Objective: To assess longitudinal impact of changes in childhood BMI on cardiac structure and function. Background: Childhood obesity has increased dramatically in the US since 1980 and is associated with cardiovascular disease in adulthood. Echocardiographic studies have demonstrated cardiac remodeling and alterations in myocardial structure and function in obese adults. Associations between weight and cardiac structure and function in children are less well documented. Methods: Project HeartBeat! recruited 678 children grouped in cohorts aged 8, 11, and 14 years at baseline. Anthropometric, including BMI, and transthoracic echo data were collected at 4-month intervals for 4 years (1991–1995) for a total of 5779 person-exams. Fractional shortening (FS), left atrial dimension, left ventricular systolic and diastolic dimensions, and left ventricular mass indexed to body surface area (LVMi) were assessed as outcomes. Cross-sectional association between baseline BMI and baseline outcomes were assessed with linear regression models. We used random effects models for repeated measures, adjusted for covariates (age, sex, race and blood pressure), to model: 1) associations between baseline BMI and change in echo measures over time, and 2) associations between change in BMI and echo measures over time. Results: Reference Table 1 Conclusions: Elevated baseline BMI and increasing BMI over time are associated with higher baseline and greater increases in LVMi. Elevated baseline BMI and increases in BMI over time were also associated with increased left atrial and left ventricular dimensions. While there was no association between baseline BMI and baseline FS, higher baseline BMI and increased in BMI over time were associated with mild increases in FS. The results demonstrate that higher baseline BMI and increases in BMI over time negatively impact the heart in children as early as 8 years of age and through adolescence.
Primary pulmonary vein stenosis is a severe and unrelenting disease often characterized by the development of multivessel obstruction. Endovascular stents have proven to be an effective intervention,1Balasubramanian S. Marshall A.C. Gauvreau K. et al.Outcomes after stent implantation for the treatment of congenital and postoperative pulmonary vein stenosis in children.Circ Cardiovasc Interv. 2012; 5: 109-117https://doi.org/10.1161/CIRCINTERVENTIONS.111.964189Crossref PubMed Scopus (83) Google Scholar,2Khan A. Qureshi A.M. Justino H. Comparison of drug eluting versus bare metal stents for pulmonary vein stenosis in childhood.Catheter Cardiovasc Interv. 2019; 94: 233-242https://doi.org/10.1002/ccd.28328Crossref PubMed Scopus (38) Google Scholar but as the disease extends to previously healthy vessels over time, treatment is obligatorily piecemeal, and de novo lesions often develop near a preexisting stent. This is a particular challenge in patients with pulmonary vein anatomic subtypes involving common or adjacent venoatrial connections. In such cases, any intervention on the new lesion runs the risk of obstructing access to or damaging the previously placed stent. To address this challenge, stents can be deployed using a "double barrel" orientation. When a preexisting stent is adjacent to a de novo lesion, the second stent is implanted while a balloon is inflated within the first stent, thus ensuring the de novo wire has not crossed through a side-cell and that the new stent does not crush or obstruct the adjacent vessel. Alternatively, if adjacent lesions are being addressed during the same case, simultaneous stents can be deployed after accessing each individual vessel. This yields immediately satisfactory results with a double-barrel stent orientation, but with subsequent interventions, it can be technically challenging to pass a wire through the true central lumens of each stent. To mitigate this problem, we have modified techniques used to address coronary artery bifurcation lesions.3Raphael C.E. O'Kane P.D. Johnson T.W. et al.Evolution of the crush technique for bifurcation stenting.J Am Coll Cardiol Intv. 2021; 14: 2315-2326https://doi.org/10.1016/j.jcin.2021.08.048Crossref Scopus (17) Google Scholar Herein we describe our first instance of using the double-barrel stent side-cell crush technique to address complex pulmonary vein anatomy. The patient is a singleton male born at 28 weeks gestation with comorbidities including pulmonary hypertension and bronchopulmonary dysplasia requiring tracheostomy and ventilator dependence. At 5 months of age, he underwent his first intervention with a 3.5 × 8 mm Onyx drug-eluting stent (Medtronic) placed in a recanalized atretic right upper pulmonary vein and balloon angioplasty of a second lesion involving the left upper pulmonary vein (LUPV) venoatrial junction. He then manifested severe progression of disease; at 8 months of age, disease recurred in the LUPV (Figure 1A), which was treated with a 5 × 12 Synergy drug-eluting stent (Boston Scientific) (S1). At 10 months of age, the disease extended to the proximal left lower pulmonary vein (LLPV) (Figure 1B) which was addressed with a 6 × 12 mm Formula 418 bare metal stent (Cook Medical) (S2). The left upper and lower pulmonary veins shared a common origin from the left atrium, so the left upper and lower pulmonary vein stents were deployed in a double-barrel orientation (Figure 1C). At 13 months of age, he presented for ongoing rehabilitation with distal extension of disease in the LLPV; at this point, the orientation of his left vein stents became a technical challenge. Using a 6.5F Destino steerable sheath (Oscar Inc), a 0.014" guide wire was placed through the central lumen of the stent with the greatest potential diameter, in this case S2 in the LLPV (Figure 1D). Next, using a microcatheter placed within the long sheath, apart from the LLPV wire, the side-cells of both stents were crossed, and distal wire position was established through S1. Starting with a 2 mm coronary balloon the side-cells are dilated to the target diameter appropriate for upper vein rehabilitation (Figure 1E). This leaves a proximal gap between the 2 stents (Figure 1F). Leaving the upper wire in position, a second balloon is advanced into the lower vein, which is then rehabilitated as indicated. In this case, disease progressed and an additional stent was placed peripherally in the LLPV. Finally, to create a common origin at the venoatrial junction, both LUPV and LLPV balloons are aligned with the proximal edge of the stents and simultaneously inflated to effectively crush the proximal portion of S1 and dilate the proximal portion of S2 to create a stented "Y" at the vein bifurcation (Figure 1G). Retrograde pulmonary vein angiogram demonstrates patency of both vessels and a single functional orifice relative to the left atrium (Figure 1H). The final position of each stent is illustrated in the image (Figure 1I). In the 2.5 years since stent modification, the patient has undergone 4 additional interventional procedures with access to the primary vessel and distal branches preserved (Figure 1J). His most recent CTA performed at 3.5 years of age demonstrates preserved left vein patency with no extension of disease. Stents are an essential tool in the treatment of pulmonary vein stenosis, but they have several well-known limitations. As illustrated in this case, disease progression is unpredictable, and previously placed stents can render future interventions more challenging. The side-cell crush technique can be used to simplify pulmonary vein access in the setting of multivessel disease with a common venoatrial origin. Paul Tannous is a consultant for Ascend Cardiovascular. Conor P O'Halloran, Matthew Cornicelli, and Amanda Hauck reported no financial interests. This work was not supported by funding agencies in the public, commercial, or not-for-profit sectors.
The coincident occurrence of tricuspid atresia and aortopulmonary window (APW) is exceedingly rare, with one previous case reported in the literature. We present a patient with tricuspid atresia, pulmonary atresia, and APW. Postnatal echocardiograms demonstrated no visible pulmonary valve, and additional defects including a bicuspid aortic valve, right aortic arch and anomalous coronary arteries raised suspicion for tricuspid atresia with persistent truncus arteriosus. However, fetal echocardiography and direct visualization of the anatomy confirmed the alternate diagnosis. The patient underwent successful palliation consisting of APW repair, atrial septectomy and a 3.5 mm modified Blalock–Taussig shunt, followed by a bidirectional cavopulmonary connection.
Abstract Introduction Limited evidence suggests that serum alkaline phosphatase activity may decrease after cardiac surgery in adults and children. The importance of this finding is not known. Recent studies, however, have identified a potential role for alkaline phosphatase as modulator of inflammation in multiple settings, including during adult cardiopulmonary bypass. We sought to describe the change in alkaline phosphatase activity after cardiothoracic surgery in infants and to assess for a correlation with intensity and duration of post-operative support, markers of inflammation, and short-term clinical outcomes. Methods Sub-analysis of a prospective observational study on the kinetics of procalcitonin in 70 infants (≤90 days old) undergoing cardiothoracic surgery. Subjects were grouped based on the use of cardiopulmonary bypass and delayed sternal closure. Alkaline phosphatase, procalcitonin, and C-reactive protein (CRP) levels were obtained pre-operation and on post-operative day 1. Mean change in alkaline phosphatase activity was determined in each surgical group. Generalized linear modeling and logistic regression were employed to assess for associations between post-operative alkaline phosphatase activity and post-operative support, inflammation, and short term outcomes. Primary endpoints were vasoactive-inotropic score at 24 hours and length of intubation. Secondary endpoints included procalcitonin/CRP levels on post-operative day 1, length of hospital stay, and cardiac arrest or death. Results Mean decrease in alkaline phosphatase was 30 U/L (p = 0.01) in the non-bypass group, 114 U/L (p<0.0001) in the bypass group, and 94 U/L (p<0.0001) in the delayed sternal closure group. On multivariate analysis, each 10 U/L decrease in alkaline phosphatase activity on post-operative day 1 was independently associated with an increase in vasoactive-inotropic score by 0.7 (p<0.0001), intubation time by 6% (p<0.05), hospital stay by 5% (p<0.05), and procalcitonin by 14% (P<0.01), with a trend towards increased odds of cardiac arrest or death (OR 1.3; p = 0.06). Post-operative alkaline phosphatase activity was not associated with CRP (p = 0.7). Conclusions Alkaline phosphatase activity decreases after cardiothoracic surgery in infants. Low post-operative alkaline phosphatase activity is independently associated with increased procalcitonin, increased vasoactive/inotropic support, prolonged intubation time, and prolonged hospital stay. Alkaline phosphatase may serve as a biomarker and potential modulator of post-operative support and inflammation following cardiothoracic surgery in infants.
