Congenital heart diseases causing significant hemodynamic and functional consequences require surgical repair. Understanding of the precise surgical anatomy is often challenging and can be inadequate or wrong. Modern high resolution imaging techniques and 3D printing technology allow 3D printing of the replicas of the patient’s heart for precise understanding of the complex anatomy, hands-on simulation of surgical and interventional procedures, and morphology teaching of the medical professionals and patients. CT or MR images obtained with ECG-gating and breath-holding or respiration navigation are best suited for 3D printing. 3D echocardiograms are not ideal but can be used for printing limited areas of interest such as cardiac valves and ventricular septum. Although the print materials still require optimization for representation of cardiovascular tissues and valves, the surgeons find the models suitable for practicing closure of the septal defects, application of the baffles within the ventricles, reconstructing the aortic arch, and arterial switch procedure. Hands-on surgical training (HOST) on models may soon become a mandatory component of congenital heart disease surgery program. 3D printing will expand its utilization with further improvement of the use of echocardiographic data and image fusion algorithm across multiple imaging modalities and development of new printing materials. Bioprinting of implants such as stents, patches and artificial valves and tissue engineering of a part of or whole heart using the patient’s own cells will open the door to a new era of personalized medicine.

OBJECTIVES: The current Australian epidemiology of Kawasaki disease (KD) is poorly defined. Previous enhanced surveillance (1993–1995) estimated an incidence of 3.7/100 000 <5 years. METHODS: We identified all patients hospitalized in Western Australia (current population ∼2.4 million) 1979 through 2009 with a discharge diagnosis of KD. We reviewed demographic, clinical, laboratory, and echocardiographic data from individual patient files and derived age-specific population estimates. KD diagnosis was made using standard criteria. RESULTS: There were 353 KD cases, with incomplete KD in 34 (9.6%). Male to female ratio was 1.7:1 and median age was 3.8 years (interquartile range 12–60 months). Fifty (18.1%) patients were Asian. Mean annual incidence increased from 2.82 per 100 000 children aged <5 years (95% confidence interval, 1.93–3.99) in 1980 to 1989, to 7.96 (6.48–9.67) in 1990 to 1999, to 9.34 (7.72–11.20) in 2000 to 2009. The highest incidence was 15.7 in 2005. A total of 293 children (83%) received intravenous immunoglobulin and 331 (95.4%) aspirin. Of 282 children who completed echocardiographic studies, 47 (16.7%) had coronary artery (CA) ectasia/dilatation and 19 (6.8%) had CA aneurysms; male gender was significantly associated with CA abnormalities. CONCLUSIONS: KD epidemiology in Western Australia mirrors that of other industrialized, predominantly European-Caucasian populations. The rising incidence likely reflects both improved ascertainment and a real increase in disease burden. The current Australian incidence is threefold higher than previously reported and similar to the United Kingdom. The CA outcomes, which include the pre-intravenous immunoglobulin era, are comparable to those reported elsewhere.

Kawasaki disease is an acute systemic vasculitis predominantly affecting young children. It is due to an abnormal host response to as yet unidentified infectious trigger(s). Kawasaki disease may cause coronary artery damage, long-term cardiovascular morbidity and occasionally mortality, especially if the diagnosis is missed or timely treatment is not given. This is the first of two updates on Kawasaki disease. Here we review recent advances in epidemiology, possible aetiologies, host susceptibility and pathogenesis of this fascinating condition.

No abstract

No abstract

This is the second of two updates on Kawasaki disease. The first review focused on epidemiology and aetio-pathogenesis. Here, we review the clinical features and diagnosis of Kawasaki disease, as well as recent evidence on treatment, follow-up and cardiovascular outcomes.

No abstract

Children after rTOF do not have elevated LV native T1 or LV extracellular volume, but show evidence of increased RV native T1 suggestive of diffuse RV fibrosis, for which volume loading seems to be a risk factor. Surgical bypass and cross-clamp times are associated with fibrotic remodeling over a decade later.