Diastolic heart failure: standard doppler approach and beyond

Vitarelli, Antonio; Gheorghiade, Mihai

doi:10.1016/s0002-9149(98)00067-8

Cited by 37 publications

(23 citation statements)

References 73 publications

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“…However, others have found similar (10,41) or increased (26,40) ratios. In adults with progressing diastolic dysfunction, a lowered E/A ratio is followed by "pseudo-normalization" and a subsequent increase of the ratio (53). Conflicting results could thus potentially reflect different stages of diastolic dysfunction.…”

Section: Diastolic Dysfunctionmentioning

confidence: 99%

Intrauterine growth restriction: impact on cardiovascular development and function throughout infancy

et al. 2016

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Intrauterine growth restriction (IUGR) refers to the situation where a fetus does not grow according to its genetic growth potential. One of the main causes of IUGR is uteroplacental vascular insufficiency. Under these circumstances of chronic oxygen and nutrient deprivation, the growth-restricted fetus often displays typical circulatory changes, which in part represent adaptations to the suboptimal intrauterine environment. These fetal adaptations aim to preserve oxygen and nutrient supply to vital organs such as the brain, the heart, and the adrenals. These prenatal circulatory adaptations are thought to lead to an altered development of the cardiovascular system and "program" the fetus for life long cardiovascular morbidities. In this review, we discuss the alterations to cardiovascular structure, function, and control that have been observed in growth-restricted fetuses, neonates, and infants following uteroplacental vascular insufficiency. We also discuss the current knowledge on early life surveillance and interventions to prevent progression into chronic disease. Intrauterine growth restriction (IUGR) refers to the situation where a fetus does not grow according to its genetic growth potential. The main cause of IUGR in developed countries is uteroplacental vascular insufficiency (1), which drives the fetus to redistribute its cardiac output to preserve oxygen and nutrient supply to the brain, heart, and adrenals. Although these adaptive circulatory changes are beneficial during intrauterine life, they are thought to cause dysfunctional development of the cardiovascular system and "program" the fetus for life long cardiovascular morbidities (2). This is also known as the Developmental Origins of Health and Disease hypothesis, which postulates that insults during intrauterine and early postnatal development can permanently change the body's structure, function, and metabolism and influence susceptibility to adult noncommunicable diseases (2). Despite their increased risk of cardiovascular disease, infants born growth restricted usually do not receive long-term cardiovascular follow-up. Depending on the definition used, IUGR can occur in up to 10% of pregnancies, and as cardiovascular disease is the number one cause of death worldwide (3), early identification of cardiovascular risk factors and targeted interventions in this high-risk population are of major clinical importance. In this review, we discuss the alterations of cardiovascular structure, function, and control that have been observed in infants born growth restricted and their implications for surveillance and intervention to prevent progression into chronic disease. CHALLENGES IN IDENTIFYING IUGRThe current literature uses many different definitions of IUGR, which may explain some of the contradicting findings discussed in this review. Traditionally, and most commonly, IUGR is defined as a birth weight below the 10th percentile for gestational age on the normative population growth curve (4). This definition, however, merely describes those who ...

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Section: Diastolic Dysfunctionmentioning

confidence: 99%

Intrauterine growth restriction: impact on cardiovascular development and function throughout infancy

et al. 2016

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“…The recorded velocity profile of left ventricular inflow shows an early filling wave (E-wave) and a late filling wave during atrial contraction (A-wave). A multitude of indices such as peak E and A velocity, their ratio, and acceleration and deceleration times are derived from this velocity pattern and proposed as markers for diastolic function [1][2][3][4][5] . Intensive research, using numerical [6][7][8][9] and in vitro [10] models, next to observations in animals and humans [8,[11][12][13][14][15][16] , have clearly elucidated the physical and physiological determinants of the transmitral velocity pattern.…”

Section: Introductionmentioning

confidence: 99%

Diastolic Filling and Pressure Imaging: Taking Advantage of the Information in a Colour M-mode Doppler Image

Mey

Sutter

Vierendeels

et al. 2001

European Journal of Echocardiography

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The ability to derive non-invasively information on left ventricular diastolic function on one hand and pressure gradients on the other hand, makes Doppler ultrasound a very attractive tool in clinical practice. However, the limitations of the standard Doppler approaches in differentiating between normal and pseudonormal filling patterns, together with the limitations of the simplified Bernoulli equation for assessing pressure gradients, are well described. In this manuscript the role of colour M-mode Doppler echocardiography as a tool that can overcome these limitations is discussed. Relevant key concepts of the haemodynamics of left ventricular filling and its relationship with colour M-mode Doppler echocardiography are introduced.

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“…Tissue Doppler imaging (TDI) is an ultrasound imaging modality that directly measures myocardial velocity during the cardiac cycle and allows wall movement to be directly www.intechopen.com Coronary Artery Disease -Current Concepts in Epidemiology, Pathophysiology, Diagnostics and Treatment 236 analyzed (Vitarelli &, Gheorghiade, 1998;Dokainish, 2004). The myocardial portion commonly studied is above the mitral annulus at either the septal or lateral walls.…”

Section: Echocardiography Evaluationmentioning

confidence: 99%