(s):  
Juliet Varghese ◽  
Jason Craft ◽  
Christopher D. Crabtree ◽  
Yingmin Liu ◽  
Ning Jin ◽  
...  
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 < 0.0001), fetal acidosis (pH 7.11 vs. 7.24 at 150 min, P < 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.


Author(s):  
Miroslava Svobodova ◽  
Elena S. Di Martino

The heart is a very efficient mechanical pump whose function is to controls the blood flow in the body. Two physical systems, namely mechanical for the pumping action and electrical for the control interact within the heart. Cardiac function can only be studied if both mechanical and electrical systems are considered. In particular, we are interested in the electromechanical control of the atrium pump function which is less studied then the electromechanical control of the ventricle pump function and none the less is a crucial factor in the development of atrial fibrillation.


Author(s):  
Barnali Basu ◽  
Ranjan Shetty ◽  
Krishnendu Gupta

Background: One of the consequences of IUGR is the development of cardiac diastolic dysfunction in fetuses. Tissue doppler in echocardiography is a new technique to detect myocardial tissue function and can act as a useful tool in the identification of this complication. Hence we decided to undertake this study to assess the utility of myocardial tissue doppler in detecting foetal cardiac dysfunction in IUGR. It was a prospective case control study in a tertiary care teaching hospital.Methods: Foetal cardiac function in the third trimester of pregnancy was evaluated with the help of myocardial tissue doppler and compared between IUGR and normal growth babies and correlated with vessel doppler findings and neonatal outcomes.Results: There were sixty two IUGR and fifty eight normal growth babies in the study. In babies with IUGR, particularly the ones with severe IUGR, abnormal vessel doppler and adverse neonatal outcomes, right ventricular MPI was found to be significantly lower. However, the variable had a poor sensitivity (40%) in detecting fetuses at risk for poor neonatal outcomes.Conclusions: Myocardial tissue doppler shows right sided cardiac dysfunction in IUGR babies in comparison to normal growth babies It is however not a sensitive indicator of adverse perinatal outcome in IUGR babies.


Nosotchu ◽  
1984 ◽  
Vol 6 (2) ◽  
pp. 223-229 ◽  
Author(s):  
Tomoaki Terada ◽  
Haruhiko Kikuchi ◽  
Jun Karasawa ◽  
Ikuo Ihara ◽  
Izumi Nagata

2021 ◽  
Vol 12 ◽  
Author(s):  
Wenkai Yang ◽  
Hanjian Tu ◽  
Kai Tang ◽  
Haozhong Huang ◽  
Shi Ou ◽  
...  

This study investigated the effects of reynoutrin on the improvement of ischemic heart failure (IHF) and its possible mechanism in rats. The rat heart failure model was established by permanently ligating the left anterior descending coronary artery (LAD) and administering different doses of reynoutrin. Cardiac function, inflammatory factors releasing, oxidative stress, cardiomyocytes apoptosis, and myocardial fibrosis were evaluated. Western blotting was used to determine protein expression levels of S100 calcium-binding protein A1 (S100A1), matrix metallopeptidase 2(MMP2), MMP9, phosphorylated (p-) p65, and transforming growth factor -β1 (TGF-β1) in myocardial tissue of the left ventricle. Results showed that reynoutrin significantly improved cardiac function, suppressed the release of inflammatory factors, reduced oxidative stress, inhibited cardiomyocytes apoptosis, and attenuated myocardial fibrosis in rats with IHF. In rat myocardial tissue, permanent LAD-ligation resulted in a significant down-regulation in S100A1 expression, whereas reynoutrin significantly up-regulated S100A1 protein expression while down-regulating MMP2, MMP9, p-p65, and TGF-β1 expressions. However, when S100A1 was knocked down in myocardial tissue, the above-mentioned positive effects of reynoutrin were significantly reversed. Reynoutrin is a potential natural drug for the treatment of IHF, and its mechanism of action involves the up-regulation of S100A1 expression, thereby inhibiting expressions of MMPs and the transcriptional activity of nuclear factor kappa-B.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Eisei Yamamoto ◽  
Hitoshi Takano ◽  
Hiroyuki Tajima ◽  
Jun Tanabe ◽  
Hidekazu Kawanaka ◽  
...  

Background: Renal artery stenosis (RAS) often plays an important role not only in malignant hypertension but also in sudden development of heart failure (HF) so called ‘flash pulmonary edema’ or chronic HF refractory to medical treatment. One of the possible mechanisms whereby RAS affects these unique conditions of HF is suppression of LV compliance through the complex interaction between neurohormonal systems originating from the reduction of renal blood flow. Renal artery angioplasty is expected to be an effective treatment for restoring renal blood flow in patients with RAS. The aim of the present study was whether the angioplasty can improve the impaired neurohormonal systems and diastolic cardiac function in patients with RAS. Methods: A prospective analysis was performed in 18 HF patients with RAS (age: 72±6, 3 females, NYHA I/II/III: 5/9/4) who underwent renal artery angioplasty between 2005 and 2007. Four patients with significant bilateral RAS and 3 patients with unilateral RAS in the vessel supplying a functional solitary kidney were included. We monitored the changes of biochemical and neurohormonal markers and blood pressure. Cardiac function was evaluated by tissue Doppler echocardiogram before and 3 months after the procedure. Results: Technical success was achieved in all interventions. The results are shown in table . Systolic arterial blood pressure significantly decreased by renal angioplasty. B-type natriuretic peptide (BNP) was significantly reduced 3 months after the angioplasty, whereas the change of sCr or angiotensinII was not statistically significant. Myocardial early diastolic velocity (Em), a parameter of diastolic LV function, was significantly improved compared with that measured before the procedure. Conclusions: In patients with either overt or latent HF possessing RAS, renal artery angioplasty not only decreases arterial blood pressure but also improves diastolic cardiac function in parallel with the reduction of BNP level.


Stroke ◽  
1970 ◽  
Vol 1 (5) ◽  
pp. 330-347 ◽  
Author(s):  
EDWARD S. COOPER ◽  
JAMES W. WEST ◽  
MARVIN E. JAFFE ◽  
HERBERT I. GOLDBERG ◽  
J. KAWAMURA ◽  
...  

Perfusion ◽  
2018 ◽  
Vol 34 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Terje Aass ◽  
Lodve Stangeland ◽  
Christian Arvei Moen ◽  
Atle Solholm ◽  
Geir Olav Dahle ◽  
...  

Introduction: This experimental study compares myocardial function after prolonged arrest by St. Thomas’ Hospital polarizing cardioplegic solution (esmolol, adenosine, Mg2+) with depolarizing (hyperkalaemic) St. Thomas’ Hospital No 2, both administered as cold oxygenated blood cardioplegia. Methods: Twenty anaesthetized pigs on tepid (34°C) cardiopulmonary bypass (CPB) were randomised to cardioplegic arrest for 120 min with antegrade, repeated, cold, oxygenated, polarizing (STH-POL) or depolarizing (STH-2) blood cardioplegia every 20 min. Cardiac function was evaluated at Baseline and 60, 150 and 240 min after weaning from CPB, using a pressure-conductance catheter and epicardial echocardiography. Regional tissue blood flow, cleaved caspase-3 activity and levels of malondialdehyde were evaluated in myocardial tissue samples. Results: Preload recruitable stroke work (PRSW) was increased after polarizing compared to depolarizing cardioplegia 150 min after declamping (73.0±3.2 vs. 64.3±2.4 mmHg, p=0.047). Myocardial tissue blood flow rate was high in both groups compared to the Baseline levels and decreased significantly in the STH-POL group only, from 60 min to 150 min after declamping (p<0.005). Blood flow was significantly reduced in the STH-POL compared to the STH-2 group 240 min after declamping (p<0.05). Left ventricular mechanical efficiency, the ratio between total pressure-volume area and blood flow rate, gradually decreased after STH-2 cardioplegia and was significantly reduced compared to STH-POL cardioplegia after 150 and 240 min (p<0.05 for both). Conclusion: Myocardial protection for two hours of polarizing cardioplegic arrest with STH-POL in oxygenated blood is non-inferior compared to STH-2 blood cardioplegia. STH-POL cardioplegia alleviates the mismatch between myocardial function and perfusion after weaning from CPB


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