Age-dependent ventricular response to pressure overload. Considerations for the arterial switch operation.
Success with the arterial switch operation for D-transposition of the great arteries and the concept of left ventricular suitability for systemic work stimulated this literature review of the age-dependent mechanisms in normal cardiac growth and pressure-induced left ventricular hypertrophy. Normal postnatal myocardial growth is markedly influenced by hemodynamic factors. It consists of an early hyperplastic phase of both myocytes and capillaries that is followed by a myocyte hypertrophic phase. Similarly, imposition of a pressure overload induces both myocyte hyperplasia/hypertrophy and increased angiogenesis in neonates, but only myocyte hypertrophy at a later age. The functional consequences of ventricular hypertrophy are the result of adaptive and nonadaptive changes resulting from the overload stimulus, for example, induction of protooncogene expression, myosin isoenzyme shifts, degree of coronary perfusion, responsiveness to beta-adrenergic stimulation, and myocyte capacity to re-accumulate or sequester cytosolic calcium. Strikingly, both the capacity and the rapidity of left ventricular hypertrophy decrease with increasing age. This experimental information supports the current use of primary arterial switching for neonates with D-transposition of the great arteries and the use of "rapid" two-stage arterial switching in infants more than 3 to 4 weeks of age; it raises some concern about the practice of late retraining of the left ventricle in cases of failed atrial inversion operation.
Di Donato
R M
RM
Department of Cardiovascular Surgery, Children's Hospital, Boston, Mass. 02115.
Fujii
A M
AM
Jonas
R A
RA
Castañeda
A R
AR
D000367:Age Factors; D002118:Calcium / Q000378:metabolism; D006332:Cardiomegaly / Q000209:etiology*; D003326:Coronary Circulation; D003600:Cytosol / Q000378:metabolism; D006321:Heart / Q000254:growth & development; D006352:Heart Ventricles / Q000166:cytology / Q000473:pathology; D006801:Humans; D006965:Hyperplasia; D006984:Hypertrophy; D007231:Infant, Newborn; D009218:Myosins / Q000378:metabolism; D009389:Neovascularization, Pathologic; D014188:Transposition of Great Vessels / Q000503:physiopathology* / Q000601:surgery*
D009218:Myosins; D002118:Calcium