Sequential development of fetal aortic valve stenosis and endocardial fibroelastosis during the second trimester of pregnancy

Mielke, G.; Mayer, Ralf W.; Hassberg, D.; Breuer, Johannes

doi:10.1016/s0002-8703(97)70160-1

Cited by 11 publications

(6 citation statements)

References 11 publications

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“…In pulmonary valve stenosis, reduced diameters of the pulmonary valve anulus are observed 16 . Reference ranges for cardiac dimensions in the first half of the second trimester of pregnancy are rare but increasingly important, as early diagnosis of congenital heart defects has become possible 17,18 .…”

Section: Discussionmentioning

confidence: 99%

Reference ranges for two‐dimensional echocardiographic examination of the fetal ductus arteriosus

Mielke

Benda

2000

Ultrasound in Obstet & Gyne

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Section: Discussionmentioning

confidence: 99%

Reference ranges for two‐dimensional echocardiographic examination of the fetal ductus arteriosus

Mielke

Benda

2000

Ultrasound in Obstet & Gyne

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“…There is an overlap of pathology between these three entities. [8][9][10] In this report, we describe our own experience in intervention in a fetus suspected of developing hypoplasia of the left heart.…”

Section: Arious Physiologic Mechanisms Have Beenmentioning

confidence: 99%

How to grow a heart: fibreoptic guided fetal aortic valvotomy

Suh¹,

Quintessenza

Huhta

et al. 2006

Cardiol Young

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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

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“…Instead of cellular hypertrophy and concentric LV hypertrophy, fetal myocardial adaptations are characterized by myocyte hyperplasia, LV dilation, endocardial fibroelastosis, myocardial fibrosis, and early systolic and diastolic dysfunction . The mechanisms that cause the unique response of the fetal myocardium to pressure load are not entirely understood but may include increased wall stress leading to upregulation of profibrotic factors, impaired myocardial oxygen delivery related to elevated LV end‐diastolic pressure and subendocardial ischemia, and/or altered intracellular calcium handling …”

Section: Introductionmentioning

confidence: 99%

“…[2][3][4][5][6] The mechanisms that cause the unique response of the fetal myocardium to pressure load are not entirely understood but may include increased wall stress leading to upregulation of profibrotic factors, impaired myocardial oxygen delivery related to elevated LV end-diastolic pressure and subendocardial ischemia, and/or altered intracellular calcium handling. [7][8][9][10][11][12][13][14][15] N-terminus brain pro-natriuretic peptide (NT-BNP) and troponin are markers of cardiac function and health that are excreted via the urinary tract and are therefore detectable in amniotic fluid. 16 NT-BNP is a cleavage product of cardiac peptide BNP which is released in response to myocardial stretch and has become a well-established marker of heart failure.…”

Section: Introductionmentioning

confidence: 99%

Myocardial injury in fetal aortic stenosis: Insights from amniotic fluid analysis

et al. 2018

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Sequential development of fetal aortic valve stenosis and endocardial fibroelastosis during the second trimester of pregnancy

Cited by 11 publications

References 11 publications

Reference ranges for two‐dimensional echocardiographic examination of the fetal ductus arteriosus

Reference ranges for two‐dimensional echocardiographic examination of the fetal ductus arteriosus

How to grow a heart: fibreoptic guided fetal aortic valvotomy

Myocardial injury in fetal aortic stenosis: Insights from amniotic fluid analysis

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