ABC | Volume 114, Nº3, March 2020

Statement Brazilian Position Statement on Resistant Hypertension – 2020 Arq Bras Cardiol. 2020; 114(3):576-596 Chart 2 – Key information obtained from ambulatory blood pressure monitoring • Multiple measurements over an observation period • Blood pressure assessment during daytime • Correlation of daytime measurements with activities and symptoms • Blood pressure assessment during sleep • Possibility of correlating blood pressure variability with symptoms, activities, and medications • Complement to the patient's diagnosis and prognosis • Evaluation of the antihypertensive effect 4.3. Home Blood Pressure Monitoring and Blood Pressure Self-Measurement Home BP measurements are more accurate than casual BP measurements and offer a better prediction of risk for CV outcomes, contributing to greater adherence to drug treatment. 35,38,39 In this context, HBPM and BP self- measurement (BPSM) are viable and effective alternatives for proper diagnosis and improved adherence. 40,41 4.4. Measurement of Central Arterial Pressure Arterial stiffness is recognized as an important prognostic index and potential therapeutic target in patients with hypertension. As a result, central systolic blood pressure (cSBP) and PWV have been recently investigated in a population of patients with RHTN. 42 The mean age of the population was 58.7 ± 15.3 years, and 65% (n = 53) were women. Brachial and central blood pressures were elevated in all patients. Additionally, the PWV value was higher than the reference value for age, and the difference was statistically higher for PWV in women. Another study 23 analyzing associations between RHTN and arterial stiffness has shown that patients with RHTN have increased vascular stiffness compared with patients with well-controlled hypertension. PWV increased with arterial stiffness and correlated with BP levels, justifying the need for adequate BP control. 5. Target-Organ Damage Coordinator: Roberto Dischinger Miranda. Authors: José Fernando Vilela-Martin, Juan Carlos Yugar- Toledo, Wilson Nadruz Júnior, and Cibele Isaac Saad Rodrigues. 5.1. Introduction Both C-RHTN and UC-RHTN are associated with a higher prevalence of TOD and higher CV risk and mortality compared with controlled hypertension. 43-45 Therefore, the investigation of TOD in RHTN is fundamental to complement the risk stratification and establish the prognosis. 44 5.2. Vascular Changes Patients with RHTN present structural and functional vascular changes resulting not only from uncontrolled hypertension but also from early vascular aging. This is a complex process involving biochemical, enzymatic, and cellular changes that modify the function and structure of the artery, culminating in early and progressive degeneration of the arterial health. 43-47 Pathophysiological mechanisms include increased oxidative stress, endothelial dysfunction, vascular remodeling, smooth muscle cell hypertrophy, increased arterial stiffness due to changes in collagen/elastin distribution, vascular inflammation, and increased expression of inflammatory mediators and matrix repair metalloproteinases, in addition to increased advanced glycation end-products and parietal calcification. 48,49 The molecular mechanisms of vascular aging include genetic alterations in segments involved in DNA protection and repair 50 and mitochondrial metabolic activity. 51 In the microcirculation, endothelial dysfunction promotes vasoconstriction, eutrophic remodeling (increased media/ lumen [M/L] ratio without external changes), decreased vasodilatory reserve and vascular rarefaction, the latter evaluated by in vivo capillaroscopy, 52 gluteus biopsy, or yet, measurement of the M/L ratio with laser Doppler flowmetry of retinal arteries 53 and optical videomicroscopy. In large arteries, parietal remodeling leads to increased arterial stiffness. 49,54-56 Arterial stiffness is estimated by carotid-femoral PWV (c-f PWV) and calculation of the augmentation index (AIx) by applanation tonometry. 57,58 These changes in arterial stiffness hemodynamic parameters and cellular biomarkers are associated with increased morbidity and mortality. 59,60 The macrovascular involvement is further characterized by carotid, cerebral, coronary, and peripheral atherosclerotic diseases. 61,62 5.3. Cerebral Changes The cerebrovascular involvement in RHTN is subtle and insidious. Microscopic white matter lesions begin early and may progress irreversibly, leading to cognitive impairment and progression to vascular dementia. 63,64 Patients with RHTN have a higher risk of cerebral infarction and transient cerebral ischemia, a fact that has been pointed out by the Kaiser Permanente 16 and REGARDS studies, 65 which showed risk increases of 17 and 14%, respectively. Atherosclerosis of the carotid and small cerebral vessels is responsible for ischemic and thromboembolic phenomena. Retinal artery occlusion is a marker of small vessel injury and has been associated with an increased risk of cerebral events. 66 Uncontrolled hypertension is the leading cause of hemorrhagic stroke. Patients with RHTN have microangiopathy (Charcot-Bouchard aneurysms), which affect the penetrating arteries in the brain and cause intraparenchymal hemorrhage. 67 Changes in large artery stiffness are also associated with increased occurrence of microvascular changes and a greater predisposition to cerebrovascular events. 68 5.4. Cardiac Changes Several cardiac changes may be observed in patients with RHTN, including LVH, left ventricular diastolic dysfunction (LVDD), and myocardial ischemia. 69 LVH is an independent 583