A possible role of visceral fat-related inflammation in linking obstructive sleep apnea to left ventricular hypertrophy.

A Possible Role of Visceral Fat-Related Inflammation in Linking Obstructive Sleep Apnea to Left Ventricular Hypertrophy To the Editor: We read with great interest the article by Avelar et al1 titled “Left Ventricular Hypertrophy in Severe Obesity. Interactions Among Blood Pressure, Nocturnal Hypoxemia, and Body Mass.” Although the contribution of obstructive sleep apnea to the development of left ventricular remodeling is not confirmed by all of the previous studies, the authors pointed out that a reduced oxygen saturation resulted as the strongest independent predictor of left ventricular hypertrophy, with body mass index and high blood pressure amplifying the effect.1 In the accompanying editorial commentary, de Simone2 discussed widely the role of various pathophysiologicals possibly involved in this association. However, it does not make mention of the putative implication of visceral adipose tissue (VAT) and its related inflammatory background.3,4 We have suggested recently, in uncomplicated morbid obesity, that the activation of inflammatory pathways within the myocardium could be responsible for a correlative and causative relationship between abdominal VAT and subclinical echocardiographic abnormalities.3,4 This was suggested by the association of both echocardiac parameters and VAT area with the levels of bioactive proteins involved in ventricular remodeling (eg, monocyte-chemoattractant protein-1, C-reactive protein, and soluble interleukin-6 receptor/interleukin-6 complex).3,4 Thus, it is reasonable to consider a role for inflammation in ventricular remodeling, starting before the occurrence of cardiovascular complications (eg, hypertension). Abdominal fat accumulation also represents the anatomic precondition for an altered nocturnal ventilatory drive. An increased VAT-related inflammatory background was also described for obstructive sleep apnea5,6 with its treatment leading to an improvement.6 However, this reduction in cytokines reaches levels comparable to those of obese controls,6 thus suggesting a worsening proinflammatory role of obstructive sleep apnea. In this sense, the higher predictive role of hypoxemia may find a further possible explanation.1 However, the poorer association between left ventricular hypertrophy and body mass index could be ascribed to the high degree of obesity of the population studied by Avelar et al.1 Although fitting well to populationbased studies, body mass index should be regarded as an index of weight excess, because it does not distinguish between VAT from subcutaneous abdominal fat, particularly in morbid obesity. The quantitative assessment of VAT, other than by echography (eg, by computed tomography),3,4 is not of clinical use. However, the quantification of VAT surrogates (eg, waist circumference, waist/hip ratio, or epicardial fat by echocardiography) is feasible. Considering the inflammatory background associated with fat distribution, future research might provide further clarifications of the association between obstructive sleep apnea and left ventricular hypertrophy.