Key result
Extremely low birth weight links to stiffer arteries and altered cardiac structure despite preserved ventricular-arterial coupling.
Why the study?
Premature birth disrupts intrauterine maturation of the left ventricle and arteries, prompting investigation into its impact on ventricular-arterial coupling as a potential precursor of adult cardiovascular disease.
Does premature birth (extremely-low-birth-weight) alter ventricular-arterial coupling and cardiovascular hemodynamics in 11-year-old children?
Case-Control (n=180)
Single-blind
No
Does premature birth (extremely-low-birth-weight) alter ventricular-arterial coupling and cardiovascular hemodynamics in 11-year-old children?
Extremely-low-birth-weight children have preserved ventricular-arterial coupling at age 11 due to compensatory mechanisms, despite having altered cardiovascular hemodynamics and structure.
Answers are grounded in this paper and cite their sources.
Preserved coupling despite altered hemodynamics in ELBW children suggests compensation; leaves open long-term cardiovascular risk.
BACKGROUND: Premature birth disrupts the intra-uterine structural and functional maturation of the left ventricle (LV) and arteries. The study investigated the impact of premature birth on ventricular-arterial coupling (VAC), a potential precursor of cardiovascular disease in adulthood. METHODS: This case-control study in Northern Belgium (2011-2016) included 93 extremely-low-birth-weight (ELBW) cases and 87 sex and age-matched term-born controls. Main outcomes included SBP and DBP, central arterial properties, echocardiographic structure and function, and VAC. RESULTS: Compared with controls, cases were shorter by 4.1 cm [95% confidence interval (95% CI): 1.3-7.0] and lighter by 4.1 kg (95% CI: 1.3-6.9). Cases had higher central SBP/DBP (+7.3/3.0 mmHg; 95% CI: 4.7-9.9/1.1-4.8), lower left ventricular end-diastolic and end-systolic dimensions, and 9.2 g (95% CI: 3.7-14.6) lower left ventricular mass. Left ventricular volumes and mass correlated with body size without significant between-group differences ( P ≥ 0.12). Cardiac output was 0.38 l/min lower in cases, who also had higher arterial resistance (29.5 vs. 24.4 mmHg × min/l) and augmentation ratio (1.10 vs. 1.05). The tension-time index was 231 mmHg × ms (95% CI: 128-335) higher in cases. Ea and Ees were higher in cases (0.40 and 0.65 mmHg/ml, respectively), but VAC did not differ between groups ( P = 0.48). CONCLUSION: Compensatory mechanisms maintain the anatomical and functional integrity of the cardiovascular system in ELBW youth, but mask their vulnerability to cardiovascular disease in adulthood and necessitate careful follow-up during adolescence.
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Zhang et al. (2025) conducted a case-control in Extremely low birth weight (ELBW) (n=180). Extremely low birth weight (ELBW) vs. Term-born controls was evaluated on Ventricular-arterial coupling (VAC) (p=0.48). Extremely low birth weight children had stiffer central arteries and altered cardiac structure compared to term-born controls, but ventricular-arterial coupling was preserved.
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