IJCS | Volume 32, Nº5, September/October 2019

530 Mourilhe-Rocha and Salvino Obesity and heart failure Int J Cardiovasc Sci. 2019;32(5):527-535 Review Article symptoms of HF, such as fatigue and lower limb edema, can be frequently found in obese individuals. In addition, brain natriuretic peptide (BNP), an important marker commonly used in the diagnosis and follow-up of HF, has a limited use in obesity, 6,12 and its levels are inversely proportional to BMI, independently of the presence or severity of HF. 6 In the FraminghamHeart Studywith5,881participants, 11.0% of the HF in men and 14.0% of the HF in women were solely attributed to obesity, even after adjusting for other known cardiovascular risk factors. 8 The duration of morbid obesity is the strongest predictor of HF development in obese patients. 6,26 The presence of morbid obesity for 20 years is associated with a 70% chance of developing HF, which increases to 90% after 30 years. 9 Most publications analyzed in this review used the term ‘obesity cardiomyopathy’, encompassing all patients with preserved and reduced ejection fraction. Obesity paradox Several studies have shown a paradoxical association between obesity and the prognosis of patients with coronary disease and HF, called the paradox of obesity. 5,7-9,12,29 According to that theory and contrary to what is expected, individuals with established cardiac disease and overweight or obesity have a better prognosis than under- or normal-weight individuals. 5,7,8,12,30 That favorable prognosis is observed for both men and women, in acute HF, HFpEF and HFrEF. 9 However, obesity hinders the treatment of patients with advanced HF, 8 and both morbid obesity and HF markedly reduce functional capacity. 17 In addition, no study has reported that weight-reducing interventions of patients with morbid obesity increase the mortality or morbidity of HF. 4 A meta-analysis 8 has shown a reduction in the hospitalization and cardiovascular and all-causemortality of patients withHF and overweight as compared to those of patients with normal BMI. However, more severely obese patients have not had the same benefit. 8 Other studies have suggested that when BMI exceeds 40 kg/m 2 , obesity is once again associated with worse prognosis. 9 There are several theories to explain that paradox, whosemechanismremains unclear. Observational studies demonstrating that paradox have not proven that weight loss is beneficial to obese patients with coronary artery disease, because most of them analyzed only baseline body weight values, with no follow-up data. 5 In addition, most of themare retrospective analysis. 9 Another relevant factor is that lowBMI values are frequently associatedwith sarcopenia, a conditionassociatedwith increasedmortality. It is postulated that, because BMI does not distinguish fat from lean mass, individuals with coronary artery disease and overweight or obesity can have a higher amount of preservedmusclemass. Thus, whenBMI reaches very high values that direct to body adiposity, the obesity paradox disappears. 5 Supporting that theory, studies using other measures to assess obesity and the prognosis of HF, such as Dual-Energy X-Ray Absorptiometry (DEXA), 9 have attained more controversial results. On the other hand, obese individuals with HF can be diagnosed earlier, at a stage of lower myocardial dysfunction, than non-obese individuals, 7-9 causing the impression of better cardiovascular outcome. In addition, cardiac cachexia, which occurs late in HF, is associated with worse prognosis. 7-9,12 Thus, once advanced HF becomes catabolic, causing muscle mass loss and cachexia, obesity can progress with increased metabolic reserves in the form of adipose tissue, which can delay the catabolic stage. However, further investigation is required to determine if that is a mechanism. 9,12 Although the obesity paradox can represent a statistical phenomenon, the likelihood of a real protective effect on the physiology of obesity should be considered. 7,8 Cardiac morphofunctional benefits related toweight reduction Substantial weight loss has been associated with the reversion of hemodynamic abnormalities and with the reverse LV remodeling of patients with obesity and HF. 4,21,31 There is a linear relationship between weight loss and LV mass regression, 14,32 in addition to the improvement of functional capacity. 33 Bariatric surgery has been more successful than diet and exercise to reverse those alterations. Because it is used for patients with more severe obesity, it produces substantial weight reduction and more evident neuro- hormonal and metabolic improvement than the weight loss modalities based on diet and exercise usually used for less obese individuals. 20 There is evidence that surgical weight reduction can increase ejection fraction in the presence of previous systolic dysfunction, 1,10,17,34 mainly in individualswith long-