Tricuspid regurgitation during pregnancy: Two-dimensional and pulsed doppler echocardiographic observations

Limacher, Marian C.; Ware, J. Anthony; O'Meara, Michael E.; Fernandez, Genaro C.; Young, James B.

doi:10.1016/0002-9149(85)90746-5

Cited by 27 publications

(7 citation statements)

References 20 publications

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“…No data are available regarding changes in pulmonary artery and mitral orifice areas during pregnancy. However Limacher et al (1985) reported a significant increase in tricuspid annulus diameter as well as right atrial and ventricular dimensions during pregnancy. It would appear therefore that dilatation involves not only all the intracardiac chambers but their respective outflow valves as well.…”

Section: Discussionmentioning

confidence: 95%

Haemodynamic changes during the puerperium: a Doppler and M‐mode echocardiographic study

Robson

Dunlop

Moore

et al. 1987

BJOG

272

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Summary. Serial haemodynamic investigations were performed in 15 women at 38 weeks gestation and then 2, 6, 12 and 24 weeks after delivery. Cardiac output was measured by Doppler and cross‐sectional echocardiography at the aortic, pulmonary and mitral valves. Cardiac chamber size and ventricular function were investigated by M‐mode echocardiography. Flow measurements at the three intracardiac sites correlated closely. Cardiac output fell from a mean of 7.421/min at 38 weeks to 4.961/min at 24 weeks after delivery, a fall of 33%. Most of this decrease (28%) had occurred by 2 weeks. This was associated with a 20% reduction in heart rate and an 18% reduction in stroke volume. By 2 weeks after delivery there was a significant decrease in left atrial dimension and left ventricular end‐diastolic dimension. Left ventricular wall thickness and mass declined throughout the period of study as did aortic, pulmonary and mitral valve areas. M‐mode derived indices of myocardial contractility were all significantly reduced by 2 weeks and thereafter showed no further change. No haemodynamic differences were found between lactating and non‐lactating mothers.

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Section: Discussionmentioning

confidence: 95%

Haemodynamic changes during the puerperium: a Doppler and M‐mode echocardiographic study

Robson

Dunlop

Moore

et al. 1987

BJOG

272

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“…In the current study, tPVR was calculated directly from mPAP and CO measured in the PA (tPVR = mPAP/CO); in the prior study, CO was computed from SV times HR, which will overestimate CO if significant tricuspid regurgitation exists. Since tricuspid regurgitation is likely estrogen-dependent 20 and often observed in PAH patients 30 , we anticipate that the SV-method overestimated CO and thus underestimated tPVR in the estrogen-treated SuHx animals, which accounts for the discrepancy between these studies.…”

Section: Discussionmentioning

confidence: 93%

Estrogen Preserves Pulsatile Pulmonary Arterial Hemodynamics in Pulmonary Arterial Hypertension

Liu¹,

Hacker

Eickhoff

et al. 2016

Ann Biomed Eng

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Pulmonary arterial hypertension (PAH) is caused by extensive pulmonary vascular remodeling that increases right ventricular (RV) afterload and leads to RV failure. PAH predominantly affects women; paradoxically, female PAH patients have better outcomes than men. The roles of estrogen in PAH remain controversial, which is referred to as “the estrogen paradox”. Here, we sought to determine the role of estrogen in pulsatile pulmonary arterial hemodynamic changes and its impact on RV functional adaption to PAH. Female mice were ovariectomized and replenished with estrogen or placebo. PAH was induced with SU5416 and chronic hypoxia (SuHx). In vivo hemodynamic measurements showed that (1) estrogen prevented loss of pulmonary vascular compliance with limited effects on the increase of pulmonary vascular resistance in PAH; (2) estrogen attenuated increases in wave reflections in PAH and limited its adverse effects on PA systolic and pulse pressures; and (3) estrogen maintained the total hydraulic power and preserved transpulmonary vascular efficiency in PAH. This study demonstrates that estrogen preserves pulmonary vascular compliance independent of pulmonary vascular resistance, which provides a mechanical mechanism for ability of estrogen to delay disease progression without preventing onset. The estrogenic protection of pulsatile pulmonary hemodynamics underscores the therapeutic potential of estrogen in PAH.

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“…However, functional tricuspid regurgitation is common in pregnant women, which may give rise to murmur in a clinically and hemodynamically stable patient. 15 Again, tricuspid regurgitation may be secondary to underlying severe mitral valve disease.…”

Section: Tricuspid Valve Diseasementioning

confidence: 99%

Valvular heart disease in pregnancy: A review

Khanom

Hossain²

2015

Journal of Indian College of Cardiology

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Available online xxx Keywords:Valvular heart disease Pregnancy Maternal mortality a b s t r a c t Pregnancy is associated with significant hemodynamic changes that can aggravate valvular heart disease and increase the risk of thrombo-embolic events. Risk during pregnancy is dependent on the valve lesion, its severity, maternal pre-pregnancy functional capacity and the degree of left ventricular systolic function. For stenotic lesions, maternal and fetal risk increases when mitral or aortic valve area is less than 1.5 cm 2 .Pregnancy is usually well tolerated in women with chronic left sided valve regurgitation without left ventricular dysfunction. In patients with heart valve prostheses, hemodynamic tolerance is generally good, the issue is with anticoagulation. Many women with valvular heart disease can be successfully managed throughout pregnancy, labor and delivery with conservative medical measures designed to optimize intravascular volume, systemic loading conditions, blood pressure and rhythm. High risk patients require multidisciplinary close follow-up, so that any deterioration in symptom can be detected early and managed in a timely way.

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Tricuspid regurgitation during pregnancy: Two-dimensional and pulsed doppler echocardiographic observations

Cited by 27 publications

References 20 publications

Haemodynamic changes during the puerperium: a Doppler and M‐mode echocardiographic study

Haemodynamic changes during the puerperium: a Doppler and M‐mode echocardiographic study

Estrogen Preserves Pulsatile Pulmonary Arterial Hemodynamics in Pulmonary Arterial Hypertension

Valvular heart disease in pregnancy: A review

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