Myocyte growth is seen in all forms of myocardial hypertrophy. In certain disease states, particularly arterial hypertension, components of the hypertrophic remodelling process, other than myocyte growth, distort myocardial structure and thereby adversely alter its mechanical behaviour. Such a pathologic structural remodelling includes a perivascular and interstitial fibrosis that impairs myocardial stiffness and a medial thickening of intramyocardial coronary arteries that attenuates its vasodilator reserve to ischaemic and pharmacologic provocation. The concept of cardioreparatíon embodies both a regression in myocyte hypertrophy and the pathologic components of the structurally remodelled myocardium and in so doing restores structure and function to normal. Implicit in this concept is the supposition that heart failure will be reversible. The concept of reparation was tested in 14-week-old male spontaneously hypertensive rats having left ventricular hypertrophy, diastolic dysfunction with myocardial fibrosis, and impaired coronary vascular reserve to adenosine, using the angiotensin-converting enzyme inhibitor lisinopril. A regression in left ventricular hypertrophy, perivascular and interstitial fibrosis, and medial thickening of intramural vessels were obtained after 12 weeks of oral lisinopril administration. It would now seem logical to determine whether cardioreparation can be achieved with lisinopril in patients with hypertension and left ventricular hypertrophy, in whom pathologic remodelling of the myocardium is responsible for symptomatic heart failure.