Archives of Cardiovascular Diseases最新文献

Background

Aims

Methods

Results

Conclusion

Background

Aim

Methods

Results

Conclusions

Background

Methods

Conclusions

Introduction

Children with congenital heart disease often undergo painful procedures due to surgeries and associated care. While medications are commonly used for pain management during procedures like chest tube removal, they can have side effects. Non-pharmacological methods, such as therapeutic hypnosis, have shown effectiveness in reducing procedural pain and anxiety in children. However, there is limited research in this area, particularly in children, and none in children with congenital heart disease.

Objective

The objective of this study is to prove the non-inferiority of therapeutic hypnosis as a co-analgesic compared to standard analgesics during intrathoracic drain removal in children with congenital heart disease.

Methods

This study is a non-inferiority, randomized, controlled trial. Patients are randomized by computer. One group receive the conventional analgesia protocol including ketamine, midazolam, and MEOPA. The other group only receives MEOPA and lower doses of ketamine and undergo a hypnosis session by one of the service's professionals trained in medical hypnosis. Patient pain is self-assessed before and after the procedure. Patients are filmed throughout the drain removal so that per-procedure pain can be blindly evaluated from the randomization arm at a distance from the intervention. Finally, indirect signs of pain (HR, RR, SpO₂) are recorded before, during, and after the intervention.

This study has been authorized by a French Committee of Ethics.

Clinicaltrial.gov: NCT06373627.

Expected results

Therapeutic hypnosis, when combined with minimal sedation-analgesia, is non-inferior to conventional sedation-analgesia in managing pain during chest tube removal in children with congenital heart disease.

Perspectives

This study would pave the way for wider adoption of therapeutic hypnosis as a co-analgesic method for children undergoing painful medical procedures, potentially reducing reliance on medications and enhancing patient experience.

Introduction

Sudden cardiac death (SCD) is the most common cause of death in childhood hypertrophic cardiomyopathy (HCM). Recently, two risk scores have been developed to estimate the 5-year risk of SCD.

Objective

We aimed to assess their respective performances in an independent cohort of primary prevention children with HCM.

Methods

All patients with HCM < 18-year-old from a single-center were retrospectively included between 2003 and 2023. Secondary and syndromic causes of HCM were excluded as well as children with inaugural sustained ventricular arrythmias. HCM Risk-Kids and PRIMaCY risk scores were calculated at diagnosis and during follow-up. The primary composite outcome included sustained ventricular arrhythmia, appropriate ICD therapy, aborted cardiac arrest, or SCD.

Results

Hundred primary prevention children were included (mean age 7.1 ± 5.6 years, 59.0% males), with a mean follow-up of 8.6 ± 5.5 years.13 (13.0%) patients experienced the primary composite outcome. When only considering events during the 5 first years, Harrel's C index was 0.52 (95% CI: 0.27–0.77) for HCM Risk-Kids (≥ 6%) and 0.70 (95% CI: 0.59–0.80) for PRIMaCY (> 8.3%), with 1 patient potentially treated by ICD for every 25 ICDs implanted for HCM Risk Kids and 1 for every 14 ICDs implanted for PRIMaCY. When risk scores were repeated and all primary outcomes during follow-up considered, all events except one (93.2%) were correctly identified using both risk scores, with 1 patient potentially treated by ICD for every 5.6 ICDs implanted for HCM Risk Kids and 1 for every 5.3 ICDs implanted for PRIMaCY. Among 44 (44.0%) patients implanted with an ICD, all primary prevention patients who had ≥ one appropriate ICD therapy during follow-up had HCM Risk-Kids ≥ 6% and PRIMaCY > 8.3% at implantation.

Conclusion

Our findings suggest imperfect discrimination between low and high-risk HCM patients using these two risk scores. The performance or risk scores was substantially improved by periodic re-assessment during follow-up.

Introduction

The primary genetic risk factor for heritable pulmonary arterial hypertension (PAH) is the presence of monoallelic mutations in the BMPR2 gene. The incomplete penetrance of BMPR2 mutations implies that additional triggers are necessary for PAH occurrence. Pulmonary artery stenosis directly raises pulmonary artery pressure, while the redirection of blood flow to unobstructed arteries lead to endothelial dysfunction and vascular remodeling.

Objective

We aimed to evaluate the effect of right pulmonary artery occlusion (RPAO) in rats. Then, we evaluated the effect of BMPR2 loss of function on cardiac and pulmonary vascular remodeling.

Methods

Male and female rats with a 71 bp monoallelic deletion in exon 1 of BMPR2 and their wild-type (WT) siblings underwent acute and chronic RPAO. They were subjected to full high-fidelity hemodynamic characterization. We also examined how chronic RPAO can mimic the pulmonary gene expression pattern associated with installed PH in unobstructed territories.

Expected results

RPAO induced pre-capillary PH in male and female rats, both acutely and chronically. BMPR2 mutant and male rats manifested more severe PH compared to their counterparts. While WT rats adapted to RPAO, BMPR2 mutant rats experienced heightened mortality. RPAO induced a decline in cardiac contractility index, particularly pronounced in male BMPR2 rats. Chronic RPAO resulted in elevated pulmonary interleukin-6 (IL-6) expression and decreased Gdf2 expression (corrected P-value < 0.05 and log2 fold change > 1). In this context, male rats expressed higher pulmonary levels of endothelin-1 and IL-6 than females (Fig. 1).

Perspectives

Our novel two-hit rat model presents a promising avenue to explore the adaptation of the right ventricle and pulmonary vasculature to PH, shedding light on pertinent sex and gene-related effects.