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It is hard to determine the relationship between heart rate variability and brain damage

We read the article by Dr Tsuyomu Ikenoue et al. about hypoxic ischemia–lipopolysaccharide (LPS)induced heart rate pattern changes and its relations to brain damage with interest. Periventricular white matter (WM) injury is a major brain injury and accounts for the most prominent determinant of neurological deficits in infants. Epidemiological observations show that hypoxic ischemia and inflammation are the two major risk factors for WM injury or cerebral palsy in very preterm infants. In our opinion, the work using fetal heart rate (FHR) patterns to predict brain damage is very useful. However, a question still remains because the model is not a good model for brain damage. Although the authors found that the specificity and sensitivity of FHR pattern changes in this model were sufficient, there still remains a phenomenon that only 5/16 rats developed brain damage; that is, using this model to research the relationship between brain damage and FHR is not suitable. Intraperitoneally injected LPS is not a good way to induce brain damage compared with intracerebral injection. In fact, by using an intraventricular injection of LPS (1 mg/kg), inducing hypoxia with a 10% oxygen concentration for 90 min, ligating the right common carotid and using the P9 day detection method, our lab also carried out similar work several years ago, but obtained a negative result. We placed 40 rats into an experimental group and a non-LPS group, and an additional five rats in a control group. We found that in experimental group, 21/30 rats developed brain damage (neuron loss) and exhibited behavior deficits (as determined using a water maze); however, although the baseline heart rates were different, the heart rate variability was not statistically different between the brain-damaged rats and the health ones in the experimental group. Finally, using the heart rate pattern to predict fetal brain damage is an easy and practical method, and its development would be worthwhile; however, in the article by Ikenoue’s et al., the model was not a good one for the induction of brain damage. Besides that, although the authors obtained exciting results, the number of rats was not large enough for the development of a useful conclusion; also, repetitive hypoxia may cause hypoxia pre-conditioning, which is not a natural condition. All these drawbacks will limit future work. We would like to draw your attention to the article’s Methods section, which states: ‘Intermittent hypoxia was repeated at 10-min intervals for a total of 10 times, in which the duration of each hypoxic period was 6 min.’ This should be 150 min in total; however, in Figures 2 and 3, the x-axis showed just 110 min and finished total 10 times hypoxia.