ABC | Volume 110, Nº6, June 2018

Artigo Original Catharina et al Síndrome metabólica na hipertensão Arq Bras Cardiol. 2018; 110(6):514-521 Methods Study population In this cross-sectional study, a convenience sample of 107 resistant and 129 mild to moderate hypertensive patients regularly followed at the Resistant Hypertension Outpatient Clinic and Hypertension Outpatient Clinic of the University of Campinas (Campinas, Brazil) were enrolled, and classified into those with MetS (n = 157) and without MetS (n = 79). Suitable subjects who agreed to participate in the study were screened for a 6-month period of clinical follow-up to exclude (i) secondary hypertension (pheochromocytoma, aortic coarctation, Cushing's or Conn's syndrome, renal artery stenosis and obstructive sleep apnea) and (ii) pseudoresistance hypertension, including poor medication adherence (verified by pill counts) and white coat hypertension (verified by ambulatory blood pressure monitoring-ABPM). The diagnosis of “true” RHTN was done according to the 2008 American Heart Association Scientific Statement, 9 the last guideline published which properly defines a condition as (1) high blood pressure (BP) levels despite the use of at least three antihypertensive agents of different classes or (2) controlled BP after the use of four or more drugs. Ideally, one of the three agents should be a diuretic and all agents should be prescribed at optimal doses. Mild to moderate hypertensive subjects (grade I and II hypertension) were defined in accordance to the 2013 European Society of Hypertension (ESH) guidelines, 10 the last guideline on essential hypertension. Exclusion criteria were clinically-evident coronary artery disease or cerebrovascular disease, significant impaired renal or liver function, myocardial infarction and peripheral vascular disease. Diagnosis of MetS Diagnosis of MetS was determined according to the criteria proposed by the NCEP-ATPIII revised in 2005, 3 as the presence of at least three of the following criteria: (i) waist circumference (WC) ≥ 88 cm for women or ≥ 102 cm for men, (ii) HDL‑cholesterol < 50 mg/dL for women or 40 mg/dL for men, (iii) triglycerides ≥ 150 mg/dL (or in current use of fibrate), (iv) cutoff BP values of ≥ 130/85 mmHg (or current antihypertensive treatment), and (v) fasting glucose ≥ 100 mg/ dL (or current treatment for type 2 diabetes). Bioelectrical impedance analysis (BIA) Fat-free mass (FFM), fat mass (FM), total body water (TBW) and basal metabolic rate (BMR) were determined by BIA using the Bioimpedance Analyser 450 (Biodynamics Corporation, Seattle, USA). The measurements were performed after 4-hour period of fasting. Also, patients were instructed to avoid physical activity and smoking prior to the examination. Office and Ambulatory BP measurements Office systolic BP (SBP) and diastolic BP (DBP) were evaluated at approximately 08:00 a.m. in the right arm using a validated digital sphygmomanometer (HEM-907XL, OMRON Healthcare Inc., Bannockburn, IL, USA). The 24-h ABPM measurements were performed with a validated automatic device (Spacelabs 90217, Spacelabs Inc, Redmon, WA, USA), and measurements were taken every 20min. Patients were instructed to maintain their usual daily activities and inform them in a personal diary. Both office and ambulatory BP measurements were performed according to 2013 ESH guidelines. 10 Biochemical measurements The laboratory exams analyzed were: fasting blood glucose (FBG), insulin, glycated hemoglobin (HbA1c), serum sodium and potassium, plasma cortisol, total cholesterol, low and high-density lipoprotein-cholesterol (LDLc and HDLc, respectively), triglycerides, urea, creatinine and renin. The values between 30 and 300 mg/g of urine albumin/creatinine ratio grouped the patients as having microalbuminuria (MA) for comparisons of early renal damage. Plasma concentrations of adiponectin and leptin (R&D Systems, Minneapolis, USA) were determined by ELISA and aldosterone (Immunotech SAS, Marseille, France) by chemiluminescence, according to the manufacturer's instructions. Pulse wave velocity Arterial stiffness was determined by pulse wave velocity (PWV), in meters per second (m/s), dividing the distance between the right carotid and femoral arteries by the pulse transit time through these two sites of interest. We used the Sphygmocor device (AtCor Medical, USA), synchronized with the electrocardiogram. We used the mean of two PWV values in the analyses, or the median of three consecutive readings if the difference between the two measurements was greater than 0.5 m/s. The patients were considered as having arterial rigidity if PWV ≥ 10 m/s, for comparisons of vascular damage. 11 Echocardiography Left ventricular (LV) measurements were performed according to the recommendations of the American Society of Echocardiography using two-dimensional M-mode echocardiography. 12 Examinations were performed by an echocardiography expert and reviewed by two blinded investigators, following standard technique, using a cardiovascular ultrasound machine (Siemens Acuson CV70, Munich, Bavaria, Germany) with a multi-frequency sector transducer (2-4 MHz). We calculated LV mass index (LVMI), and considered those with LVMI > 95 g/m 2 (females) and > 115 g/m 2 (males) as having left ventricular hypertrophy (LVH). The intraobserver and interobserver coefficients of variation were less than 9.5% for the LVMI. Statistical analyses For continuous variables we calculated the mean and standard deviation or median (1st, 3rd quartiles), according to normal distribution, measured by the Kolmogorov-Smirnov test. We compared them using either unpaired Student´s t-test or Mann-Whitney test, according to distribution of data. Categorical variables were presented in absolute 515