Altered maternal left ventricular contractility and function during normal pregnancy

Estensen, Mette-Elise; Beitnes, Jan Otto; Grindheim, Guro; Aaberge, Lars; Smiseth, Otto A.; Henriksen, Tore; Aakhus, Svend

doi:10.1002/uog.12296

Cited by 77 publications

(73 citation statements)

References 38 publications

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“…The response of cardiomyocytes to volume overload includes the addition of sarcomeres in series to existing sarcomeres, resulting in increased chamber diameter without increasing wall thickness. Additionally, this type of cardiac remodeling has been shown to enhance contractile function, an essential requirement in pregnancy to allow for the maternal system to successfully adapt to the increased metabolic need of the fetus [1][2][3].…”

Section: Discussionmentioning

confidence: 98%

“…Although ANP À/À dams exhibit larger hearts at this time point postpartum, it is important to mention that identical trends in cardiac change were observed in both hypertensive dams and control groups, suggesting that the presence of chronic hypertension and/or lack of ANP expression did not influence pregnancy-related cardiac remodeling in pregnant mice. Other investigations have also reported sustained pregnancy-induced CH postpartum in normal [1,7,31] and pre-eclamptic [32] pregnancies. Thus, along with our data set, there is a growing body of evidence to suggest that the critical window of significant maternal cardiac change occurs early postpartum.…”

Section: Cardiac Hypertrophy In Pregnancy Peaks Postpartummentioning

confidence: 91%

“…In normal pregnancy, the cardiovascular system undergoes significant physiological changes to allow for normal maternal function during pregnancy and to provide adequate oxygenation and nutrient supply to the fetus through uteroplacental circulation [1][2][3]. Along with the characteristic hemodynamic changes associated with pregnancy, such as increased cardiac output [4,5], increased stroke volume, increased heart rate, and decreased vascular resistance [6], the maternal heart is also subject to extensive remodeling [3,7,8].…”

Section: Introductionmentioning

confidence: 99%

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Onset and Regression of Pregnancy-Induced Cardiac Alterations in Gestationally Hypertensive Mice: The Role of the Natriuretic Peptide System1

Ventura

Tse

et al. 2015

Biology of Reproduction

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Pregnancy induces cardiovascular adaptations in response to increased volume overload. Aside from the hemodynamic changes that occur during pregnancy, the maternal heart also undergoes structural changes. However, cardiac modulation in pregnancies complicated by gestational hypertension is incompletely understood. The objectives of the current investigation were to determine the role of the natriuretic peptide (NP) system in pregnancy and to assess alterations in pregnancy-induced cardiac hypertrophy between gestationally hypertensive and normotensive dams. Previously we have shown that mice lacking the expression of atrial NP (ANP; ANP(-/-)) exhibit a gestational hypertensive phenotype. In the current study, female ANP(+/+) and ANP(-/-) mice were mated with ANP(+/+) males. Changes in cardiac size and weight were evaluated across pregnancy at Gestational Days 15.5 and 17.5 and Postnatal Days 7, 14, and 28. Nonpregnant mice were used as controls. Physical measurement recordings and histological analyses demonstrated peak cardiac hypertrophy occurring at 14 days postpartum in both ANP(+/+) and ANP(-/-) dams with little to no change during pregnancy. Additionally, left ventricular expression of the renin-angiotensin system (RAS) and NP system was quantified by real-time quantitative polymerase chain reaction. Up-regulation of Agt and AT(1a) genes was observed late in pregnancy, while Nppa and Nppb genes were significantly up-regulated postpartum. Our data suggest that pregnancy-induced cardiac hypertrophy may be influenced by the RAS throughout gestation and by the NP system postpartum. Further investigations are required to gain a complete understanding of the mechanistic aspects of pregnancy-induced cardiac hypertrophy.

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Section: Discussionmentioning

confidence: 98%

Section: Cardiac Hypertrophy In Pregnancy Peaks Postpartummentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Onset and Regression of Pregnancy-Induced Cardiac Alterations in Gestationally Hypertensive Mice: The Role of the Natriuretic Peptide System1

Ventura

Tse

et al. 2015

Biology of Reproduction

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“…Initially there is a decrease in blood pressure (BP) and systemic vascular resistance (SVR) followed by an increase during the third trimester [16]. Cardiac morphological changes during pregnancy are characterised by reversible left ventricular hypertrophy and chamber enlargement [17], and studies on cardiac function report altered left ventricular systolic and diastolic performance [17],[18]. The cardiovascular system of the pregnant women may respond differently to a variety of challenges.…”

Section: Introductionmentioning

confidence: 99%

Effect of Passive Leg Raising on Systemic Hemodynamics of Pregnant Women: A Dynamic Assessment of Maternal Cardiovascular Function at 22–24 Weeks of Gestation

2014

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ObjectiveTo investigate functional hemodynamic response to passive leg raising in healthy pregnant women and compare it with non-pregnant controls.Materials and MethodsThis was a prospective cross-sectional study with a case-control design. A total of 108 healthy pregnant women at 22–24 weeks of gestation and 54 non-pregnant women were included. Cardiac function and systemic hemodynamics were studied at baseline and 90 seconds after passive leg raising using non-invasive impedance cardiography.Main outcome measuresTrends and magnitudes of changes in impedance cardiography derived parameters of cardiac function and systemic hemodynamics caused by passive leg raising, and preload responsiveness defined as >10% increase in stroke volume or cardiac output after passive leg raising compared to baseline.ResultsThe hemodynamic parameters in both pregnant and non-pregnant women changed significantly during passive leg raising compared to baseline, but the magnitude and trend of change was similar in both groups. The stroke volume increased both in pregnant (p = 0.042) and non-pregnant (p = 0.018) women, whereas the blood pressure and systemic vascular resistance decreased (p<0.001) following passive leg raising in both groups. Only 14.8% of pregnant women and 18.5% of non-pregnant women were preload responsive and the difference between groups was not significant (p = 0.705).ConclusionStatic measures of cardiovascular status are different between healthy pregnant and non-pregnant women, but the physiological response to passive leg raising is similar and not modified by pregnancy at 22–24 weeks of gestation. Whether physiological response to passive leg raising is different in earlier and later stages of pregnancy merit further investigation.

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“…4) It has been reported that cardiac output during pregnancy increases by 20%. 5) Such cardiac burdens are considered to be prominent from the second half of pregnancy to the early postpartum period. 1) Although peripartum cardiomyopathy (PPCM) is one of the most severe conditions seen in obstetric practice, reliable screening methods for pregnant women at high risk of developing severe myocardial disorders have not been established.…”

mentioning

confidence: 99%

Detection of Peripartum Myocardial Burden by Vector-Projected 187 Channel Electrocardiography and Serum NT-proBNP

et al. 2013

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SummaryThere is no reliable method of screening for pregnant women at high risk of developing severe myocardial disorders. In this study, we used vector-projected 187 channel electrocardiography (DREAM-ECG) and serum biochemical markers to evaluate peripartum myocardial burden in pregnant women. Forty-one pregnant women were examined at 36-37 weeks gestation (GW36), 7 days postpartum (PPD7), and 1 month postpartum (PPM1). Ten non-pregnant control women were assessed at a single time point. Heart rate, sympathetic index, and repolarization index (RTc dispersion) were quantified using the DREAM-ECG system, and serum levels of NT-proBNP, cardiac troponin T, estrogen, and progesterone were determined. Heart rate and the sympathetic index decreased from GW36 to PPM1 (P = 0.0031). The repolarization index decreased over time and was greater than in non-pregnant controls (31 ± 13 ms). Estrogen and progesterone at PPD7 and PPM1 were significantly lower than those at GW36 (P < 0.0001, P < 0.001). NT-proBNP at PPD7 was greater than at GW36 (median 29 pg/mL at GW36, 86 pg/mL at PPD7), and decreased at PPM1 in comparison to PPD7 (median 18.5 pg/mL). Troponin T was in the normal range during the whole period (< 0.003 ng/mL). In conclusion, these results indicate that the peripartum myocardial burden in pregnant women does not return to normal nonpregnant levels by PPM1. We propose that both repolarization indexes such as RTc dispersion by DREAM-ECG and serum biochemical markers may identify pregnant women at high risk of developing severe myocardial damage in the peripartum period. (Int Heart J 2013; 54: 140-145)

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Altered maternal left ventricular contractility and function during normal pregnancy

Cited by 77 publications

References 38 publications

Onset and Regression of Pregnancy-Induced Cardiac Alterations in Gestationally Hypertensive Mice: The Role of the Natriuretic Peptide System1

Onset and Regression of Pregnancy-Induced Cardiac Alterations in Gestationally Hypertensive Mice: The Role of the Natriuretic Peptide System1

Effect of Passive Leg Raising on Systemic Hemodynamics of Pregnant Women: A Dynamic Assessment of Maternal Cardiovascular Function at 22–24 Weeks of Gestation

Detection of Peripartum Myocardial Burden by Vector-Projected 187 Channel Electrocardiography and Serum NT-proBNP

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