Obesity adversely affects myocardial metabolism, efficiency, and diastolic function. Our objective was to determine if weight loss can ameliorate obesity-related myocardial metabolism and efficiency derangements and that these improvements directly relate to improved diastolic function in humans. We studied 30 obese (body mass index [BMI]>30kg/m2) subjects with positron emission tomography (myocardial metabolism, blood flow) and echocardiography (structure, function) before and after marked weight loss from gastric bypass surgery (N=10) or moderate weight loss from diet (N=20). Baseline BMI, insulin resistance, hemodynamics, left ventricular (LV) mass, systolic function, myocardial oxygen consumption (MVO2), and fatty acid (FA) metabolism were similar between the groups. MVO2/gram decreased after diet-induced weight loss (P=0.009). Total MVO2 decreased after dietary (P=0.02) and surgical weight loss (P=0.0006) and was related to decreased BMI (P=0.006). Total myocardial FA utilization decreased (P=0.03), and FA oxidation trended lower (P=0.06) only after surgery. FA esterification and LV efficiency were unchanged. After surgical weight loss, LV mass decreased by 23%, (Doppler-derived) E/E’ by 33%, and relaxation increased (improved) by 28%, and. Improved LV relaxation related significantly to decreased BMI, insulin resistance, total MVO2, and LV mass but not FA utilization. Decreased total MVO2 predicted LV relaxation improvement independent of BMI change (P=0.02). Weight loss can ameliorate the obesity-related derangements in myocardial metabolism and LV structure and diastolic function. Decreased total MVO2 independently predicted improved LV relaxation, suggesting that myocardial oxygen metabolism may be mechanistically important in determining cardiac relaxation.
During the past twenty years, there has been a dramatic increase in obesity and the cardiometabolic syndrome (CMS). In the United States alone, there are an estimated 42 million persons affected by CMS.1 In addition to complications from diabetes and hypertension, this population is at risk for the development of both ischemic and nonischemic heart failure.2 Although it is fairly well accepted that obesity and other aspects of CMS contribute to left ventricular (LV) remodeling and diastolic dysfunction, controversy does exist as to the effects of CMS on systolic function.2 This is partly due to the fact that obesity is associated with an increase in plasma volume.2 Thus, any load-dependent measures of systolic function, e.g., cardiac output, are necessarily affected by alterations in volume as well as contractility. Different methods for indexing LV systolic function measures in obese subjects may also affect systolic function results. For example, cardiac output may be increased in obesity but when indexed for body surface area, cardiac index may be low. Thus, newer, more load-independent noninvasive methods are necessary for better characterizing LV systolic function.Tissue Doppler imaging (TDI), an echocardiographic method previously described in the Images in CMS section of the Journal of the Cardiometabolic Syndrome, is considered to be relatively load-independent.3 Although, TDI is relatively easy to perform and measure, it does have some limitations. TDI provides a longitudinal assessment of the function of an entire wall rather than of a segment, so localization of the segmental wall motion abnormalities using TDI is limited.4 Additionally, because it is a Doppler-derived parameter, it is necessarily angle-dependent, and so TDI-derived measures of function are angle-dependent.A new echocardiographic technique called strain imaging, overcomes some of the limitations of TDI. Like TDI, strain imaging is thought to be relatively load-independent, but strain imaging has other advantages as well. Strain imaging allows for segmental wall motion quantification and (when quantified using speckle tracking) is not angle-dependent. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptIn order to explain this technique it is first important to define "strain" as it pertains to LV systolic function. Strain means deformation and is calculated as the change in length divided by the original length.4 As such, strain is dimensionless and typically represented as a negative fractional or percentage change in dimension. Since LV contraction in systole causes LV deformation (strain), strain is a measure of contractility.4 (The rate at which the LV deforms may also be measured echocardiographically and is termed "strain rate," but this imaging article will focus on strain). LV contraction is a three-dimensional process that involves radial and longitudinal cardiac muscle fibers. As longitudinal fibers shorten the ventricle, radial fibers squeeze in and twist in a clockwise direction at the base and counte...
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