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The Australian and New Zealand population of patients alive after a Fontan procedure will double over the next 20years increasing the demand for heart-failure services and cardiac transplantation. Greater consideration for the needs of this mostly adult Fontan population will be necessary.

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Background-Patients with systemic ventricles of right ventricular morphology are at high risk of contractile dysfunction, the cause of which has not been fully elucidated. Objective-To assess whether ischaemia or infarction contributes to ventricular impairment in unoperated patients with uncomplicated congenitally corrected transposition of the great arteries (TGA) by studying myocardial perfusion and function. Setting-Paediatric and adult congenital cardiac clinics of a tertiary referral centre. Patients-Five patients with congenitally corrected TGA but without associated structural cardiac defects (aged 3.5 to 34 years). Interventions-Maximal exercise stress testing using standard or modified Bruce protocols. Sestamibi (technetium-99m methoxy isobutyl isonitrile) scanning after isotope injection at maximal exercise and rest. Main outcome measures-Maximum exercise capacity; right ventricular myocardial perfusion, regional wall motion, and thickening; right ventricular ejection fraction. Results-The two youngest patients (3.5 and 11 years) had normal exercise capacity for age, while the others had reduced exercise performance. Sestamibi scanning showed reversible myocardial ischaemia in four patients and fixed defects indicating infarction in five. Irreversible defects were mostly associated with impaired wall motion and thickening. The ejection fraction was normal (65%) in the youngest patient but < 55% in the others (mean (SD) 47(11)%). Conclusions-Patients with unoperated congenitally corrected TGA have a high prevalence of myocardial perfusion defects, with consequent abnormalities of regional wall motion and thickening, and impaired ventricular contractility. These data suggest that ischaemia and infarction are important in the pathogenesis of ventricular failure in this condition. (Heart 1998;80:322-326)

OBJECTIVETo better understand the cardiac limitations during exercise in adolescents with type 2 diabetes mellitus (T2DM), we measured left ventricular performance with magnetic resonance imaging (MRI) during exercise in diabetic and nondiabetic adolescents. RESEARCH DESIGN AND METHODSThirteen subjects with T2DM, 27 overweight/obese nondiabetic (ObeseND) subjects, and 19 nondiabetic nonobese control subjects were recruited. Cardiac (left ventricular) MRI scans were performed at rest and during submaximal exercise. RESULTSVO 2 peak indexed to fat-free mass was reduced in T2DM and ObeseND subjects compared with control subjects (P < 0.0001). Indexed cardiac output increased less during exercise and was 20% lower in T2DM subjects due to reduced stroke volume. This was a consequence of reduced ventricular filling with smaller enddiastolic volume, which decreased further during exercise in T2DM subjects, but not in ObeseND or control subjects. End-systolic volume was also smaller in T2DM subjects. These changes were associated with increased resting and exercise diastolic blood pressure, and total peripheral resistance in T2DM subjects. CONCLUSIONSIndependently of obesity, T2DM impairs cardiac function during exercise in adolescents. Diabetes Care 2014;37:143937: -144637: | DOI: 10.233737: /dc13-2031 Exercise is a standard recommendation in the management and prevention of type 2 diabetes mellitus (T2DM) (1,2). Regrettably, people with diabetes often have reduced cardiac reserve (3,4) and a resultant decrease in aerobic capacity (3,5). Adults with T2DM have smaller left ventricular stroke volume (6) and reduced heart rates (3,7) during peak exercise. These factors may present a barrier to exercise participation because recommended "moderate intensity" exercise (2) requires a greater proportion of their aerobic capacity (8).Several authors suggest that reduced early left ventricular diastolic filling (i.e., diastolic dysfunction) is responsible for lower aerobic capacity in people with T2DM,

Pulmonary regurgitation and RVOT aneurysm/akinesia were independently associated with RV dilation and the latter with RV hypertrophy late after rTOF. The RVOT aneurysm/akinesia was common but related only in part to RVOT or transannular patching. Both RV hypertrophy and RVOT aneurysm/akinesia were associated with lower RVEF. Left ventricular systolic dysfunction correlated with RV dysfunction, suggesting an unfavorable ventricular-ventricular interaction. Measures to maintain or restore pulmonary valve function and avoid RVOT aneurysm/akinesia are mandatory for preserving biventricular function late after rTOF.