October 3, 2017 Circulation. 2017; 136: 1273–1275. DOI: 10.1161/CIRCULATIONAHA. 117.030730 1274 hypertrophy, as occurs in patients with mitral or aortic regurgitation, fails to normalize diastolic wall stress despite the correction of systolic wall stress. This observation in eccentric hypertrophy raised the prospect that the extent of LV hypertrophy may not always be “adequate” to the level of wall stress; persistently “uncompensated” wall stress in the setting of modest hypertrophy was posited to promote contractile dysfunction. Thus, important work in preclinical and clinical models correlated the presence of LVH with a variety of physiological variables, including wall stress and oxygen consumption. Nowadays, we call these variables surrogate markers, and we are acutely aware that such markers can, at times, mislead. In any event, the concept of compensatory hypertrophy has persisted as a hypothesis that has never been tested.