Abstract

With the recognition that left ventricular (LV) mass (LVM) contributed to the prediction of cardiovascular morbidity and mortality, independent of conventional risk factors, including those that partially determined LVM (body size, blood pressure, and tobacco), interest in better understanding the clinical and epidemiological roles of LVM measurement accelerated.1 Over the last 2 decades, substantial progress has been made in this regard. For example, clinical trials have been designed to demonstrate the independent contribution of pharmacological LVM reduction, beyond blood pressure reduction in hypertensive patients, to improvement in cardiovascular outcomes.2 The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents incorporates LVM measurement in its evaluation algorithm with intensification of antihypertensive management recommended in the presence of LV hypertrophy.3 Despite this success, the role of LVM in clinical practice has not been firmly established. There are a number of controversies surrounding the measurement of LVM. These include the fact that LVM is principally determined by body size so that some component of LVM is adaptive rather than pathological, that LVM can be increased by healthful behaviors (eg, physical training) and cardiovascular risk factors, that there are significant problems in standardizing echocardiographic measurement of LVM by echocardiography across laboratories, that MRI provides more accurate measurement of LVM than echocardiography, and that a firm definition of LV hypertrophy based on the calculation of heart weight has not been established by consensus. Historically, one method for overcoming these several limitations has been indexing LVM to body size. Most commonly this is done by dividing LVM by body surface area or height elevated to some power, usually height2 or height2.7.1,4,5⇓⇓ Driving these analyses has been a concern for accommodating the strong relationship of LVM to lean body mass (and …

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