Dilating and fracturing side struts of open cell stents frequently used in pediatric cardiac interventions-An in vitro study.

BACKGROUND: Open cell stents are frequently used in interventional therapy of congenital heart disease. Overstenting of vessel branches may necessitate strut dilation. METHODS AND RESULTS: The strut size achievable in Bard Valeo and Cook Formula stents, and the pressure necessary to fracture struts was assessed. In addition, a self expanding stent (Optimed SinusflexDS) was also tested. With the original balloon at nominal pressure, in Valeo stents side struts could be dilated to approximately 90% of the nominal stent diameter, in Formula stents to approximately 80%. With larger high pressure woven balloons, strut size increased to approximately 125% in Valeo stents, and to approximately 105% in the Formula. Strut fracture can connect two adjoining struts. Pressures were dependent on the balloon utilized. Sidestruts of the Sinusflex could lastingly overdilated with large balloons only. CONCLUSION: Dilation and overdilation of side struts in open cell stents can be achieved. Dependent on the clinical context, the original balloon used to place the premounted stent can be used to achieve strut dilation, but woven high pressure balloons maybe safer for patients. Should a larger diameter be required, these high pressure woven balloons can achieve bigger diameters and even strut fracture.

Pulmonary arterial wall distensibility assessed by intravascular ultrasound in children with congenital heart disease: an indicator for pulmonary vascular disease?

BACKGROUND: Both pulmonary hypertension and pulmonary overflow are associated with functional and structural changes of the pulmonary arterial wall. Current techniques to evaluate the pulmonary vasculature neglect the pulsatile nature of pulmonary flow. STUDY OBJECTIVES: To determine whether the dynamic properties of the pulmonary arterial wall are altered in patients with abnormal pulmonary hemodynamics due to congenital heart defects, and whether these changes are associated with the progression of pulmonary vascular disease (PVD). PATIENTS AND METHODS: In 43 children with PVD due to congenital heart defects and 12 control subjects, pulmonary arterial pulsatility (the relative increase in vessel area during the cardiac cycle) and distensibility (the inverse of the stress/strain elastic modulus) were determined with intravascular ultrasound. Results were correlated with clinical and hemodynamic parameters. RESULTS: Pulsatility correlated with pulmonary pulse pressure (p < 0.001), pulmonary-to-systemic vascular resistance ratio (PVR/SVR) [p = 0.001], and hemoglobin concentration (p = 0.01). However, when corrected for these variables, pulsatility did not differ between patients and control subjects. In contrast, arterial wall distensibility decreased with the severity of PVD and correlated independently with pulmonary-to-systemic arterial pressure ratio (p < 0.001) and PVR/SVR (p = 0.03), and with hemoglobin concentration (p < 0.01). Adjusted for hemodynamic variables, distensibility was still decreased in patients with PVD compared to control subjects. CONCLUSIONS: These results demonstrate that pulmonary arterial wall distensibility is progressively decreased in PVD; moreover, this decreased distensibility is, in part, related to increased distending pressure as a result of pulmonary hypertension but also, in part, to stiffening of the arterial wall during the disease process. Arterial wall distensibility may be of additional value in the evaluation of pulmonary vasculature and ventricular workload.