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Ann Thorac Surg 1997;64:750-751
© 1997 The Society of Thoracic Surgeons
Pediatric Cardiothoracic Surgery, Children's Hospital of Pittsburgh, One Children's Place, 3705 Fifth Ave at DeSoto St, Pittsburgh, PA 15213-2583
This article by Yatsunami and associates is an elegant study of a subject of great interest to pediatric cardiologists and cardiac surgeons. It has been clear that left ventricular systolic and diastolic dimensions and function after the arterial switch repair for transposition are frequently found to be not entirely normal even in the large cohort of patients who are clinically quite stable and asymptomatic. The fear has been that the surgical procedure itself with the need to transpose the coronary vessels to the neoaorta may limit the potential for growth of the coronary vessels or the coronary orifice and that this surgical and growth issue may be related to nonoptimal ventricular hemodynamics. The authors of this study have shown that the coronary distribution within the left coronary system after the arterial switch correction is smaller than "normal" when compared with a group of controls, the controls in this study being patients with Kawasaki disease, who are followed up with coronary angiograms (and thus conveniently available) and who are considered to have no coronary involvement associated with their disease. Yatsunami and associates acknowledge that this is not an ideal control, but it may be the best available.
Yatsunami and associates state that there were no coronary obstructive lesions in the study population other than in the 1 patient with an occluded left system who was excluded from the study. The coronary vessels were studied by selective angiography with a specified protocol for determining the site of size measurement. No data are presented to describe neoaortic root anatomy or whether there may be some compromise of the right and left coronary orifices. Potential limitation in the growth of the coronary vessel to neoaortic connection has been of concern and if present would be expected to limit the growth of the right or left coronary system after the arterial switch operation. This was not demonstrated in this study.
The large proportion of patients in this study with the "two-stage switch repair" is a different experience than usually reported, in which most if not all of the patients have undergone their correction as a one-stage operation during their first 2 weeks of life. This difference in surgical timing and the importance of left ventricular conditioning might be expected to have a significant influence on muscle mass and coronary flow dynamics. Yatsunami and associates speculated that there may be differences in the coronary growth in patients undergoing a one-stage repair (early neonatal period) versus the two-stage repair and in patients with or without a ventricular septal defect. Interestingly, no significant difference was found, which forces one to question whether it is, in fact, the left ventricular muscle mass that determines the size and distribution of coronary vessel development in the patient with transposition.
Similar coronary studies in patients who have undergone atrial rerouting procedures as their corrective operation for transposition would help further delineate the relative contribution of muscle mass development and its relation to coronary vessel size. If muscle mass is not the most important factor in inducing coronary development in the patient with transposition, we might speculate that the smaller left coronary system is in some way determined by other causes or during prenatal cardiac development.
It is difficult to extrapolate from the size measurements presented in this article that the patients may be having coronary flow limitations with ischemia, based on coronary vessel size abnormalities, which could be responsible for the subtle left ventricular dysfunction observed in the post-arterial switch transposition population. The observations so nicely described in this study are an important step toward a better understanding of the late functional results of the arterial switch correction of transposition of the great arteries.
Related Article
Ann. Thorac. Surg. 1997 64: 746-750.
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