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Background: Heated humidified high-flow nasal cannulas (HHHFNCs) are increasingly used as an alternative strategy for weaning from nasal continuous positive airway pressure (NCPAP) in premature infants. However, the optimal pressure provided by HHHFNCs is unknown. This retrospective study investigated the pressure changes and associated factors during HHHFNC therapy in preterm infants. Methods: Clinically stable preterm neonates born with a birth weight of 2500 g or less and receiving HHHFNC therapy for weaning from NCPAP were enrolled. The flow of the HHHNFCs was adjusted to achieve an initial pressure equivalent to the positive expiratory pressure (PEEP) of NCPAP. Subsequent pressure changes in the HHHFNCs were measured by a GiO digital pressure gauge. Results: Nine premature infants were enrolled. Their gestational age (mean ± SD) was 28.33 ± 2.61 weeks, and the birth weight was 1102.00 ± 327.53 g. Overall, 437 pressure measurements were conducted. The median pressure of the HHHFNCs was 5 cmH2O. The generated pressure had a significant association with the body weight, postmenstrual age (PMA) and flow rate. A multiple regression model revealed that the measured pressure (cmH2O) = −5.769 + 1.021 × flow rate (L/min) − 0.797 × body weight (kg) + 0.035 × PMA (days) (r2 = 0.37, p < 0.001). Conclusions: The pressure provided by HHHFNCs is influenced by body weight, PMA, and flow rate. It is feasible to set the delivered pressure of HHHFNCs to match the applied PEEP of NCPAP initially, facilitating the weaning of preterm infants from NCPAP to HHHFNCs. [ABSTRACT FROM AUTHOR]

Ductus arteriosus closure may be delayed in preterm infants, and prostaglandin, a vasodilator, can affect ductal patency. Furosemide can increase renal prostaglandin synthesis, so its net effect on patent ductus arteriosus (PDA) is uncertain. Our goal is to explore the relationship between furosemide and spontaneous ductal closure in very-low-birth-weight preterm infants. Our treatment for PDA involves fluid restriction initially and furosemide administration for hemodynamically significant PDA until closure is confirmed by the echocardiogram. We enrolled 105 infants from 1 January 2019 to 30 June 2022 and evaluated the impact of furosemide on ductal closure, including exposure duration and cumulative dose. There is no correlation between furosemide exposure and spontaneous ductal closure (p = 0.384). Furosemide exposure does not delay the postmenstrual age at which spontaneous ductal closure occurs (p = 0.558). The time for spontaneous ductal closure is positively associated with furosemide prescription days (coefficient value = 0.547, p = 0.026) and negatively with gestational age (coefficient value = −0.384, p = 0.062). The prescription of furosemide does not impact the probability or time duration of ductus arteriosus spontaneous closure. The cumulative dose of furosemide has minimal impact on ductal closure. The correlation between furosemide exposure duration and ductal patency duration is likely due to our treatment protocol, with gestational age being a significant factor. [ABSTRACT FROM AUTHOR]

In recent years, the utilization of minimally invasive surfactant therapy (MIST) and Non-invasive ventilation (NIV) as the primary respiratory assistance has become increasingly prevalent among preterm infants with neonatal respiratory distress syndrome (RDS). This study aims to compare the outcomes between MIST administered with nasal continuous positive airway pressure (NCPAP) versus nasal intermittent positive pressure ventilation (NIPPV), with the objective of exploring the respiratory therapeutic benefits of these two approaches. This retrospective study collected data from the neonatal intensive care unit of Kaohsiung Medical University Hospital spanning from January 2016 to June 2021. Infants were divided into two groups based on the type of NIV utilized. The NCPAP group comprised 32 infants, while the NIPPV group comprised 22 infants. Statistical analysis revealed significant differences: the NIPPV group had a smaller gestational age, lower birth weight, higher proportion of female infants, and earlier initiation of MIST. Additionally, the NIPPV group exhibited higher incidence rates of retinopathy of prematurity, longer respiratory support duration, prolonged hospitalization, and mortality. However, upon adjustment, these differences were not statistically significant. Analysis of venous blood gas and respiratory parameter changes indicated that both the NCPAP and NIPPV groups experienced improvements in oxygenation and ventilation following MIST. [ABSTRACT FROM AUTHOR]

Given the limited availability of evidence-based methods for assessing the timing of extubation in intubated preterm infants, we aimed to standardize the extubation protocol in this single-center, retrospective study. To accomplish this, we established an extubation evaluation form to assess the suitability of extubation in preterm infants. The form comprises six indicators: improved clinical condition, spontaneous breath rate ≥ 30 breaths per minute, peak inspiratory pressure (PIP) ≤ 15 cmH2O, fraction of inspired oxygen (FiO2) ≤ 30%, blood pH ≥ 7.2, and mixed venous carbon dioxide tension (PvCO2) < 70 mmHg. Each positive answer is given one point, indicating a maximum of six points. We enrolled 41 intubated preterm infants (gestational age < 32 weeks, birth weight < 1500 g) who were receiving mechanical ventilation support for over 24 h. Among them, 35 were successfully extubated, and 6 were not. After completing the extubation evaluation form and adjusting for birth weight and postextubation device, we observed that the total score of the form was significantly associated with successful extubation; the higher the score, the greater the chance of successful extubation. Thus, we infer that the extubation evaluation form may provide a more objective standard for extubation assessment in preterm infants. [ABSTRACT FROM AUTHOR]

Background and Purpose: Mitochondrial dysfunction plays a role in the progression of cardiovascular diseases including heart failure. 3-Hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins), which inhibit ROS synthesis, show cardioprotective effects in chronic heart failure. However, the beneficial role of statins in mitochondrial protection in heart failure remains unclear.Experimental Approach: Rats were treated with angiotensin II (1.5 mg·kg-1 ·day-1 ) or co-administered simvastatin (oral, 10 mg·kg-1 ) for 14 days; and then administration was stopped for the following 14 days. Cardiac structure/function was examined by wheat germ agglutinin staining and echocardiography. Mitochondrial morphology and the numbers of lipid droplets, lysosomes, autophagosomes, and mitophagosomes were determined by transmission electron microscopy. Human cardiomyocytes were stimulated, and intracellular ROS and mitochondrial membrane potential (ΔΨm ) changes were measured by flow cytometry and JC-1 staining, respectively. Autophagy and mitophagy-related and mitochondria-regulated apoptotic proteins were identified by immunohistochemistry and western blotting.Key Results: Simvastatin significantly reduced ROS production and attenuated the disruption of ΔΨm . Simvastatin induced the accumulation of lipid droplets to provide energy for maintaining mitochondrial function, promoted autophagy and mitophagy, and inhibited mitochondria-mediated apoptosis. These findings suggest that mitochondrial protection mediated by simvastatin plays a therapeutic role in heart failure prevention by modulating antioxidant status and promoting energy supplies for autophagy and mitophagy to inhibit mitochondrial damage and cardiomyocyte apoptosis.Conclusion and Implications: Mitochondria play a key role in mediating heart failure progression. Simvastatin attenuated heart failure, induced by angiotensin II, via mitochondrial protection and might provide a new therapy to prevent heart failure. [ABSTRACT FROM AUTHOR]