Abstract

Left ventricular hypertrophy (LVH) is generally considered to be an adaptive response that allows for normal ejection fraction despite abnormal pressure and/or volume load.1 However, this adaptation is associated with increased cardiac morbidity and mortality, including acute myocardial infarction, heart failure, arrhythmia, and stroke.2–4 Insight into the prevalence and consequences of LVH and response to treatment was made possible by the advent of echocardiography,5 which has been used to measure left ventricular mass for the past 3 decades6 in cross-sectional and epidemiological studies and serially in clinical trials.7 Cardiac MRI is accepted as a more precise means to measure LV mass8,9 and is being used in large-scale clinical and epidemiological studies.10,11 The article by Khouri et al in this issue of Circulation: Cardiovascular Imaging 12 reflects this maturation of cardiac MRI; these authors used MRI-derived mass and volume to refine the paradigm of LV hypertrophic response in a large (2803 subjects) cross-sectional study of participants in the Dallas Heart Study. Article see p 164 To understand the importance of this work, some context should be provided. Hypertrophy, defined as an increase in LV mass in relation to body size (ie, high LV mass index), is produced by an increase in chamber size, an increase in wall thickness, or both. For decades, concentric hypertrophy was considered the appropriate, even universal, response to a pressure load, as the heart adapted to maintain normal stroke volume despite high systolic pressure.13 In 1992, Ganau et al13 proposed a simple quantitative classification paradigm based on their study of …

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