ABC | Volume 110, Nº6, June 2018

Artigo Original Catharina et al Síndrome metabólica na hipertensão Arq Bras Cardiol. 2018; 110(6):514-521 Table 2 – Biochemical parameters of hypertensive patients with and without metabolic syndrome Patients with MetS (n = 157) Patients without MetS (n = 79) p-value Cholesterol (mg.dL –1 ) 166 (139 – 192) 179 (150 – 200) 0.06 LDL-c (mg.dL –1 ) 88 (70 – 111) 98 (73 – 118) 0.19 HDL-c (mg.dL –1 ) 43 (37 – 49) 57 (51 – 65) < 0.01 Triglycerides (mg.dL –1 ) 142 (97 – 199) 81 (68 – 115) < 0.01 FBG (mg.dL –1 ) 107 (95 – 130) 91 (86 – 97) < 0.01 HbA1c (%) 6.30 (6– 7.40) 5.90 (5.50 – 6) < 0.01 hs-CRP (mg.dL –1 ) 0.39 (0.17 – 0.65) 0.25 (0.11 – 0.48) 0.02 Na (mEq.dL –1 ) 141 (140 – 143) 142 (138 – 143) 0.61 K (mEq.dL –1 ) 4.40 (4.10 – 4.70) 4.30 (4.20 – 4.60) 0.82 PAC (ng.dL –1 ) 83 (48 – 162) 65 (41 – 125) 0.10 CC (ml.min –1 .(1,73m 2 ) –1 ) 80 (55 – 97) 71 (53 – 94) 0.53 Creatinine (mg.dL –1 ) 0.93 (0.80 – 1.12) 0.95 (0.77 – 1.20) 0.97 Renin (pg.ml – 1 ) 23 (12 – 64) 30 (11 – 80) 0.78 Urea (mg.mL –1 ) 35 (26 – 44) 36 (28 – 44) 0.81 Cortisol (ug.dL –1 ) 14 (10 – 20) 14 (10 – 16) 0.44 Leptin (ng.mL –1 ) 21.0 (14.40–41.60) 15.70 (6.30–33.20) < 0.01 Adiponectin (µg.dL –1 ) 5.30 (2.60– 7.80) 7.50 (3.80 – 11.90) < 0.01 LAR 4.81 (2.14 – 10.80) 2.22 (1.10 – 5.20) < 0.01 LAR > 3.72, n (%) 85 (54) 24 (30) < 0.01 Values are expressed as mean ± standard deviation or median (1st, 3rd quartiles), according to data distribution. Continuous variables were compared using unpaired Student´s t-test or Mann-Whitney test, according to data distribution. Categorical variables were compared by chi-square test. MetS: metabolic syndrome; LDL-c: low density lipoprotein-c; HDL-c: high density lipoprotein-c; FBG: fasting blood glucose; HbA1C: glycated hemoglobin; hs-CRP: high-sensitivity c-reactive protein; Na: serum sodium; K: serum potassium; PAC: plasma aldosterone concentration; CC: creatinine clearance; LAR > 3.7: leptin adiponectin ratio > 3.7 (the cutoff value was determined by median value). Finally, pharmacological approaches should be carried out in order to improve obesity, dyslipidemia, hyperglycemia and hypertension 33 for renal protection. However, the cornerstone of treating MetS remains lifestyle modification, 3 which mainly involves healthy diet, aerobic exercise, and behavioral counseling. To date, current guidelines do not specifically address the management of mild to moderate hypertension and RHTN in the patient with MetS. However, considering the increased risk of developing diabetes in these patients, it seems reasonable that the first consideration in antihypertensive treatment is to be focused on the inhibition of the renin-angiotensin system with either angiotensin converting enzyme or angiotensin II receptor inhibitors. 34 There has been increasing interest in combination strategies of antihypertensive agents in RHTN patients with MetS to reduce the pill burden. Future works are still needed to define the best antihypertensive therapy in this group of high-risk patients. The limitations of this study include: (i) the cross-sectional design with no cause-effect inference; (ii) a small sample size and (iii) inclusion of patients from one outpatient clinic only. Although studies have shown significant differences between patients with mild to moderate hypertension and RHTN, 35,36 we did not dichotomize the hypertensive population because they both had a high prevalence of SMet with similar metabolic profile, then contributing to the objective of evaluating the influence of SMet on all these subjects together. Conclusion In summary, our study showed that MetS is significantly associatedwithMA, RHTN and adipokines levels. These findings suggest that hypertensive patients with MetS tend to develop early manifestations of end-organ damage with metabolic/ hormonal changes, culminating in increased cardiovascular risk and renal impairment. However, as we mentioned earlier, we cannot infer from this cross-sectional study the exact nature of the association between MetS, MA, RHTN and adipokines levels. Early diagnosis of MetS in hypertensive patients may enable more accurate prediction of adverse cardiovascular events and renal impairment, as well as the implementation of more efficient strategies in terms of primary prevention. Besides that, prompt identification of MetS in resistant hypertensive patients allows modification of multiple risk factors that promote resistance to antihypertensive therapy, as well as guide the treatment to individual components of the syndrome. Thus, targeted treatment to individual components of the syndrome along with weight loss and lifestyle modifications can prevent resistance to antihypertensive treatment, as well as contribute to effective therapy in resistant hypertensive patients 518