Fetal Hemodynamic Responses to Arterial Occlusion of Acardiac Twins

2021 ◽  
pp. 1-7
Author(s):  
Kuntharee Traisrisilp ◽  
Suchaya Luewan ◽  
Fuanglada Tongprasert ◽  
Kasemsri Srisupundit ◽  
Theera Tongsong
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Critical Period ◽  
Ultrasound Guidance ◽  
Arterial Occlusion ◽  
Tei Index ◽  
Small Series ◽  
Twin Pregnancies ◽  
Normal Cardiac Function ◽  
Isovolumic Relaxation

Abstract The objective of this study was to comprehensively assess fetal hemodynamic adaptions to occlusive procedures. Twin pregnancies complicated with acardiac twin and hydrops fetalis of the pump twin were recruited. The occlusive procedures — either alcoholization, radiofrequency ablation, coil embolization or occlusive glue — were performed under ultrasound guidance. Various hemodynamic parameters were assessed before, shortly after, then every 6 h for 48 h and 2−4 weeks after the procedures. Seven pregnancies were recruited. The median (range) gestational age of intervention was 21 (17−26) weeks of gestation. Before the procedures, all cases showed normal cardiac function. Just after the procedures, all cases showed an increase in Tei index and isovolumic relaxation time but returned to preocclusion levels within 6−48 h, except for two cases that were persistently high. Increased preload and poor shortening fraction were observed in two cases, leading to heart failure, with one recovery and one death in utero. Five out of the seven cases got through the critical period with a gradual return to normal hemodynamics, ending with the disappearance of hydrops and successful outcomes. It was concluded that the occlusive procedure could aggravate the overworked heart, leading to heart failure. Preocclusion preload index and Tei index may predict risk of heart failure due to the occlusion. This small series strongly suggests that the occlusion should be performed before the deterioration of cardiac function.

scholarly journals A Randomized Controlled Trial to Study the Effect of Yoga Therapy on Cardiac Function and N Terminal Pro BNP in Heart Failure

2014 ◽  
Vol 9 ◽  
pp. IMI.S13939 ◽  
Author(s):  
Bandi Hari Krishna ◽  
Pravati Pal ◽  
G. K. Pal ◽  
J. Balachander ◽  
E. Jayasettiaseelon ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Medical Therapy ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Tei Index ◽  
Ventricular Ejection Fraction ◽  
Yoga Therapy ◽  
Standard Medical Therapy

Aims The purpose of this study was to evaluate whether yoga training in addition to standard medical therapy can improve cardiac function and reduce N terminal pro B-type natriuretic peptide (NT pro BNP) in heart failure (HF). Methods 130 patients were recruited and randomized into two groups: Control Group (CG) ( n = 65), Yoga Group (YG). In YG, 44 patients and in CG, 48 patients completed the study. Cardiac function using left ventricular ejection fraction (LVEF), myocardial performance index (Tei index), and NT pro BNP, a biomarker of HF, was assessed at baseline and after 12 weeks. Result Improvement in LVEF, Tei index, and NT pro BNP were statistically significant in both the groups. Furthermore, when the changes in before and after 12 weeks were in percentage, LVEF increased 36.88% in the YG and 16.9% in the CG, Tei index was reduced 27.87% in the YG and 2.79% in the CG, NT pro BNP was reduced 63.75% in the YG and 10.77% in the CG. The between group comparisons from pre to post 12 weeks were significant for YG improvements (LVEF, P < 0.01, Tei index, P < 0.01, NT pro BNP, P < 0.01). Conclusion These results indicate that the addition of yoga therapy to standard medical therapy for HF patients has a markedly better effect on cardiac function and reduced myocardial stress measured using NT pro BNP in patients with stable HF.

Genomic and Proteomic Biomarkers That Distinguish Ischemic and Non-Ischemic Heart Failure and Subjects with Normal Cardiac Function

2007 ◽  
Vol 13 (6) ◽  
pp. S107
Author(s):  
Zsuzsanna Hollander ◽  
David Lin ◽  
Gabriela Cohen Freue ◽  
Janet Wilson-McManus ◽  
Robert Balshaw ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Ischemic Heart ◽  
Ischemic Heart Failure ◽  
Normal Cardiac Function

Abstract 18575: The Transcriptional Cofactor Eyes Absent 4 is a Critical Regulator for Maintaining Normal Cardiac Function

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tatjana Williams ◽  
Moritz Hundertmark ◽  
Peter Nordbeck ◽  
Sabine Voll ◽  
Anahi Paula Arias-Loza ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Interstitial Fibrosis ◽  
Critical Role ◽  
Cardiac Physiology ◽  
Eyes Absent ◽  
Age Dependent ◽  
Normal Cardiac Function

Introduction: E193, a human mutation in the transcription cofactor Eyes absent 4 (EYA4) causes hearing impairment followed by terminal heart failure, defining an important role for Eya4 in maintaining normal cardiac function. METHODS AND RESULTS: First, in-vitro experiments show that overexpression of Eya4 and the mutant isoform alter the expression of p27kip1 on both, transcript and protein levels. Next, we generated transgenic mice with cardiomyocyte-specific Eya4 or E193 overexpression to elucidate the in vivo function of Eya4 upon cardiac physiology. Luciferase and CHIP assays revealed that Eya4 and E193 bind to and regulate p27 expression in a contradictory manner, as already seen in vitro. Activity and phoshorylation of the downstream molecules CK2α and HDAC2 were significantly elevated in Eya4 mice, whereas they were significantly reduced in E193 animals compared to WT littermates. MRI and hemodynamic analysis indicate that a constitutive overexpression of Eya4 results in the age-dependent development of hypertrophy already under baseline conditions with no obvious functional effects, whereas E193 overexpressing animals develop onset of dilative cardiomyopathy as seen in human patients carrying the E193 mutation. Morphometric analysis proved ventricular hypertrophy or dilation of the LV associated with a thinning of the myocardial wall, interstitial fibrosis of myocardial tissue and alterations in cell size. Re-activation of fetal genes also occured in both TG models, characteristic for cardiac disease. Both cardiac phenotypes were aggravated upon pressure overload. Finally, we identified a new human heterozygous truncating Eya4 mutation, E215, which leads to similar clinical features of disease and a stable myocardial expression of the mutant protein. Conclusion: Our results implicate that Eya4 plays a critical role in regulating normal cardiac physiology and function via Six1/p27/CK2α/HDAC2 and that an imbalance within the Eya4/Six1 transcriptional complex leads to an age dependent onset of cardiomyopthy and heart failure.

Abstract MP170: Increased Ga o Expression Regulated by NRSF Plays a Key Role in the Development of Heart Failure Through the Impairment of Ca 2+ Homeostasis

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Hideaki Inazumi ◽  
Yasuaki Nakagawa ◽  
Kenji Moriuchi ◽  
Koichiro Kuwahara
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Cardiac Dysfunction ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Troponin T ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Cardiac Gene ◽  
Normal Cardiac Function

Background: In the development of heart failure, pathological intracellular signaling reactivates fetal cardiac gene program, which leads to pathological cardiac remodeling. We previously reported that a transcriptional repressor, neuron restrictive silencer factor (NRSF) represses fetal cardiac gene program and maintains normal cardiac function, while pathological stimuli de-repress this NRSF mediated repression via activation of CaMKII. Molecular mechanisms by which NRSF maintains cardiac function remains to be determined, however. Purpose: To elucidate molecular mechanisms by which NRSF maintains normal cardiac function. Methods and Results: Newly generated cardiac-specific NRSF knockout mice (NRSF-cKO) showed cardiac dysfunction and premature deaths accompanied with lethal arrhythmias, as was observed in our previously reported cardiac-specific dominant-negative mutant of NRSF transgenic mice (dnNRSF-Tg). Expression of Gnao1 gene encoding Gα o , a member of inhibitory G proteins, was commonly increased in ventricles of dnNRSF-Tg and NRSF-cKO. ChIP-seq analysis, reporter assay and electrophoretic mobility shift assay identified that NRSF transcriptionally regulates Gnao1 gene expression. Genetic Knockdown of Gα o in dnNRSF-Tg and NRSF-cKO ameliorated the reduced systolic function, increased arrhythmogenicity and reduced survival rates. Conversely cardiac-specific GNAO1 overexpression was sufficient to show impaired cardiac function. Mechanistically, Gα o increases current density in surface sarcolemmal L-type Ca 2 + channel and then activates CaMKII without affecting protein kinase A activity, which finally leads to impaired Ca 2+ handling and systolic dysfunction. Furthermore, expression of Gα o is also increased in ventricles of transverse aortic constriction model mice and cardiac troponin T mutant DCM model mice, in both of which, genetic reduction of Gα o prevented the progression of cardiac dysfunction. Conclusions: Increased expression of Gα o , induced by attenuation of NRSF-mediated repression forms a pathological circuit via activation of CaMKII and progresses heart failure by impairing Ca 2+ homeostasis. Gα o is a potential therapeutic target for heart failure.

4968Increased Gao expression underlies cardiac dysfunction and lethal arrhythmias accompanied with abnormal Ca2+ handling

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Inazumi ◽  
K Kuwahara ◽  
Y Kuwabara ◽  
Y Nakagawa ◽  
H Kinoshita ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Knockout Mice ◽  
Cardiac Dysfunction ◽  
Troponin T ◽  
Systolic Dysfunction ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Electrical Stability ◽  
Normal Cardiac Function

Abstract Background We previously demonstrated that a transcriptional repressor, neuron restrictive silencer factor (NRSF), maintains normal cardiac function and electrical stability. Transgenic mice expressing a dominant-negative mutant of NRSF in their hearts (dnNRSF-Tg) exhibit systolic dysfunction with cardiac dilation and premature death due to lethal arrhythmias like human dilated cardiomyopathy (DCM). Underlining mechanisms remain to be elucidated, however. Purpose We studied underling mechanisms by which NRSF maintains normal cardiac function to identify novel therapeutic targets for heart failure. Methods and results We generated cardiac-specific NRSF knockout mice (NRSFcKO) and confirmed that cardiac phenotypes of NRSFcKO are similar to those of dnNRSF-Tg. cDNA microarray analysis revealed that cardiac gene expression of GNAO1 that encodes Gαo, a member of inhibitory G protein Gαi family, is increased in both dnNRSF-Tg and NRSFcKO ventricles. We confirmed that GNAO1 is a direct target of NRSF through ChIP-seq analysis, reporter assay and electrophoretic mobility shift assay. In dnNRSF-Tg, pharmacological inhibition of Gαo with pertussis toxin improved systolic dysfunction and knockdown of Gαo by crossing with GNAO1 knockout mice improved not only systolic function but also frequency of ventricular arrhythmias and survival rates. Electrophysiological and biochemical analysis in ventricular myocytes obtained from dnNRSF-Tg demonstrated that genetic reduction of Gαo ameliorated abnormalities in Ca2+ handling, which include increased current density in surface sarcolemmal L-type Ca2+ channel, reduced content of sarcoplasmic reticulum Ca2+ and lowered peak of Ca2+ transient. Furthermore, genetic reduction of Gαo attenuated increased phosphorylation levels of CAMKII in dnNRSF-Tg ventricles, which presumably underlies the improvement in Ca2+ handling. In addition, we identified increased Gαo expression in ventricles of heart failure model mice induced by transverse aortic constriction and cardiac troponin T mutant DCM model mice, in both of which, genetic reduction of Gαo ameliorated cardiac dysfunction. Figure 1 Conclusions We found that increased expression of Gαo, induced by attenuation of NRSF-mediated repression, plays a crucial role in the progression of cardiac dysfunction and lethal arrhythmias by evoking Ca2+ handling abnormality. These data demonstrate that Gαo is a potential therapeutic target for heart failure.

scholarly journals The Control of Diastolic Calcium in the Heart

2020 ◽  
Vol 126 (3) ◽  
pp. 395-412 ◽  
Author(s):  
David A. Eisner ◽  
Jessica L. Caldwell ◽  
Andrew W. Trafford ◽  
David C. Hutchings
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Reduced Ejection Fraction ◽  
Intracellular Ca ◽  
Cardiac Relaxation ◽  
Low Levels ◽  
Normal Cardiac Function

Normal cardiac function requires that intracellular Ca 2+ concentration be reduced to low levels in diastole so that the ventricle can relax and refill with blood. Heart failure is often associated with impaired cardiac relaxation. Little, however, is known about how diastolic intracellular Ca 2+ concentration is regulated. This article first discusses the reasons for this ignorance before reviewing the basic mechanisms that control diastolic intracellular Ca 2+ concentration. It then considers how the control of systolic and diastolic intracellular Ca 2+ concentration is intimately connected. Finally, it discusses the changes that occur in heart failure and how these may result in heart failure with preserved versus reduced ejection fraction.

Assessment of Cardiac Function and Heart Failure by Cardiac Time Analysis (Tei Index)

2009 ◽  
Vol 15 (7) ◽  
pp. S138
Author(s):  
Toshinori Yuasa ◽  
Mihoko Kouno ◽  
Akira Kisanuki ◽  
Nami Ueya ◽  
Kenichi Nakashiki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Time Analysis ◽  
Tei Index

Role of kinins in chronic heart failure and in the therapeutic effect of ACE inhibitors in kininogen-deficient rats

2000 ◽  
Vol 278 (2) ◽  
pp. H507-H514 ◽  
Author(s):  
Yun-He Liu ◽  
Xiao-Ping Yang ◽  
Dharmesh Mehta ◽  
Manohar Bulagannawar ◽  
Gloria M. Scicli ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Infarct Size ◽  
Receptor Antagonist ◽  
Cardiac Remodeling ◽  
Myocardial Infarct ◽  
Brown Norway ◽  
Myocardial Infarct Size ◽  
Normal Cardiac Function

Using Brown Norway Katholiek (BNK) rats, which are deficient in kininogen (kinin precursor) due to a mutation in the kininogen gene, we examined the role of endogenous kinins in 1) normal cardiac function; 2) myocardial infarction (MI) caused by coronary artery ligation; 3) cardiac remodeling in the development of heart failure (HF) after MI; and 4) the cardioprotective effect of angiotensin-converting enzyme inhibitors (ACEI) on HF after MI. Two months after MI, rats were randomly treated with vehicle or the ACEI ramipril for 2 mo. Brown Norway rats (BN), which have normal kininogen, were used as controls. Left ventricular (LV) end-diastolic volume (EDV), end-systolic volume (ESV), end-diastolic pressure (EDP), and ejection fraction (EF) as well as myocardial infarct size (IS), interstitial collagen fraction (ICF), cardiomyocyte cross-sectional area (MCA), and oxygen diffusion distance (ODD) were measured. We found that 1) cardiac hemodynamics, function, and histology were the same in sham-ligated BN and BNK rats; 2) IS was similar in BN and BNK; 3) in rats with HF treated with vehicle, the decrease in LVEF and the increase in LVEDV, LVESV, LVEDP, ICF, MCA, and ODD did not differ between BNK and BN; and 4) ACEI increased EF, decreased LVEDV and LVESV, and improved cardiac remodeling in BN-HF rats, and these effects were partially blocked by the bradykinin B2 receptor antagonist icatibant (HOE-140). In BNK-HF rats, ACEI failed to produce these beneficial cardiac effects. We concluded that in rats, lack of kinins does not influence regulation of normal cardiac function, myocardial infarct size, or development of HF; however, kinins appear to play an important role in the cardioprotective effect of ACEI, since 1) this effect was significantly diminished in kininogen-deficient rats and 2) it was blocked by a B2 kinin receptor antagonist in BN rats.

An educational tool for understanding the cardiopulmonary changes associated with heart failure.

1994 ◽  
Vol 267 (6) ◽  
pp. S37 ◽  
Author(s):  
Y Chen ◽  
S E DiCarlo
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Cardiac Function ◽  
Physiological Data ◽  
Educational Tool ◽  
Approach To Learning ◽  
Innovative Method ◽  
Normal Cardiac Function

We wanted a new and innovative method of engaging students in interactive learning. To this end, we developed an educational tool that compares and contracts the cardiopulmonary responses to exercise in an individual with heart failure with an individual with normal cardiac function. This exercise provides a unique opportunity to analyze, integrate, and interpret the changes associated with heart failure because more is learned about how a system operates when it is forced to perform than when it is idle. In this laboratory, basic anatomical and physiological data about heart failure are provided. Subsequently, figures are presented that illustrate the response of specific cardiopulmonary variables during exercise (e.g., heart rate, cardiac output, blood pressure), and the students are challenged to analyze and assimilate information from figures, answer questions, make calculations, and plot graphs. The answers to the questions are provided. The students reported that this tool was an interesting and thoughtful approach to learning cardiopulmonary physiology. We conclude that this method is pedagogically sound inasmuch as students are forced to draw conclusions with directed exercises and questions.

scholarly journals The genetic basis of cardiac function: dissection by zebrafish ( Danio rerio ) screens

2000 ◽  
Vol 355 (1399) ◽  
pp. 939-944 ◽  
Author(s):  
Kerri S. Warren ◽  
Justina C. Wu ◽  
Florence Pinet ◽  
Mark C. Fishman
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Danio Rerio ◽  
Heart Diseases ◽  
Single Gene ◽  
Cardiac Contractility ◽  
Gene Mutations ◽  
Genetic Screens ◽  
Endothelial Lining ◽  
Normal Cardiac Function

The vertebrate heart differs from chordate ancestors both structurally and functionally. Genetic units of form, termed ‘modules’, are identifiable by mutation, both in zebrafish and mouse, and correspond to features recently acquired in evolution, such as the ventricular chamber or endothelial lining of the vessels and heart. Zebrafish ( Danio rerio ) genetic screens have provided a reasonably inclusive set of such genes. Normal cardiac function may also be disrupted by single–gene mutations in zebrafish. Individual mutations may perturb contractility or rhythm generation. The zebrafish mutations which principally disturb cardiac contractility fall into two broad phenotypic categories, ‘dilated’ and ‘hypertrophic’. Interestingly, these correspond to the two primary types of heart failure in humans. These disorders of early cardiac function provide candidate genes to be examined in complex human heart diseases, including arrhythmias and heart failure.

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