# Maternal Ramadan fasting and fetal cardiac function: subclinical hemodynamic alterations revealed by doppler evaluation

**Authors:** Deniz Taşdemir

PMC · DOI: 10.1186/s12884-026-08683-4 · 2026-02-05

## TL;DR

This study found that maternal Ramadan fasting is linked to subtle changes in fetal heart function and fluid levels, but not to signs of distress.

## Contribution

The study reveals subclinical hemodynamic changes in fetuses of mothers who fast during Ramadan using Doppler echocardiography.

## Key findings

- Fasting mothers had fetuses with higher left ventricular MPI and middle cerebral artery PI.
- Fasting was associated with lower amniotic fluid index and higher cardiothoracic ratio.
- No overt signs of fetal distress were observed despite these hemodynamic differences.

## Abstract

To assess the association between maternal Ramadan fasting and fetal cardiac function and hemodynamics using comprehensive Doppler echocardiography, with a focus on subclinical myocardial and circulatory changes.

In this cross-sectional Doppler ultrasound study, 203 healthy singleton pregnancies between 24 and 32 weeks of gestation were examined, comprising 102 women who fasted for ≥ 10 days during Ramadan and 101 non-fasting controls. The study was prospectively registered with the National Clinical Trial (ClinicalTrials.gov Identifier: NCT06900257, registration date 23 March 2025). Doppler assessments included umbilical artery, middle cerebral artery, and ductus venosus pulsatility indices (PI), cerebroplacental ratio, and fetal cardiac parameters, including left and right myocardial performance indices (LV MPI, RV MPI), tricuspid and mitral annular plane systolic excursions (TAPSE, MAPSE), cardiothoracic ratio (CTR), and amniotic fluid index (AFI). Statistical analyses were performed using IBM SPSS v25.0 and Python 3.10, including group comparisons, correlation analysis, multivariable regression, and receiver operating characteristic (ROC) analysis.

Fasting pregnancies demonstrated significantly higher MCA PI (p < 0.001), LV MPI (p < 0.001), RV MPI (p = 0.041), and CTR (p < 0.001), and lower AFI (p < 0.001) than controls. Umbilical and ductus venosus PI, TAPSE, and MAPSE did not differ significantly.LV MPI correlated positively with CTR (r = 0.33) and inversely with AFI (r = –0.42). In multivariable regression analysis, fasting status was independently associated with higher LV MPI and lower AFI. ROC analysis demonstrated that LV MPI had no clinically meaningful predictive value for low amniotic fluid volume (AUC = 0.52).

Maternal Ramadan fasting was associated with mild differences in fetal cardiac and hemodynamic parameters, characterized by increased MPI and MCA PI and reduced AFI, without overt Doppler evidence of fetal distress. These findings highlight the adaptive capacity of the fetal cardiovascular system; however, given the cross-sectional design, causality and reversibility cannot be established, but support individualized monitoring during fasting in pregnancy.

ClinicalTrials.gov Identifier NCT06900257. Registered on 23 March 2025. (The record currently appears as “Update Not Released” on ClinicalTrials.gov due to the temporary U.S. government shutdown, but the submission has been completed and will be publicly released once the database reopens.)

The online version contains supplementary material available at 10.1186/s12884-026-08683-4.

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** impairment of myocardial performance (MESH:D009202), IVRT (MESH:D000377), cardiomegaly (MESH:D006332), venous congestion (MESH:D006940), cardiac compromise (MESH:D006331), thyroid or renal disease (MESH:D007674), hypoxic (MESH:D002534), fetal distress (MESH:D005316), gestational diabetes (MESH:D016640), ET (MESH:D054160), water restriction (MESH:D002313), hypertension (MESH:D006973), Amniotic Fluid (MESH:D004619), oligohydramnios (MESH:D016104), MPI (MESH:C566784), fetal growth restriction (MESH:D005317), polyhydramnios (MESH:D006831), chromosomal fetal anomalies (MESH:D000013), dehydration (MESH:D003681), cerebrovascular resistance (MESH:D002561), preeclampsia (MESH:D011225), DV (MESH:C562830), hypoglycemia (MESH:D007003), placental dysfunction (MESH:D010922), diabetes mellitus (MESH:D003920)
- **Chemicals:** ketone bodies (MESH:D007657), glucose (MESH:D005947), oxygen (MESH:D010100), PI (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12964637/full.md

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Source: https://tomesphere.com/paper/PMC12964637