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Updated: Jan 28, 2026

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Cardiac adaptation in asphyxiated infants treated with therapeutic hypothermia
A Sehgal1,2, N Linduska1, C Huynh1
1Monash Newborn, Monash Children's Hospital, Clayton, Australia.
Background:
Hypoxic ischemic encephalopathy (HIE) affects one to two newborns per 1,000 live births and oftentimes involves multi-organ insult. The objectives were to assess the evolution of cardiac function in infants with HIE treated with therapeutic hypothermia using echocardiography (ECHO).
Methods:
Archived data during the period 2010-2016 was assessed. Amongst the infants with baseline ECHO assessments, a sub-cohort which had assessments in all the three phases (baseline/pre-active cooling [T1], cooling [T2] and rewarming [T3]) was analyzed separately.
Results:
Thirty three infants formed part of the overall cohort, the gestation and birthweight were 39.6 ± 1.6 weeks and 3306 ± 583 g, respectively. Baseline (T1) information noted impaired cardiac performance (right ventricle stroke volume 1.08 ± 0.04 ml/kg, fractional area change [FAC] 24 ± 0.5% and tricuspid annular peak systolic excursion [TAPSE] 7.46 ± 0.11mm). Serial information was available for 24 of 33 infants. Cardiac function improved significantly between the cooling and the re-warming kphases. This included changes in right ventricular output (127 ± 34 vs 164 ± 47 ml/kg/min, p <0.01) and FAC (20 ± 3 vs 28 ± 2%, p<0.01). Pairwise comparisons for fractional shortening did not show significant changes. From the cooling to the rewarming phase, maximum change was noted in FAC (26.3 ± 9.8%) while minimum change was noted in fractional shortening (median, interquartile range) of 4.6% (1.4, 9.1). Significant correlation between TAPSE and time to peak velocity as a proportion of right ventricular ejection time was noted (r2 = 0.68, p <0.001).
Conclusions:
In infants with moderate to severe HIE, cardiac function evolves during various phases of therapeutic hypothermia. Low output state during cooling may be due to a combination of the disease state (HIE) and cooling therapy.
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