Ultraschall Med
DOI: 10.1055/a-2782-7679
Letter to the Editor

Aortic pulsatile diameter changes in fetuses with growth restriction

Letter regarding: Lobmaier SM et al. Fetal cardiovascular function in a late-onset SGA and FGR cohort. Ultraschall in Med 2025; 46:270-277Pulsatiler Aorten-Durchmesser bei Feten mit Wachstumsrestriktion

Authors

  • Markus Gonser

    1   Prenatal Medicine & Sonography, Tübingen, Germany
    2   Obstetric Research Unit, University of Zurich, Zurich, Switzerland (Ringgold ID: RIN27217)
  • Ladina Vonzun

    3   Department of Obstetrics, University Hospital Zurich, Zurich, Switzerland (Ringgold ID: RIN27243)
  • Nicole Ochsenbein-Kölble

    3   Department of Obstetrics, University Hospital Zurich, Zurich, Switzerland (Ringgold ID: RIN27243)

10.1055/a-2390-2010

In this article, Lobmaier et al. studied cardiovascular functions, particularly pulsatile distensibility of the fetal aorta in late-onset SGA fetuses, including an FGR subgroup [1]. The investigation of pulsatile diameter changes of the fetal aorta is important to obtain a comprehensive fetal cardiovascular evaluation [2].

In this context it is important to ask whether aortic pulsatile distension increases in FGR due to increased fetal hypertension or aortic distensibility is already reduced due to vascular remodeling with loss of elasticity.

Using a 3–8 MHz multifrequency transducer to study aortic diameter changes with M-mode, Lobmaier et al. found significantly lower systolic/diastolic diameter changes in late-onset SGA than in controls, and even lower diameter changes in the FGR subgroup. They compared their results with the findings of Visentin et al., who, in contrast, found significantly greater systolic/diastolic aortic diameter changes in FGR than in controls (using a 2–8 MHz multifrequency transducer with cine-loop) [3].

As shown by Lobmaier in table 2, the pulsatile systolic-diastolic diameter changes were 1.1mm in the control group, 1.0mm in SGA, and 0.9mm in FGR (Anova, p = 0.001), i.e. these small group differences of 0.1mm and 0.2mm were considered to be statistically significant.

However, the accuracy of vessel diameter measurements is limited by the axial resolution of ultrasound, in particular by the wavelength λ in tissue and blood. Using a 3–8 MHz multifrequency transducer, the smallest detectable difference is 0.2mm under optimal measurement conditions (8 MHz, depth 3cm), but 0.4mm is more realistic (5 MHz, depth 5cm) [4]. Harmonics may enhance axial resolution to some degree. Was this an option in M-mode? However, if 8 MHz is the maximal recording frequency, then 0.2mm remains the axial resolution limit. Hence, it is hardly possible to objectify such small group differences.

Vessel diameter changes can be measured much more precisely using the ultrasonic echo-tracer technique, with the smallest detectable vessel wall movement being less than 0.01mm (7.8 μm). This technique was extensively used by Karel Marsal and his team in Lund, Sweden, to study fetal aortic diameter changes [2]. In fact, they found significantly lower aortic pulse amplitudes in FGR than in controls, even after adjusting for GA and for fetal weight. This retrospectively confirms the observations of Lobmaier and may be interpreted as vascular remodeling in FGR, a deteriorating developmental process with loss of aortic elasticity.

This analysis of pulsatile aortic diameter changes draws attention to an important feature in fetal cardiovascular physiology, namely pulse wave (PW) reflection, a well-established hemodynamic concept in adults. Refinements of the echo-tracer technique made it possible to visualize the effect of PW reflection on fetal aortic distension waveforms [5].

Pulsatile aortic distension waveforms are similar in shape to aortic pressure waveforms. These waveforms can be divided into 2 components: an early systolic component as the result of ventricular contraction, and a 2nd component showing an additional diameter augmentation, i.e., a mid-systolic shoulder, caused by the reflected wave, RW, returning from the fetal periphery [2] [5] [6].

Thus, the RW additionally augments the aortic diameter by distending the aorta from diameter D1, taken at the inflection point of the waveform shoulder, to D2, the peak of the 2nd systolic component ([Fig. 1]). The magnitude of this additional distension is given by the augmentation index, AI = D2/D1 (%) [5] [6].

Zoom
Fig. 1 Diameter pulse wave of the fetal aorta. D: aortic diameter; T: cardiac cycle; D1: ejection wave diameter; D2: peak diameter; ΔD: diameter augmentation showing the contribution of the reflection wave; AI = D2/D1, augmentation index.

The AI was found to be increased in fetuses with abnormal umbilical artery Doppler [6]. Obviously, in addition to vascular remodeling, fetal aortic diameter changes carry important information about the fetal arterial system, in particular fetal hypertension and vasoconstriction, conditions which modulate the pulsatile aortic distension waveform. Therefore, consideration of ultrasonic echo-tracing and fetal PW reflection is advocated when studying fetal aortic distensibility.

Footnotes:

  • The paper of Visentin et al., referenced with number 25 in the discussion section [1], is not shown in the reference list.

  • Common cardiac output (CO), given in tables 1 and 2, should be the sum of left and right CO. Rearranging the left, right, and common CO and converting the units “mm3/s” to “ml/min”, as commonly used, does not seem to resolve the problem.

However, this is beyond the scope of this letter.



Publication History

Received: 18 October 2025

Accepted: 02 January 2026

Article published online:
10 February 2026

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