(Circulation. 2006;113:405-413.)
© 2006 American Heart Association, Inc.
Imaging |
From the Adult Congenital Heart Unit (S.V.B.-N., W.L., O.G., P.A.D., M.A.G.) and the Cardiovascular Magnetic Resonance Unit (S.V.B.-N., P.J.K., J.C.M., D.J.P.), Royal Brompton Hospital, London, United Kingdom; and the National Heart and Lung Institute (S.V.B.-N., P.J.K., W.L., M.K., S.Y.H., D.J.P., M.A.G.), Imperial College, London, United Kingdom.
Correspondence to Dr Sonya V. Babu-Narayan, Adult Congenital Heart Unit, Royal Brompton Hospital, Sydney St, London SW3 6NP, United Kingdom. E-mail sonya{at}doctors.org.uk
Received March 11, 2005; revision received October 28, 2005; accepted November 21, 2005.
Background Late morbidity and mortality remain problematic after repair of tetralogy of Fallot (TOF). We hypothesized that fibrosis detected by late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) would be present in adults with repaired TOF and would be related to adverse markers of outcome.
Method and Results LGE was scored in the right and left ventricles (RV and LV) of 92 adult patients who had undergone TOF repair. RV LGE was seen in all patients at surgical sites located in the outflow tract (99%) or the site of ventricular septal defect patching (98%) and in the inferior RV insertion point (79%) and trabeculated myocardium (24%). LV LGE (53%) was located at the apex consistent with apical vent insertion (49%), in the inferior or lateral wall consistent with infarction (5%), or in other areas (8%). Patients with supramedian RV LGE score were older (38 versus 27 years, P<0.001) and more symptomatic (38% versus 8% in New York Heart Association class II or greater, P=0.001), had increased levels of atrial natriuretic peptide (7.3 versus 4.9 pmol/L, P=0.041), and had a trend to higher brain natriuretic peptide (12.3 versus 7.2 pmol/L, P=0.086), exercise intolerance (maximum
O2 24 versus 28 mL · min1 · kg1, P=0.021), RV dysfunction (RV end-systolic volume 61 versus 55 mL/m2, P=0.018; RV ejection fraction 50% versus 56%, P=0.007), and clinical arrhythmia (26% versus 10%, P=0.039). Nonapical vent LV LGE also correlated with markers of adverse outcome. In a multivariate model, RV LGE remained a predictor of arrhythmia.
Conclusions RV and LV LGE were common after TOF repair and were related to adverse clinical markers, including ventricular dysfunction, exercise intolerance, and neurohormonal activation. Furthermore, RV LGE was significantly associated with clinical arrhythmia.
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