ABSTRACT
OBJECTIVE: To evaluate whether preprocedural transthoracic echocardiography (TTE) can be used to predict Amplatzer septal occluder (ASO) size for device closure of atrial septal defect (ASD). DESIGN: Retrospective review of patients who underwent ASD device closure at our institution between August 2006 and August 2013 was performed. Patients with complex congenital heart disease, devices other than the ASO, multiple devices, or inadequate TTE images were excluded. Those who had transesophageal echocardiography (TEE)-guided device placement were evaluated. A blinded observer reviewed their preprocedural TTE images and applied a scaled formula to predict device size. RESULTS: A total of 186 patients underwent ASO placement during the study period, 87 had TEE guidance, of which 45 met inclusion criteria. The mean predicted device size by the scaled formula was 18.0 ± 5.11 mm, compared to the mean implanted device size of 18.8 ± 5.22 mm. The mean absolute difference between each predicted and final deployed device size was 1.44 mm with 95% CI [1.08, 1.81]. The Pearson correlation showed that the predicted device size had a positive correlation coefficient of 0.94. CONCLUSION: Preprocedural TTE assessment of ASD size using a scaling formula in patients with adequate TTE windows can accurately predict ASO device size and aid in device selection.
Subject(s)
Cardiac Catheterization/instrumentation , Decision Support Techniques , Echocardiography, Transesophageal , Heart Septal Defects, Atrial/diagnostic imaging , Heart Septal Defects, Atrial/therapy , Septal Occluder Device , Adolescent , Adult , California , Child , Child, Preschool , Female , Humans , Infant , Male , Models, Biological , Observer Variation , Patient Selection , Predictive Value of Tests , Prosthesis Design , Reproducibility of Results , Retrospective StudiesABSTRACT
BACKGROUND: Endomycocardial biopsies have demonstrated that subclinical myocarditis is a universal feature of acute Kawasaki disease (KD). METHODS: We investigated biochemical evidence of myocardial strain, oxidative stress, and cardiomyocyte injury in 55 acute KD subjects (30 with paired convalescent samples), 54 febrile control (FC), and 50 healthy control (HC) children by measuring concentrations of cardiovascular biomarkers. RESULTS: Levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and soluble ST2 (sST2) were elevated in acute vs. convalescent KD, FC, and HC (p≤0.002), while γ-glutamyl transferase and alanine amino transferase as measures of oxidative stress were increased in acute vs. FC (p≤0.0002). Cardiac troponin I (cTnI) levels, using a highly sensitive assay, were elevated in 30% and 40% of paired acute and convalescent KD subjects, respectively, and normalized within two years of disease onset. NT-proBNP and sST2 negatively correlated with deceleration time, but only NT-proBNP correlated with MV E:A ratio and internal diameter of the coronary arteries (RCA/LAD Zworst). CONCLUSIONS: NT-proBNP and sST2 were elevated in acute KD subjects and correlated with impaired myocardial relaxation. These findings, combined with elevated levels of cTnI, suggest that both cardiomyocyte stress and cell death are associated with myocardial inflammation in acute KD.
