How to grow a heart: fibreoptic guided fetal aortic valvotomy

2006 ◽  
Vol 16 (S1) ◽  
pp. 43-46 ◽  
Author(s):  
Elsa Suh ◽  
James Quintessenza ◽  
James Huhta ◽  
Ruben Quintero
Keyword(s):  
Left Ventricle ◽  
Aortic Stenosis ◽  
Fetal Echocardiography ◽  
Left Ventricular ◽  
Left Heart ◽  
Endocardial Fibroelastosis ◽  
Fetal Diagnosis ◽  
Ventricular Afterload ◽  
Systolic And Diastolic Function ◽  
Additional Support

Various physiologic mechanisms have been proposed to account for the development of hypoplasia of the left heart. The mechanism thus far most widely accepted suggests that the entity starts as severe or critical aortic stenosis during fetal gestation. Obstruction at the level of the abnormal aortic valve is then held to increase left ventricular afterload, resulting in decreased systolic and diastolic function. Shunting across the patent oval foramen is then reversed, so that blood flows from left to right. This reversal of flow during fetal gestation decreases the volume of blood crossing the mitral valve, thus decreasing the further potential for growth of the left ventricle.1 Additional support for this postulated physiologic mechanism was provided with the advent of fetal echocardiography during the 1980s.2–4 It was the group of Allan, working at Guy's Hospital in London, which first documented the fetal development of hypoplasia of the left heart by serial echocardiographic observation.4 In their retrospective study of 7000 pregnancies, 462 fetuses were diagnosed to have a structural cardiac defect at the time of the initial echocardiogram. Among those, 28 patients had dilated and dysfunctional left ventricles and aortic valves. The majority of these patients were also found to have concomitant endocardial fibroelastosis. Out of 15 patients in the series who were followed with serial echocardiograms, five progressed to develop hypoplasia of the left heart. With echocardiographic technology undergoing refinement over the same period, it was during this era that the first fetal cardiac intervention was performed using echocardiographic guidance.2,5,6 With still further technologic advances, fetal diagnosis of hypoplasia of the left heart can now be made as early as 13 weeks gestational age.7 One entity which is frequently associated with the hypoplastic left ventricle and aortic stenosis is endocardial fibroelastosis. There is an overlap of pathology between these three entities.8–10 In this report, we describe our own experience in intervention in a fetus suspected of developing hypoplasia of the left heart.

scholarly journals A ventricular-vascular coupling model in presence of aortic stenosis

2005 ◽  
Vol 288 (4) ◽  
pp. H1874-H1884 ◽  
Author(s):  
Damien Garcia ◽  
Paul J. C. Barenbrug ◽  
Philippe Pibarot ◽  
André L. A. J. Dekker ◽  
Frederik H. van der Veen ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Left Ventricle ◽  
Aortic Stenosis ◽  
Vascular System ◽  
Severe Aortic Stenosis ◽  
Left Ventricular ◽  
Arterial System ◽  
Coefficient Of Determination ◽  
Ventricular Afterload ◽  
Good Agreement

In patients with aortic stenosis, the left ventricular afterload is determined by the degree of valvular obstruction and the systemic arterial system. We developed an explicit mathematical model formulated with a limited number of independent parameters that describes the interaction among the left ventricle, an aortic stenosis, and the arterial system. This ventricular-valvular-vascular (V3) model consists of the combination of the time-varying elastance model for the left ventricle, the instantaneous transvalvular pressure-flow relationship for the aortic valve, and the three-element windkessel representation of the vascular system. The objective of this study was to validate the V3 model by using pressure-volume loop data obtained in six patients with severe aortic stenosis before and after aortic valve replacement. There was very good agreement between the estimated and the measured left ventricular and aortic pressure waveforms. The total relative error between estimated and measured pressures was on average (standard deviation) 7.5% (SD 2.3) and the equation of the corresponding regression line was y = 0.99 x − 2.36 with a coefficient of determination r2 = 0.98. There was also very good agreement between estimated and measured stroke volumes ( y = 1.03 x + 2.2, r2 = 0.96, SEE = 2.8 ml). Hence, this mathematical V3 model can be used to describe the hemodynamic interaction among the left ventricle, the aortic valve, and the systemic arterial system.

Assessment of Left Ventricular Endocardial Fibroelastosis in Fetuses With Aortic Stenosis and Evolving Hypoplastic Left Heart Syndrome

2010 ◽  
Vol 106 (12) ◽  
pp. 1792-1797 ◽  
Author(s):  
Doff B. McElhinney ◽  
Melanie Vogel ◽  
Carol B. Benson ◽  
Audrey C. Marshall ◽  
Louise E. Wilkins-Haug ◽  
...  
Keyword(s):  
Aortic Stenosis ◽  
Hypoplastic Left Heart Syndrome ◽  
Left Ventricular ◽  
Left Heart ◽  
Endocardial Fibroelastosis ◽  
Hypoplastic Left Heart ◽  
Left Heart Syndrome

Impact of Aortic Prosthetic Heart Valve Dysfunction on Left Ventricular Afterload and on the Accuracy of Echo-Doppler Measurements

2011 ◽  
Author(s):  
Othman Smadi ◽  
Zahra Keshavarz-Motamed ◽  
Ibrahim Hassan ◽  
Philippe Pibarot ◽  
Lyes Kadem
Keyword(s):  
Left Ventricle ◽  
Heart Valve ◽  
Heart Valves ◽  
Mechanical Heart Valve ◽  
Prosthetic Heart Valve ◽  
Left Ventricular ◽  
Heart Valve Disease ◽  
Thromboembolic Events ◽  
Left Heart ◽  
Ventricular Afterload

Left heart side (left ventricle and left atrium) is responsible for delivering the oxygenated blood to all body organs, where a relatively strong left ventricle contraction is needed to deliver around 5 liters of blood per minute. As a consequence, the left heart side experiences a high pressure (∼150 mmHg). Therefore, the dysfunction (stenosis or incompetence) in the aortic and/or mitral heart valves in the left side of the heart is more common than the dysfunction in the pulmonary and tricuspid heart valves in the right side of the heart (Yoganathan et al., 2004). Heart valve surgical replacement is the most effective solution in severe functional heart valve disease (Pibarot and Dumesnil, 2009). Almost, half of the total implants of prosthetic heart valves (∼300,000) are mechanical (mainly bileaflet). In case of mechanical heart valve (MHV), a lifelong anti-coagulant should be taken to avoid thromboembolic events. Despite the significant improvement in valve design resulting in minimizing prosthetic valve complications (thromboembolic events or pannus formation), these complications are still possible with MHV Implantation.

Echocardiographic assessment of the aortic valve and left ventricular outflow tract

2005 ◽  
Vol 15 (S1) ◽  
pp. 27-36 ◽  
Author(s):  
Alfred Asante-Korang ◽  
Robert H. Anderson
Keyword(s):  
Aortic Valve ◽  
Left Ventricle ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Left Heart ◽  
Transesophageal Echocardiogram ◽  
Left Ventricular Outflow ◽  
Echocardiographic Assessment

The previous reviews in this section of our Supplement1,2 have summarized the anatomic components of the ventriculo-arterial junctions, and then assessed the echocardiographic approach to the ventriculo-arterial junction or junctions as seen in the morphologically right ventricle. In this complementary review, we discuss the echocardiographic assessment of the comparable components found in the morphologically left ventricle, specifically the outflow tract and the arterial root. We will address the echocardiographic anatomy of the aortic valvar complex, and we will review the causes of congenital arterial valvar stenosis, using the aortic valve as our example. We will also review the various lesions that, in the outflow of the morphologically left ventricle, can produce subvalvar and supravalvar stenosis. We will then consider the salient features of the left ventricular outflow tract in patients with discordant ventriculo-arterial connections, and double outlet ventricles. To conclude the review, we will briefly address some rarer anomalies that involve the left ventricular outflow tract, showing how the transesophageal echocardiogram is used to assist the surgeon preparing for repair. The essence of the approach will be to consider the malformations as seen at valvar, subvalvar, or supravalvar levels,1 but we should not lose sight of the fact that aortic coarctation or interruption, hypoplasia of the left heart, and malformations of the mitral valve are all part of the spectrum of lesions associated with obstruction to the left ventricular outflow tract. These additional malformations, however, are beyond the scope of this review.

scholarly journals P959 Handheld echocardiography in a real world scenario: concordances compared to standard echo reports

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
L David Lechinewski ◽  
I P Vieira ◽  
N Clausell ◽  
L A Z Moura ◽  
M Barnes ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Aortic Stenosis ◽  
Right Ventricle ◽  
Pulmonary Regurgitation ◽  
Left Ventricular ◽  
K Value ◽  
Study Results ◽  
Hemodynamic Assessment ◽  
And Function ◽  
Experienced Echocardiographer

Abstract Background Handheld echocardiography devices(HH) arise as a common tool in clinical examination and screening for various cardiovascular disorders. Despite of it, studies with this method are small, with unselected patients and limited scope of diagnostic comparison. Purpose Assess the usefulness of the new miniaturized HH and compare its concordances with the standard high definition echocardiography study(STD). Methods Between April and May of 2016 adult patients who were scheduled to regular STD, were also submitted to a HH exam. Experienced sonographers performed and an experienced echocardiographer reviewed the STD exam, and an experienced echocardiographer performed and reviewed the HH study - reviewers were blinded to the other study results. STD exams included 2-dimensional images, Color Doppler and hemodynamics analysis. With the HH hemodynamic assessment was not performed as the machine does not include such technology. Agreement between the reports was analyzed. Results 110 patients were included. Mean age was 62.4 ± 16.7 years. The κ values(Table) show good correlation between HH and STD on the analysis of left ventricular global and segment functions, right ventricle size and function, mitral and aortic stenosis. On the evaluation of left ventricle hypertrophy, mitral and aortic regurgitations the correlation was modest, while poor correlation was found for pulmonary and tricuspid regurgitations. Conclusion In a daily practice scenario with experienced hands, HH demonstrates good results for the assessment of ventricles size and function, while the evaluation of right heart valves was the least reliable performance. Dissemination of HH should occur with considerations and caution. K Values for Echocardiography Analysis Echocardiography analysis K value Global estimated LV dysfunction 0.85 Wall motion abnormalities 0.78 LV hypertrophy 0.6 RV size 0.83 RV function 0.82 Mitral regurgitation 0.42 Aortic regurgitation 0.56 Mitral stenosis 0.96 Aortic stenosis 0.82 Tricuspid regurgitation 0.26 Pulmonary regurgitation 0.25 LV: left ventricle; RV: right ventricle.

scholarly journals Distention of the Immature Left Ventricle Triggers Development of Endocardial Fibroelastosis: An Animal Model of Endocardial Fibroelastosis Introducing Morphopathological Features of Evolving Fetal Hypoplastic Left Heart Syndrome

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Shogo Shimada ◽  
Christian Robles ◽  
Ben M. W. Illigens ◽  
Alejandra M. Casar Berazaluce ◽  
Pedro J. del Nido ◽  
...  
Keyword(s):  
Animal Model ◽  
Left Ventricle ◽  
Hypoplastic Left Heart Syndrome ◽  
Left Heart ◽  
Endocardial Fibroelastosis ◽  
Hypoplastic Left Heart ◽  
Fetal Imaging ◽  
Adult Rat ◽  
Human Fetal Heart ◽  
Left Heart Syndrome

Background.Endocardial fibroelastosis (EFE), characterized by a diffuse endocardial thickening through collagen and elastin fibers, develops in the human fetal heart restricting growth of the left ventricle (LV). Recent advances in fetal imaging indicate that EFE development is directly associated with a distended, poorly contractile LV in evolving hypoplastic left heart syndrome (HLHS). In this study, we developed an animal model of EFE by introducing this human fetal LV morphopathology to an immature rat heart.Methods and Results.A neonatal donor heart, in which aortic regurgitation (AR) was created, was heterotopically transplanted into a recipient adult rat. AR successfully induced the LV morphology of evolving HLHS in the transplanted donor hearts, which resulted in the development of significant EFE covering the entire LV cavity within two weeks postoperatively. In contrast, posttransplants with a competent aortic valve displayed unloaded LVs with a trace of EFE.Conclusions.We could show that distention of the immature LV in combination with stagnant flow triggers EFE development in this animal model. This model would serve as a robust tool to develop therapeutic strategies to treat EFE while providing insight into its pathogenesis.

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