Physiologic hypertrophy occurs as the result of exercise conditioning and is characterized by normal or supranormal left ventricular (LV) contractile function and reversibility of structural alterations. Whether hypertrophy produced by chronic abnormal loading can be termed ‘physiologic' is a matter of debate because in experimental pressure overload hypertrophy normal in vivo ventricular function may be associated with abnormal in vitro function of the papillary muscles. In patients with moderate LV hypertrophy from aortic valve disease (angiographic mass 20 mm Hg and/or cardiac index 2·5 l/mm/m2)interstitial fibrosis (IF) was increased to a similar extent (16 and 18%: normal <5%), whereas muscle fiber diameter (MFD normal ≤ 20 μ) was larger (P <0·05) in the patients with failure (30 μ) than in those with preserved function (27 μ). Moreover patients with depressed postoperative function had a larger (P < 001) preoperative MFD (35 μ) than those with normal postoperative function (30 μ). Seventeen months after successful aortic valve replacement IF increased (P < 0·02) and MFD decreased (P < 0·001) but did not become normal regardless whether postoperative function was normal or depressed. Thus in secondary hypertrophy myocardial structure is pathologic even in the presence of normal LV function and depressed function appears likely to be related to excessive fiber hypertrophy rather than to IF. Massive fiber hypertrophy heralds an unfavorable postoperative LV function and fibrosis is irreversible after surgical correction of the abnormal loa
