Sumário 1. Definição, Epidemiologia e Prevenção Primária 528 1.1 Definição de Hipertensão Arterial 528 […] Diretrizes Brasileiras de Hipertensão Arterial – 2020 Sumário 1. Definição, Epidemiologia e Prevenção Primária 528 1.1 Definição de Hipertensão Arterial 528 […] Diretrizes Brasileiras de Hipertensão Arterial – 2020

Recognition and treatment of secondary causes of hypertension among patients with resistant hypertension may help to control blood pressure and reduce cardiovascular risk. However, there are no studies systematically evaluating secondary causes of hypertension according to the Seventh Joint National Committee. Consecutive patients with resistant hypertension were investigated for known causes of hypertension irrespective of symptoms and signs, including aortic coarctation, Cushing syndrome, obstructive sleep apnea, drugs, pheochromocytoma, primary aldosteronism, renal parenchymal disease, renovascular hypertension, and thyroid disorders. Among 125 patients (age: 52±1 years, 43% males, systolic and diastolic blood pressure: 176±31 and 107±19 mm Hg, respectively), obstructive sleep apnea (apnea-hypopnea index: >15 events per hour) was the most common condition associated with resistant hypertension (64.0%), followed by primary aldosteronism (5.6%), renal artery stenosis (2.4%), renal parenchymal disease (1.6%), oral contraceptives (1.6%), and thyroid disorders (0.8%). In 34.4%, no secondary cause of hypertension was identified (primary hypertension). Two concomitant secondary causes of hypertension were found in 6.4% of patients. Age >50 years (odds ratio: 5.2 [95% CI: 1.9–14.2]; P 50 years, large neck circumference measurement, and snoring are good predictors of obstructive sleep apnea in this population.

Background: Obstructive sleep apnea (OSA) is associated with several cardiovascular diseases. However, the mechanisms are not completely understood. Recent studies have shown that OSA is associated with multiple markers of endothelial damage. We hypothesized that OSA affects functional and structural properties of large arteries, contributing to atherosclerosis progression. Methods and Measurements: Twelve healthy volunteers, 15 patients with mild to moderate OSA, and 15 with severe OSA matched for age, sex, and body mass index were studied by using (1) full standard overnight polysomnography; (2) carotid-femoral pulse wave velocity with a noninvasive automatic device; and (3) a high-definition echo-tracking device to measure intima-media thickness, diameter, and distensibility. All participants were free of hypertension, diabetes, and smoking, and were not on any medications. Patients with OSA were naive to treatment. Main Results: Significant differences existed between control subjects and patients with mild to moderate and severe OSA (apnea–hypopnea index, 3.1 ± 0.3, 16.2 ± 1.7, and 55.7 ± 5.9 events/hour, respectively) in pulse wave velocity (8.7 ± 0.2, 9.2 ± 0.2, and 10.3 ± 0.2 m/second; p < 0.0001), intima-media thickness (604.4 ± 25.2, 580.2 ± 29.0, and 722.2 ± 35.2 μm; p = 0.004), and carotid diameter (6,607.8 ± 126.7, 7,152.3 ± 114.4, and 7,539.9 ± 161.2 μm; p < 0.0001). Multivariate analyses showed that the apnea–hypopnea index correlated independently with pulse wave velocity and intima-media thickness variability (r = 0.61, p < 0.0001, and r = 0.44, p = 0.004, respectively), whereas minimal oxygen saturation correlated with the carotid diameter (r = −0.60, p < 0.0001). Conclusions: Middle-aged patients with OSA who are free of overt cardiovascular diseases have early signs of atherosclerosis. All vascular abnormalities correlated significantly with the severity of the OSA, which further supports the hypothesis that OSA plays an independent role in atherosclerosis progression.

Rationale: Obstructive sleep apnea (OSA) is associated with adverse cardiovascular outcomes, including myocardial infarction and stroke. Atherosclerosis is a key mechanism for these cardiovascular events. Recent cross-sectional studies showed the presence of early signs of atherosclerosis in patients with OSA who were free of comorbidities. Objectives: To determine the impact of treatment with continuous positive airway pressure (CPAP) on atherosclerosis. Methods: We randomly assigned 24 patients with severe OSA (age, 46 ± 6 yr) who were free of comorbidities to receive no treatment (control, n = 12) or CPAP (n = 12) for 4 months. Carotid intima-media thickness, arterial stiffness (evaluated by pulse-wave velocity), carotid diameter, 24-hour blood pressure monitoring, C-reactive protein, and catecholamines were determined at baseline and after 4 months. Measurements and Main Results: At baseline, all measurements were similar in both groups and did not change in the control group after 4 months. In contrast, a significant decrease occurred in carotid intima-media thickness (707 ± 105 vs. 645 ± 95 μm, P = 0.04), pulse-wave velocity (10.4 ± 1.0 vs. 9.3 ± 0.9 m/s, P < 0.001), C-reactive protein (3.7 ± 1.8 vs. 2.0 ± 1.2 mg/L, P = 0.001), and catecholamines (365 ± 125 vs. 205 ± 51 ng/ml, P < 0.001) after 4 months of CPAP. Carotid diameter did not change significantly. Regarding the whole group, changes in carotid intima-media thickness were correlated with changes in catecholamines (r = 0.41, P < 0.05). Changes in pulse-wave velocity were correlated with changes in C-reactive protein (r = 0.58, P < 0.01) and catecholamines (r = 0.54, P < 0.01). Conclusions: The treatment of OSA significantly improves early signs of atherosclerosis, supporting the concept that OSA is an independent risk factor for atherosclerosis. Clinical trial registered with www.clinicaltrials.gov (NCT00400543).

The pulse wave velocity (PWV) and the photoplethysmogram (PTG) are noninvasive methods for evaluating the pulse wave. The PWV has been associated with age and arterial hypertension, and an index of the second derivative of PTG (SDPTG) is correlated with age and other risk factors for atherosclerosis. The aim of this study was to compare SDPTG and PWV concerning the influencing factors of vascular compliance, including age and atherosclerosis, in a large hypertensive population. We studied consecutively 524 essential hypertensives, 140 with atherosclerotic alterations (AA), defined on the basis of clinical events including coronary heart disease, peripheral vascular disease, stroke, and abdominal aorta aneurysm. The PWV carotid-femoral was measured by a Complior device and the SDPTG was recorded by Fukuda FCP-3166. The augmentation index (AUI) of PTG was defined as the ratio of the late systolic peak to that of the early systolic peak in the pulse. The SDPTG consists of an a,b,c, and d wave in systole and an e wave in diastole; an SDPTG aging index (AI) was calculated as (b-c-d-e)/a. The patients with AA presented a higher PWV (14.9 +/- 4 m/sec v 12.4 +/- 2 m/sec, P < .001), PTG AUI (0.322 +/- 0.16 v 0.252 +/-0.09, P < .001), and SDPTG AI (-0.093 +/- 0.03 v -0.271 +/- 0.018, P < .001). However, in patients 60 years of age, only PWV remained higher in those with AA, whereas in patients >60 yr, both PWV and SDPTG AI remained higher in those with AA. The PWV was independently influenced by age, systolic blood pressure, glucose, AA, and plasma creatinine, whereas the PTG AUI was influenced by age and systolic pressure and the SDPTG AI by age and AA. In a logistic regression model for the presence of AA, including age, plasma creatinine, smoking, and diastolic BP, PWV was a significant independent determinant of AA, whereas SDPTG-AI weakly entered into the model. This study provides evidence that the aortic PWV reflects better than the SDPTG the modifications of the arterial compliance related to age, blood pressure, and atherosclerosis. However, the SDPTG AI may be useful for evaluation of vascular aging in hypertensives.