Background— Valve-in-valve (VIV) transcatheter aortic valve replacement (TAVR) may be less effective in small surgical valves because of patient/prosthesis mismatch. Bioprosthetic valve fracture (BVF) using a high-pressure balloon can be performed to facilitate VIV TAVR. Methods and Results— We report data from 20 consecutive clinical cases in which BVF was successfully performed before or after VIV TAVR by inflation of a high-pressure balloon positioned across the valve ring during rapid ventricular pacing. Hemodynamic measurements and calculation of the valve effective orifice area were performed at baseline, immediately after VIV TAVR, and after BVF. BVF was successfully performed in 20 patients undergoing VIV TAVR with balloon-expandable (n=8) or self-expanding (n=12) transcatheter valves in Mitroflow, Carpentier-Edwards Perimount, Magna and Magna Ease, Biocor Epic and Biocor Epic Supra, and Mosaic surgical valves. Successful fracture was noted fluoroscopically when the waist of the balloon released and by a sudden drop in inflation pressure, often accompanied by an audible snap. BVF resulted in a reduction in the mean transvalvular gradient (from 20.5±7.4 to 6.7±3.7 mm Hg, P <0.001) and an increase in valve effective orifice area (from 1.0±0.4 to 1.8±0.6 cm 2 , P <0.001). No procedural complications were reported. Conclusions— BVF can be performed safely in small surgical valves to facilitate VIV TAVR with either balloon-expandable or self-expanding transcatheter valves and results in reduced residual transvalvular gradients and increased valve effective orifice area.

Bench testing demonstrates that the frame of most, but not all, bioprosthetic surgical aortic valves can be fractured using high-pressure balloons. The safety of bioprosthetic valve fracture to optimize valve-in-valve transcatheter aortic valve replacement in small surgical valves requires further clinical investigation.

Cancer diagnostics and therapies have improved steadily over the last few decades, markedly increasing life expectancy for patients at all ages. However, conventional and newer anti-neoplastic therapies can cause short-and long-term cardiotoxicity. The clinical implications of this cardiotoxicity become more important with the increasing use of cardiotoxic drugs. The implications are especially serious among patients predisposed to adverse cardiac effects, such as youth, the elderly, those with cardiovascular comorbidities, and those receiving additional chemotherapies or thoracic radiation. However, the optimal strategy for preventing and managing chemotherapyinduced cardiotoxicity remains unknown. The routine use of neurohormonal antagonists for cardioprotection is not currently justified, given the marginal benefits and associated adverse events, particularly with long-term use. The only United States Food and Drug Administration and European Medicines Agency approved treatment for preventing anthracycline-related cardiomyopathy is dexrazoxane. We advocate administering dexrazoxane during cancer treatment to limit the cardiotoxic effects of anthracycline chemotherapy.

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With 5-year survival of children with cancer exceeding 80% in developed countries, premature cardiovascular disease is now a major cause of early morbidity and mortality. In addition to the acute and chronic cardiotoxic effects of anthracyclines, related chemotherapeutics, and radiation, a growing number of new molecular targeted agents may also have detrimental effects on the cardiovascular system. Survivors of childhood cancer also may have earlier development of conventional cardiovascular risk factors such as hypertension, dyslipidaemia, and diabetes, which further increase their risk of serious cardiovascular disease. This review will examine the epidemiology of acute and chronic cardiotoxicity relevant to paediatric cancer patients, including genetic risk factors. We will also provide an overview of current screening recommendations, including the evidence regarding both imaging (e.g. echocardiography and magnetic resonance imaging) and blood-based biomarkers. Various primary and secondary prevention strategies will also be discussed, primarily in relation to anthracycline-related cardiomyopathy. Finally, we review the available evidence related to the management of systolic and diastolic dysfunction in paediatric cancer patients and childhood cancer survivors.

In the US, children diagnosed with cancer are living longer, but not without consequences from the same drugs that cured their cancer. In these patients, cardiovascular disease is the leading cause of non-cancer-related morbidity and mortality. Although this review focuses on anthracycline-related cardiomyopathy in childhood cancer survivors, the global lifetime risk of other cardiovascular diseases such as atherosclerosis, arrhythmias and intracardiac conduction abnormalities, hypertension, and stroke also are increased. Besides anthracyclines, newer molecularly targeted agents, such as vascular endothelial growth factor receptor and tyrosine kinase inhibitors, also have been associated with acute hypertension, cardiomyopathy, increased risk of ischemic cardiac events and arrhythmias, and are summarized here. This review also covers other risk factors for chemotherapy-related cardiotoxicity (including both modifiable and non-modifiable factors), monitoring strategies (including both blood and imaging-based biomarkers) during and following cancer treatment, and discusses the management of cardiotoxicity (including prevention strategies such as cardioprotection by use of dexrazoxane).

Background Multisystem inflammatory syndrome in children associated with COVID-19 (MIS-C) causes significant cardiovascular involvement, which can be a determinant of clinical course and outcome. We aimed to investigate whether echocardiographic measures of ventricular function were independently associated with adverse clinical course and cardiac sequaele in MIS-C. Methods In a longitudinal observational study of 54 MIS-C patients (mean age 6.8 ± 4.4 years, 46% male, 56% African American), measures of ventricular function and morphometry at initial presentation, pre-discharge, and median of 3 and 10 week follow-up were retrospectively analyzed, and were compared to 108 84 age and gender matched normal controls. The magnitude of strain is expressed as an absolute value. Risk stratification for adverse clinical course and outcomes were analyzed between the tertiles of clinical and echo data using ANOVA, univariate and multivariate regression. Results Median LV apical 4-chamber longitudinal (LVA4LS) and global longitudinal strain (LVGLS) at the initial presentation were significantly decreased in MIS-C compared to normal cohort (16.2% and 15.1% vs. 22.3% and 22.0% respectively, p<0.01). Patients in the lowest LVA4LS tertile (<13%) had significantly higher CRP and hs-Troponin, need for intensive care (ICU), mechanical life support, and longer hospital length of stay (LOS) compared to those in the highest tertile (>18.5%) (p<0.01). Initial LVA4LS and LVGLS were normal in 13 of 54 and 10 of 39 patients respectively. There was no mortality. In multivariate regression, only LVA4LS was associated with both the need for ICU and LOS. At median 10 week follow-up to date, 7 of 36 patients (19%) and 6 of 25 patients (24%) had abnormal LVA4LS and LVGLS respectively. Initial LVA4LS<16.2% indicated abnormal LVA4LS at follow-up with 100% sensitivity. Conclusion Impaired LVGLS and LVA4LS at initial presentation independently indicate a higher risk of adverse acute clinical course and persistent subclinical LV dysfunction at 10 weeks follow-up, suggesting they could be applied to identify higher risk children with MIS-C.

Background: Despite their putative impact on post-operative outcomes, there is paucity of data on enteral feeding practices of neonates with congenital heart disease (CHD). Objectives: To examine feeding patterns among neonates with CHD before and after surgical repair and determine the incidence of and to identify risk factors associated with feeding-related morbidities. Methods: Retrospective data review of neonates with CHD who underwent surgical repair within the first month of life. SPSS software (version 17) was used for analyses and p < 0.05 taken as significant. Results: The median (range) gestational age of our cohort (n = 67) was 39 weeks (32–41) and birth weight 3,100 g (1,615–4,280). Ductal-dependent lesions were diagnosed in 52 infants (77.6%). Prior to surgery, feedings were initiated in 62 infants (92.5%) at a median age of 2.5 days (1–18); 100 ml/kg daily intake was achieved in 47 infants (70.1%) at 5 days (1–20) and full feeds in 22 infants (32.8%). Postoperative enteral feeds were started 3 days (1–20) after surgery in 66 infants (98.5%) and intake of 100 ml/kg/day was reached in 64 infants at 5 postoperative days (1–29). Four infants (5.9%) died; 27 (40.3%) were on at least partial gavage feedings at the time of discharge home. NEC was diagnosed in 2 infants. On regression analysis, cardiopulmonary bypass (p = 0.024) and age at which full feeds were attained prior to surgery (p = 0.039) were significantly associated with death and/or gavage at discharge. Conclusions: The majority of infants with CHD achieve moderate enteral intake prior to surgery, even while on prostaglandins. Despite this and the early initiation of postoperative enteral feeds, many infants need gavage feeds at discharge. Evidence-based feeding strategies for this high-risk population are critical to improving outcomes.