ABC | Volume 110, Nº6, June 2018

Artigo Original Catharina et al Síndrome metabólica na hipertensão Arq Bras Cardiol. 2018; 110(6):514-521 numbers and/or percentages and compared by chi-square test. A logistic regression model was applied to determine association of clinical variables with the presence of MetS, apart from potential confounders. All statistical tests were performed using SigmaPlot 12.5 version (Systat software, Inc.). A significance level of alpha = 0.05 was adopted. Results Baseline characteristics of hypertensive subjects with and without MetS are shown in Table 1. We found a MetS prevalence of 66% in all hypertensive population. No differences were found between groups regarding age, race and gender. As expected, BMI, WC, FM and TBW were higher in hypertensive patients with MetS. Office heart rate (HR) was significantly higher in patients with MetS. Neither office and ambulatory BP levels nor the proportion of patients with uncontrolled office BP (≥ 140/90 mmHg) were different between groups. The patients with MetS showed a higher prevalence of MA compared to their counterparts. The medication use was similar between groups, except for the calcium channel blockers and antidiabetics that were higher in MetS group (Table 1). As expected, the evaluation of biochemical parameters showed increased triglycerides, as well as fasting glucose and HbA1c in subjects withMetS (Table 2). Additionally, adiponectin levels were significantly lower in patients withMetS, while leptin demonstrated to be increased in those patients, compared to the subjects without MetS (Table 2). Finally, the multiple logistic regression revealed that MA, leptin/adiponectin ratio (LAR) and resistance to antihypertensive treatment were independently associated with the presence of MetS (Table 3). Discussion Our main findings suggest that MA and increased LAR are associated with the presence of MetS in hypertensive population, apart from potential confounders. Also, resistance to antihypertensive treatment is strongly associated with MetS. The high prevalence of these coexisting conditions – hypertension andMetS – may explain the increased prevalence of hypertension-related target organ damage (TOD), such as elevated urinary albumin excretion. 5 Additionally, this early renal organ damage may in part explain the increased cardiovascular risk conferred by MetS in hypertensive patients, since this marker of TOD is a well-known predictor of CV events. 13 In this sense, the identification and treatment of risk factors for cardiovascular and renal diseases, as well as an early detection of hypertension-related TODmay directly affect the prognosis of hypertensive patients with MetS. 14 Our finding of increased MA in hypertensive patients with MetS is supported by previous studies. 13 The common underlying mechanisms that may explain increased MA in patients with MetS include factors such as: (i) overactivation of the renin-angiotensin system; (ii) increase in oxidative stress and (iii) inflammation. 15 In addition, the presence of MA may affect reflect progressive endothelial and vascular dysfunction. 16 It is worth to mention that we found no difference in BP levels between the groups. Thus, in our cross-sectional study MA is probably associated with other components that comprise MetS. Another hypothesis is that the greater use of calcium channel blockers by hypertensive patients with MetS could have resulted in BP control, but not in avoiding early renal damage, in agreement with several studies. 17 Another point to be mentioned is that despite of the greater use of antidiabetic drugs by patients with MetS, HbA1c remained higher in this group. On the other hand, studies 18 have consistently shown that levels of HbA1c < 7% are associated with a reduced risk of structural and clinical manifestations of diabetic nephropathy in patients with diabetes type 1 and type 2. For instance, the U.K. Prospective Diabetes Study (UKPDS) 18 demonstrated a nearly 30% risk reduction for the development of MA in the group intensively treated for hyperglycemia (HbA1c of 7%). 18 Hypoadiponectinemia and hyperleptinemia are commonly found in hypertensive and obese patients. Previous studies have shown an inverse association between adiponectin levels and low-grade albuminuria in essential 19 and resistant hypertensive patients. 20,21 Similarly in experimental studies, adiponectin knockout rats have higher levels of albuminuria (twice above normal values), and after replacement of the protein, albuminuria returned to its normal levels. 22 Hyperleptinemia is also an independent risk factor for coronary artery disease 23 and strong predictor of acute myocardial infarction. Besides that, leptin acts as a powerful sympathostimulator, associated with increased BP and tachycardia, which consequently contributes to obesity-related hypertension and kidney damage. 24 Furthermore, a study has supported that the LAR is more beneficial than either alone for the diagnosis of MetS. 25 The use of LAR has the potential to assess insulin sensitivity and MetS in the non-fasting state, since the difference between adiponectin and leptin tends to be small in the fasting versus postprandial state. 26 Our study showed that LAR was independently associated with the presence of MetS. There are several studies that relate MetS to various cytokines and adipokines, but no biomarker is currently used in clinical practice to help in predicting and establishing MetS in individuals. Therefore, the deregulated adipokine levels (LAR) might be a valuable tool for diagnosis, prognosis or even early detection of MetS in the high-risk hypertensive population, although these associations should be tested. This may also guide a rational therapeutic approach and risk management, since adipokines are altered after lifestyle modifications and medications. 27,28 The prevalence of MetS has been increasing worldwide, 29 and it is higher in hypertensive patients than in general population. 5 In our study, we found a considerable prevalence of MetS in all hypertensive subjects (66%) – 73% in resistant and 60% in mild-to-moderate hypertensive patients. Similar data have been reported in the Global Cardiometabolic Risk Profile in Patients with hypertension disease (GOOD) study, 30 in which 58% of essential hypertensive patients had MetS. Indeed, other similar study also indicated a high proportion of RHTN among patients with MetS. 31 This high prevalence may be explained by the older age of the population in the studies, since prevalence of MetS is highly age-dependent. 1 In our study, RHTN was associated with MetS independently of potential 516