Myocardial tissue Doppler and long axis function in the fetal heart

Gardiner, Helena M.; Pasquini, Lucia; Wolfenden, Joanne; Barlow, Anna; Li, Wei; Kulinskaya, Elena; Henein, Michael Y.

doi:10.1016/j.ijcard.2005.10.029

Cited by 115 publications

(171 citation statements)

References 19 publications

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“…We specifically avoided analyzing TDI velocities offline from two-dimensional acquired data sets because of the inherent limitation of measuring maximal myocardial velocities at relatively low frame rates. Myocardial velocities increase with gestational age (8,11,32), and fetal responses to acute hypoxia are known to vary according to gestational age (20). Inasmuch as the same fetus served as its own control, the effect of gestational age was not important for the purpose of our study.…”

Section: Discussionmentioning

confidence: 93%

“…In human fetuses, higher myocardial wall velocities in the RV than LV and IVS have been attributed to segmental differences in myocardial fiber orientation (11,32). Although there are known structural differences between the ventricles with regard to myocardial fiber orientation and other morphometric parameters in sheep fetuses (39), the myocardial velocities obtained from the RV and LV were not significantly different in our study, suggesting that the amplitudes of myocardial deformation during the cardiac cycle are likely to reflect function, rather than pure anatomy, at least in the presence of increased R ua .…”

Section: Discussionmentioning

confidence: 99%

“…Echocardiography has been applied to assess fetal cardiac function noninvasively in a variety of clinical conditions, such as intrauterine growth restriction (29), hydrops (17), congenital heart disease (38), and twin-twin transfusion syndrome (36). Recently, tissue Doppler imaging (TDI) of myocardial motion has been introduced in clinical practice as a promising new technique in the assessment of fetal heart function (2,8,11,15,32,34).In human pregnancies, placental insufficiency with increased placental vascular resistance (R ua ) can lead to fetal metabolic acidosis and death. Our experiments in a chronic sheep model of increased R ua were designed to test the hypothesis that acute metabolic acidosis decreases fetal myocardial motion.…”

mentioning

confidence: 99%

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Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance

Acharya

Räsänen²,

Mäkikallio

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Acharya G, Räsänen J, Mäkikallio K, Erkinaro T, Kavasmaa T, Haapsamo M, Mertens L, Huhta JC. Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance. Am J Physiol Heart Circ Physiol 294: H498-H504, 2008. First published November 16, 2007 doi:10.1152/ajpheart.00492.2007.-We hypothesized that acute fetal metabolic acidosis decreases fetal myocardial motion in a chronic sheep model of increased placental vascular resistance (Rua). Eleven ewes and fetuses were instrumented at 118 -122 days of gestation. After 5 days of recovery and 24 h of placental embolization to increase Rua, longitudinal myocardial velocities of the right and left ventricles and interventricular septum (IVS) were assessed at the level of the atrioventricular valve annuli via tissue Doppler imaging (TDI). Ventricular inflow (E and A waves) and outflow velocities were obtained, and cardiac outputs were calculated. All measurements were performed at baseline and during fetal acidosis caused by epidural anesthesia-induced maternal hypotension, which decreased uterine artery volume blood flow, fetal oxygenation, arterial pH, and base excess and increased lactate. Compared with baseline, the peak isovolumic myocardial contraction and relaxation velocities of the ventricles and IVS, early relaxation velocity (EЈ) of the ventricles, and systolic velocity of the IVS decreased during metabolic acidosis. The proportion of isovolumic contraction time of the cardiac cycle increased but the isovolumic relaxation and ejection time proportions and the TDI Tei index did not change. The E-to-EЈ ratio for both ventricles was higher during metabolic acidosis than at baseline. During metabolic acidosis, right and left ventricular cardiac outputs remained unchanged compared with baseline. In sheep fetuses with increased Rua and acute metabolic acidosis, global cardiac function was preserved. However, acute metabolic acidosis impaired myocardial contractility during the isovolumic phase and relaxation during the isovolumic and early filling phases of the cardiac cycle. cardiac function; fetal echocardiography; tissue Doppler IN RESPONSE TO HYPOXEMIA, fetuses generally redistribute more blood toward the myocardium, brain, and adrenal glands at the expense of the lower body and viscera (3,22). The fetal heart is known to have a remarkable ability to withstand hypoxia (10, 30), but progressive hypoxia and acidosis may decrease blood supply to the heart (6) and alter myocardial energy metabolism (18,40). However, despite reduced myocardial contractility, global cardiac function is preserved during moderate acidemia (26). Echocardiography has been applied to assess fetal cardiac function noninvasively in a variety of clinical conditions, such as intrauterine growth restriction (29), hydrops (17), congenital heart disease (38), and twin-twin transfusion syndrome (36). Recently, tissue Doppler imaging (TDI) of myocardial motion has been introduced in clinical practice as a promising new techniqu...

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance

Acharya

Räsänen²,

Mäkikallio

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…Longitudinal annular motion was assessed by M mode from an apical or basal 4-chamber view. 19 Spectral tissue Doppler was used to measure systolic (S′) and early diastolic (E′) annular peak velocities at mitral and tricuspid annuli from an apical or basal 4-chamber view. 20 Peak early and late transvalvular filling (E/A) ratios were estimated by calculating the ratio between early ventricular filling (E-wave) to late ventricular filling (A-wave) from atrioventricular flows obtained from a basal or apical 4-chamber view.…”

Section: Fetal Ultrasoundmentioning

confidence: 99%

Postsystolic Shortening by Myocardial Deformation Imaging as a Sign of Cardiac Adaptation to Pressure Overload in Fetal Growth Restriction

Crispi

Bijnens

Sepulveda-Swatson

et al. 2014

Circ: Cardiovascular Imaging

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Fetal growth restriction (FGR) because of placental insufficiency affects 5% to 7% of pregnancies and represents one of the leading causes of perinatal morbidity and mortality.1 Numerous historical cohort studies 2 and animal models 3 have demonstrated that FGR has a strong association not only with metabolic but also with primary cardiovascular remodeling that lead to long-term adverse consequences in later life. The rapid cell proliferation and differentiation during fetal growth are sensitive to any of the even smallest changes damaging the environment that can lead to permanent alterations in structural and functional constitution, which may persist into the adult life. 2 The heart is a central organ in the prenatal adaptation to placental insufficiency and fetal hypoxia. Previous studies have demonstrated remodeled hearts (more globular) with signs of systolic and diastolic dysfunction and preserved ejection fraction. [4][5][6] FGR cases are associated with prenatal adverse cardiac remodeling 4,5 that persists postnatally, 6 and low birth weight was linked to increased cardiovascular mortality in adulthood.2 Chronic pressure/volume overload together with hypoxia in utero have been postulated as the potential underlying mechanistic pathway of prenatal cardiovascular remodeling in FGR. 5,6 Editorial see p 759 Clinical Perspective on p 787Although evaluation of cardiac function with echocardiography has traditionally been limited to volume-based assessment, recent developments in cardiac ultrasound allow the noninvasive measurement of cardiac deformation with direct assessment of myocardial muscle by assessing regional Background-Fetal growth restriction (FGR) is associated with global adverse cardiac remodeling in utero and increased cardiovascular mortality in adulthood. Prenatal myocardial deformation has not been evaluated in FGR to date. We aimed to evaluate prenatal cardiac remodeling comprehensively in FGR including myocardial deformation imaging. Methods and Results-Echocardiography was performed in 37 consecutive FGR (defined as birthweight <10th centile) and 37 normally grown fetuses. A comprehensive fetal echocardiography was performed including tissue Doppler and 2-dimensional-derived strain and strain rate. Postnatal blood pressure measurement at 6 months of age was also performed. FGR cases showed signs of more globular hearts with decreased longitudinal motion (left systolic annular peak velocity: controls mean 6 cm/s [SD myocardial strain and strain rate. [7][8][9] Strain is defined as change in length/thickness of a segment of myocardium relative to its resting length and is expressed as a percentage; strain rate is the velocity of this deformation.7-9 Myocardial deformation imaging has demonstrated a high sensitivity for detecting preclinical myocardial dysfunction in various pathological conditions characterized by myocardial dysfunction, despite preserved ejection fraction, such as asymptomatic carriers of hypertrophic cardiomyopathy, sarcomeric mutations, Fabry disease, or myocardial ste...

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“…It can also be applied to mitral annulus (MAPSE) 40 . Normal ranges for fetus are published 41 and recently described as a very sensitive parameter for assessing cardiac dysfunction in several fetal conditions such as fetal growth restriction 42 …”

Section: Importance Of Fetal Cardiac Functionmentioning

confidence: 99%

Ultrasound assessment of fetal cardiac function

Crispi

Valenzuela-Alcaráz

Cruz‐Lemini

et al. 2013

Australas J Ultrason Med

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Introduction: Fetal heart evaluation with US is feasible and reproducible, although challenging due to the smallness of the heart, the high heart rate and limited access to the fetus. However, some cardiac parameters have already shown a strong correlation with outcomes and may soon be incorporated into clinical practice. Materials and Methods: Cardiac function assessment has proven utility in the differential diagnosis of cardiomyopathies or prediction of perinatal mortality in congenital heart disease. In addition, some cardiac parameters with high sensitivity such as MPI or annular peak velocities have shown promising results in monitoring and predicting outcome in intrauterine growth restriction or congenital diaphragmatic hernia. Conclusion: Cardiac function can be adequately evaluated in most fetuses when appropriate expertise, equipment and time are available. Fetal cardiac function assessment is a promising tool that may soon be incorporated into clinical practice to diagnose, monitor or predict outcome in some fetal conditions. Thus, more research is warranted to further define specific protocols for each fetal condition that may affect cardiac function.

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Myocardial tissue Doppler and long axis function in the fetal heart

Cited by 115 publications

References 19 publications

Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance

Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance

Postsystolic Shortening by Myocardial Deformation Imaging as a Sign of Cardiac Adaptation to Pressure Overload in Fetal Growth Restriction

Ultrasound assessment of fetal cardiac function

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