Zidovudine treatment in HIV-infected pregnant women is associated with fetal cardiac remodelling

García‐Otero, Laura; López, Marta; Gómez, O.; Goncé, A.; Bennásar, M.; Martínez, Josep M.; Valenzuela-Alcaráz, Brenda; Rodríguez‐López, Mérida; Sitges, Marta; Loncá, Montserrat; Bijnens, Bart; Crispi, F.; Gratacós, E.

doi:10.1097/qad.0000000000001066

Cited by 33 publications

(40 citation statements)

References 41 publications

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“…However, while postnatal cardiac remodeling reverts after treating the cause, cardiac remodeling occurring in utero might persist postnatally even after the trigger has disappeared. Actually, postnatal persistence of fetal cardiac remodeling has been demonstrated in several conditions such as fetal growth restriction, maternal diabetes, exposure to antiretroviral drugs, prematurity, or assisted reproductive technologies [9,10,16,[34][35][36][37][38]. This phenomenon is explained by the fetal programming hypothesis that proposes a prenatal origin for some adult cardiovascular diseases.…”

Section: Resultsmentioning

confidence: 99%

“…Direct Myocardial Damage. Myocardium could directly be affected by a toxin (i.e., antiretroviral drugs) [9], hypoxia/ischemia (i.e., placental insufficiency [10] or anemia), or genetic cardiomyopathies inducing global/regional edema, inflammation, fiber disarray, fibrosis, or cell loss. Cardiac toxicity is frequently compensated by myocardial hypertrophy, compensating for cell loss or decreased intrinsic contractility.…”

Section: Main Determinants Of Fetal Cardiac Remodelingmentioning

confidence: 99%

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Main Patterns of Fetal Cardiac Remodeling

et al. 2020

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The heart is a central organ in the fetal adaptation to an adverse environment. Fetal cardiac changes may persist postnatally and increase the risk of cardiovascular disease in adulthood. Knowledge about fetal cardiac structural as well as functional remodeling has radically improved over the last few years. As it occurs in postnatal life, the fetal heart remodels -changing its structure and shape -to adapt to an insult. Several conditions have been reported to be associated with fetal cardiac remodeling including intrauterine growth restriction, diabetes, exposure to antiretroviral drugs, conception by assisted reproductive technologies, pulmonary stenosis, and other congenital heart diseases. Here we summarized the main observable patterns of cardiac remodeling, i.e., globular shape, hypertrophy without dilation, and hypertrophy with cardiomegaly. We discuss the potential pathophysiology behind different types of remodeling. Defining precisely the distinct patterns of fetal cardiac remodeling is critical for advancing in the understanding of fetal cardiovascular programming and its consequences on adult health, and potentially for the design of preventive strategies that might have an impact on long-term cardiovascular health.

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Section: Resultsmentioning

confidence: 99%

Section: Main Determinants Of Fetal Cardiac Remodelingmentioning

confidence: 99%

Main Patterns of Fetal Cardiac Remodeling

et al. 2020

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“…We have provided standardized and comprehensive reference values for fetal cardiac morphometric parameters across gestation in a low-risk population. An accurate measurement of heart dimensions might be very useful to identify and monitor cardiac remodeling -change in shape, size, and structure -in response to pressure/volume overload or cardiac toxicity in many conditions, such as CHD [36,37], maternal diabetes [9], twin-to-twin transfusion syndrome [38], FGR [39], conception by ART [7], fetal anemia [40], congenital diaphragmatic hernia [41], or exposure to antiretroviral drugs [8]. A better understanding and follow-up of fetal cardiac adaptations could enable early interventions and minimize long-term cardiovascular consequences [42].…”

Section: Discussionmentioning

confidence: 99%

“…Since then, technical advances have enabled a notable improvement in the assessment of cardiac structure and function. DOI The concept of cardiac remodeling -defined as changes in size, shape, structure, and function of the heart in order to adapt to an insult [4] -is now being applied in fetal life not only in CHD cases [5] but also in other prenatal conditions, such as fetal growth restriction (FGR) [6], the use of assisted reproductive techniques (ART) [7], exposure to toxics [8], and pregestational diabetes [9]. An adverse prenatal environment during the crucial period of in utero development might have a direct impact on fetal cardiac structure and long-lasting consequences on health [10].…”

Section: Introductionmentioning

confidence: 99%

Nomograms of Fetal Cardiac Dimensions at 18–41 Weeks of Gestation

et al. 2019

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Objective: There is a need for standardized reference values for cardiac dimensions in prenatal life. The objective of the present study was to construct nomograms for fetal cardiac dimensions using a well-defined echocardiographic methodology in a low-risk population. Methods: This is a prospective cohort study including 602 low-risk singleton pregnancies undergoing a standardized fetal echocardiography to accurately assess fetal cardiac, ventricular, and atrial dimensions. Parametric regressions were tested to model each measurement against gestational age from 18 to 41 weeks of gestation. Results: Nomograms were constructed for fetal cardiac dimensions (transverse and longitudinal diameters and areas) of the whole heart, atria, and ventricles, as well as myocardial wall thicknesses. All dimensions showed a progressive increase with gestational age. The best model for most parameters was a second-degree linear polynomial.Fetal cardiac, ventricular, and atrial diameters and areas were successfully obtained in 98.6% of the fetuses, while myocardial wall thicknesses could be obtained in 96.5% of the population. The results showed excellent interobserver and intraobserver reproducibility (intraclass correlation coefficient, ICC > 0.811 and ICC > 0.957, respectively). Conclusions: We provide standardized and comprehensively evaluated reference values for fetal cardiac morphometric parameters across gestation in a low-risk population. These nomograms would enable the early identification of different patterns of fetal cardiac remodeling.

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“…Diastolic dysfunction: Increased E/A ratio on the right side. Systolic dysfunction: Decreased mitral S′ (systolic annular peak velocity) and increased left ICT and IRT [25,26]. Global function: No effects ( Figure 2); however, zidovudine (NRTI) caused hypertrophy of the myocardial walls [26].…”

Section: Highly Active Antiretroviral Therapy (Haart)mentioning

confidence: 99%

Drug exposure during pregnancy and fetal cardiac function – a systematic review

Kolding

Eken

Uldbjerg

2020

Journal of Perinatal Medicine

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Background:The aim of this systematic review was to describe the effects of drug exposure during pregnancy on fetal cardiac function. Methods: We searched MEDLINE, Embase, Cochrane and SCOPUS for studies assessing fetal cardiac function in drug-exposed human pregnancies. Risk of bias was assessed by the Risk Of Bias In Non-randomized Studies of Interventions (ROBIN-I) tool. Results: We included 32 studies on eight different drug groups. They included 51 outcome variables, which were all based on ultrasound techniques primarily assessing systolic function: pulsed wave Doppler, tissue Doppler imaging (TDI), and B-and M-mode. Overall, the risk of bias was moderate. β 2 agonists increased the systolic velocity in the ductus arteriosus and the fetal heart rate. β-blockers caused unchanged or decreased systolic velocity of the pulmonary trunk. Corticosteroids increased the velocity in the ductus arteriosus. Furthermore, in growth-restricted fetuses with an increased myocardial performance index (MPI′) on the right side, corticosteroids normalized this variable. Nonsteroidal anti-inflammatory drugs (NSAIDs), but not acetylsalicylic acid, increased the flow velocities in the ductus arteriosus, decreased the shortening fraction and increased the end-diastolic ventricular diameters. Metformin and insulin normalized the diastolic strain and global longitudinal strain in diabetic pregnancies. Highly active antiretroviral therapy (HAART) exposure increased the E/A ratio on the right side, prolonged the isovolumic relaxation time (IRT) and ejection time, shortened the isovolumic contraction time (ICT), and decreased left myocardial systolic peak velocities. Chemotherapy did not cause detectable changes. Conclusion: Six of the eight drug groups caused detectable changes in fetal cardiac function. However, the evidence was hampered by only a few studies for some drugs.

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Zidovudine treatment in HIV-infected pregnant women is associated with fetal cardiac remodelling

Abstract: Fetuses from HIV-infected mothers on cART have cardiac remodelling and dysfunction, which might explain the cardiovascular changes described in childhood. Fetal cardiac remodelling was essentially associated with maternal treatment with zidovudine which challenges its use during pregnancy.

Cited by 33 publications

References 41 publications

Main Patterns of Fetal Cardiac Remodeling

Main Patterns of Fetal Cardiac Remodeling

Nomograms of Fetal Cardiac Dimensions at 18–41 Weeks of Gestation

Drug exposure during pregnancy and fetal cardiac function – a systematic review

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