Ann Thorac Surg 2001;71:1259
© 2001 The Society of Thoracic Surgeons
Invited commentary
Roberto M. Di Donato, MDa
a Department of Pediatric Cardiac Surgery, Bambino Gesù Hospital, Piazza S. Onofrio, 4, 00165 Rome, Italy
e-mail: didonato{at}opbg.net
The potential for "physiologic" growth of the myocardium (hyperplasia and angiogenesis) is lost very early in life. Myocyte response to pressure overload is considered the result of intermingling phenomena of cell replication and hypertrophy on one side, and myocyte necrosis and apoptosis on the other side, a process known as "plasticity of the myocardium." Noteworthy, a few adult cardiac myocytes seem capable to reexpress fetal proteins and proliferate following sudden pressure overload. However, after the first few weeks of age, cell hypertrophy remains the dominant type of pressure-induced myocyte response. The deterioration of diastolic function during the retraining process causes myocyte death, which, in turn, propitiates left ventricular fibrosis and dilation, aggravating the magnitude of stress on the remaining viable cells. Fiber stretching in dilated myocardium may, in fact, promote myocyte apoptosis.
In contrast to the adult, pressure-induced ventricular augmentation in the neonate involves increased angiogenesis, as in fetal life. Prolonged overload, however, causes decreased capillary density and coronary vascular reserve. These vascular changes probably reflect a switch from myocyte hyperplasia to hypertrophy as the primary mode of cardiac enlargement but may also indicate vascular abnormalities, eg, inhibition of normal vascular growth or an increase in the wall/lumen ratio because of vascular remodelling.
The extrapolation of in vitro observations to the in vivo state requires considerable caution, especially because experimental models of aortic banding determine supravalvular (ie, supracoronary) aortic stenosis, whereas clinical application of pulmonary banding in transposition is equivalent to creating "aortic" valvar stenosis. Nevertheless, the currently used criteria for selection of patients as well as timing and modalities of left ventricular reconditioning are still arbitrary. As of today, the result of a two-stage conversion from atrial to arterial switch, even if undertaken at a relatively young age, eg, in the four patients of Daebritz and colleagues, cannot be defined a truly "anatomic" repair. It relies on a structurally and functionally subnormal neosystemic pump and may be complicated by progressive atrial arrhythmias and neoaortic valve incompetence. I believe that efforts to boost up this alternative to heart transplantation for a difficult group of patients should continue. Maybe, a protocol of serial myocardial biopsies could help in directing therapeutic approaches. Maybe, strategies to genetically engineer myocyte and vascular replication could be developed. At the moment, however, we cannot rule out that a majority of these patients will eventually need a heart transplantation.
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Systemic right ventricular failure after atrial switch operation: midterm results of conversion into an arterial switch
- Sabine H. Daebritz, Andreas R. Tiete, Jörg S. Sachweh, Wolfgang Engelhardt, Götz von Bernuth, and Bruno J. Messmer
Ann. Thorac. Surg. 2001 71: 1255-1259.
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