Myocardial perfusion magnetic resonance imaging for detecting coronary function anomalies in asymptomatic paediatric patients with a previous arterial switch operation for the transposition of great arteries.

BACKGROUND: The main cause of long-term morbidity and mortality after the arterial switch operation for transposition of great arteries is complication at the coronary arteries. Myocardial perfusion magnetic resonance imaging represents a relatively novel and appealing tool for detecting myocardial ischaemia but with little experience in paediatric patients. The purpose of this paper is to report a single centre experience with myocardial perfusion magnetic resonance imaging for detecting ischaemia after the arterial switch operation for transposition of great arteries. METHODS: Twenty-eight patients aged 13-16 years with an arterial switch operation for transposition of great arteries were included in the study. Coronary pattern, operative and postoperative complications, and long-term follow-up events were reviewed. Patient functional evaluation included clinical examination, electrocardiogram and echocardiogram. Every patient underwent magnetic resonance imaging perfusion scanning at rest and under adenosine-induced stress. RESULTS: All patients were symptom free with no ischaemic signs on the electrocardiogram. All magnetic resonance imaging examinations were generally well tolerated with minor adenosine secondary effects in 36% of the patients. Two stress myocardial perfusion magnetic resonance studies were excluded from analysis for technical reasons. No perfusion stress defects were detected at the remaining 26. Myocardial delayed enhancement was performed in all 28 patients. In five subjects, a subendocardial late enhancement consistent with patch tissue for septal defect closure at the time of repair was indentified. CONCLUSION: Magnetic resonance imaging evaluation of myocardial perfusion and viability is feasible in paediatric patients long after arterial switch operation. No signs of myocardial ischaemia or necrosis were documented in this young asymptomatic population. Further studies including coronary angiography correlation are needed to validate magnetic resonance imaging results.

Late outcome of Senning and Mustard procedures for correction of transposition of the great arteries.

OBJECTIVES: To evaluate late mortality and morbidity after an atrial switch procedure for correction of transposition of the great arteries (TGA) and to assess predictive factors for adverse outcome. SETTING: Tertiary referral centre. DESIGN AND PATIENTS: Retrospective follow up study of 137 patients surviving hospitalisation for TGA atrial switch procedure (Mustard or Senning) in a single institution and divided into two groups (simple and complex) depending on presurgical anatomy. Several surgical and follow up factors were evaluated during 16.7 (5.6) years' follow up. RESULTS: Late mortality was 5.1% (95% confidence interval 1.37% to 8.84%) with sudden death as the most common cause. No significant difference was found between Mustard and Senning procedures and between the complex and simple groups in terms of mortality. Independent predictive factors for late mortality were a history of supraventricular tachyarrhythmias and advanced New York Heart Association (NYHA) functional class during follow up. A very common finding was development of sinus node dysfunction (47.6%), which had no influence on mortality. There was little need for reintervention (5.1%) and relatively few cases of right ventricular systolic dysfunction (14.6%). During follow up, most patients (96.2%) were in NYHA functional class I-II. CONCLUSIONS: Overall long term outcomes of patients with atrial repair of TGA in the present era are encouraging in terms of late mortality and quality of life. Nevertheless, better outcomes may be offered through improved diagnostic methods for right ventricular function and better management of supraventricular tachyarrhythmias.

Experience with enoxaparin in patients with mechanical heart valves who must withhold acenocumarol.

OBJECTIVES: To evaluate the incidence of thromboembolic and haemorrhagic events in a cohort of patients with mechanical heart valves who had to withhold acenocumarol and were treated with enoxaparin. DESIGN: Observational prospective study. SETTING: In hospital; after discharge, and follow up by telephone call. PATIENTS AND METHODS: All consecutive patients with mechanical heart valves admitted to the authors' hospital between May 1999 and January 2002 who had to interrupt treatment with acenocumarol and were treated with enoxaparin as an alternative to other methods were enrolled. In each patient, the following characteristics were prospectively determined: the reason for interrupting acenocumarol, demographic data, estimated global risk for thromboembolic events, international normalised ratio before starting enoxaparin treatment, number of days taking enoxaparin, and mean level of anti-Xa activity during treatment. All patients were followed up through clinical history during the hospitalisation and by telephone after discharge to detect thromboembolic events. MAIN OUTCOME MEASURE: Presence of thromboembolic or haemorrhagic events. RESULTS: 82 patients were identified and followed up for a mean of 2.8 months (range 1.5-3.5 months) after discharge. 61 of them (74%) had one or more associated thromboembolic risk factors. Acenocumarol was interrupted (to perform an invasive procedure in 74 patients and because of haemorrhagic complication in 8) an average of 11.2 days (range 3-40 days). Most patients received the standard enoxaparin dose (1 mg/kg at 12 hour intervals). Mean (SD) anti-Xa activity was 0.58 (0.3) IU/ml (median 0.51). There were 8 minor and 1 major bleeding events during enoxaparin treatment. No thromboembolic complications were clinically detected during hospitalisation or during follow up (95% confidence interval 0% to 3.6%). CONCLUSIONS: Enoxaparin may be an effective and relatively safe substitute anticoagulant for patients with mechanical heart valves who must withhold acenocumarol.