We read with interest the recent report by Mukerji et al describing the effects of weight-loss surgery on left ventricular (LV) mass and electrocardiographic findings. One of the investigators’ main conclusions is that LV mass is a key determinant of corrected QT and corrected QT dispersion in normotensive morbidly obese patients. On the basis of our observations, we offer a different interpretation, which complements the investigators’ elegant study. In patients with clinically severe obesity, we observed a negative association between the plasma levels of long-chain fatty acids and diastolic function in the setting of insulin resistance and suggested that excess fatty acids in the plasma exert lipotoxic effects on the heart. The lipotoxic effects include impaired intracellular Ca ²⁺ cycling. We also observed a dramatic reversal of increased plasma free fatty acid levels, as well as derangements in muscle metabolism and left ventricular function after bariatric surgery. Furthermore, even though parameters of obesity, including insulin resistance, free fatty acid levels, body composition, and body mass index, plateau 1 to 9 months after surgery, the benefits of bariatric surgery on left ventricular mass are sustained; that is, LV mass continues to decrease in a linear fashion over a 2-year time period. We proposed that by targeting the source of excess energy supply, weight-loss surgery reduces LV mass and improves contractile function of the heart by limiting substrate supply to the metabolically overloaded heart and to peripheral organs. In short, our earlier studies complement the work of Mukerji et al on the effects of weight loss after bariatric surgery on left ventricular repolarization. We propose that there is much more to it. Eventually, a comprehensive picture should emerge from this fascinating area of clinical research.