Aortic coarctation is a common abnormality comprising about 6% of congenital heart diseases. The narrowing of the aorta and consequent increased peak systolic stress is a potent stimulus for the development of left ventricular (LV) hypertrophy before repair. Clinically, however, the degree of hypertrophy and the progression to dilation and failure is variable. The extent of remodelling after successful repair is also difficult to predict, and persistence of hypertrophy has been demonstrated. Angiotensin converting enzyme (ACE) is responsible for the hydrolisation of angiotensin Ι into angiotensin ΙΙ, which is the principal circulating hormone of the renin–angiotensin system. It was shown that angiotensin ΙΙ stimulates myocardial growth by a direct effect on cardiac myocytes (increasing the fractional rate of protein synthesis), and also by indirect effects (increasing total peripheral vascular resistance). A single polymorphism of the ACE gene is described as follows: the insertion/larger allele, I, and the deletion/shorter allele, D, as well as a heterozygous form, ID, were located in intron 16 of chromosome 17q23. DD was associated with an increased plasma ACE activity and a high concentration of plasma angiotensin ΙΙ.¹ ACE gene polymorphism has been implicated in the pathogenesis of various cardiovascular diseases. DD has been associated with LV hypertrophy, ischaemic and idiopathic cardiomyopathy, and an increased risk of sudden death in hypertrophic cardiomyopathy.^1,2 This association between increased LV mass and ACE gene polymorphism might be expected to modify the responses to …