ABC | Volume 114, Nº4, April 2020

Statement Luso-Brazilian Position Statement on Hypertensive Emergencies – 2020 Arq Bras Cardiol. 2020; 114(4)736-751 10. Acute Aortic Syndromes Acute aortic syndrome (AAS), a term currently comprising aortic dissection (AD), intramural hematoma (IMH), and penetrating atherosclerotic ulcerations (PAU), has an incidence that ranges from 3.5 to 6.0 per 100,000 patients/year. 60 Given its high mortality rate, AAS should be considered and promptly diagnosed in patients with acute chest or back pain, especially if associated with hypertension. Computed tomography, magnetic resonance imaging, and transesophageal echocardiography are reliable imaging tests to diagnose AAS, while measurement of serum D-dimer has shown 51.7 to 100% sensitivity and 32.8 to 89.2% specificity in six studies. 61 Of all AAS types, AD is the most common (85 to 95%), followed by IMH (0 to 25%) and PAU (2 to 7%). 61 According to the Stanford classification, AAS is divided into type A, which involves the ascending aorta, and type B, which does not involve this segment. In contrast, the DeBakey classification divides AAS into type I, which involves at least the ascending aorta and the aortic arch and often also the descending aorta; type II, which is confined to the ascending aorta; and type III, which originates in the distal descending aorta and affects the left subclavian artery. 60 AAS may be associated with several risk factors including the male sex, advanced age, first-degree relatives with a history of AAS, hypertension, dyslipidemia, smoking, illicit drug use, history of major vascular arteritis ( e.g. , Takayasu arteritis), collagen vascular disease (like Marfan’s, Loeys-Dietz, and Ehlers-Danlos syndrome), blunt trauma from motor vehicle accident or vertical fall, arterial instrumentation for diagnostic or therapeutic purposes, or hereditary mutations in genes encoding proteins involved with vascular integrity (such as mutation in the ACTA2 gene). 60 10.1. Treatment Treatment of AAS requires a multidisciplinary approach involving clinical, endovascular, and surgical interventions. 62 Type A ADs have a poor prognosis and an overall in-hospital mortality of 30%, with a mortality increase of 1 to 2% per hour of progression. 63 Without intervention, the mortality is about 58%, compared with 26% with surgical intervention. 63 Open surgery is the ideal treatment for type A AAS (ascending aorta), and thoracic endovascular aortic repair is best suited to treat type B AAS (descending aorta). 64-66 Endovascular surgery has been shown to be better than medical treatment (97% vs. 43%) considering the favorable aortic remodeling, false lumen thrombosis, and absence of aortic dilation or rupture. 66 Initial management of AD involves pain control and use of antihypertensive agents. Intravenous beta-blockers (metoprolol, esmolol, or labetalol) should be administered to reduce wall stress, lowering heart rate and BP and maintaining adequate cerebral, coronary, and renal perfusion. 60 Administration of beta-blockers should be completed before BP reduction with afterload reducing agents. Guidelines recommend a SBP reduction to 100 to 120 mmHg and a heart rate below 60 bpm. 65 In case of intolerance to beta-blockers, non-dihydropyridine calcium-channel blockers (verapamil or diltiazem) should be used. 67 After proper beta blockade, afterload should be reduced. Although angiotensin-converting enzyme inhibitors (ACEIs) have not shown significant benefits in terms of mortality, they have been used as adjuvant agents to reduce BP. 68 Sodium nitroprusside may also be used after beta blockade since, as monotherapy, this agent may increase shear stress of the aortic wall resulting in progression of the dissection. 60 To date, there is no known indication for early platelet blockade in AD control. 60 Several studies have shown that the use of statins reduces the growth rate of abdominal aortic aneurysm (AAA) and decreases the likelihood of recurrent rupture after repair. 69 Still, the role of statins in AAS is unclear. 69 Effective pain management with morphine sulfate, fentanyl, or opiate should be implemented. 60 11. Hypertensive Emergencies During Pregnancy Hypertension is the most common medical problem in pregnancy, manifesting in up to 10% of all pregnancies and accounting for about 25% of prenatal hospital admissions; it is also an important cause of maternal and fetal morbidity and mortality. Women with hypertension during pregnancy are at higher risk for future hypertensive disease, stroke, and coronary artery disease. 70,71 The definition of hypertension in pregnancy follows the same criteria of the Brazilian Guideline of Arterial Hypertension, i.e., BP ≥ 140/90 mmHg. Hypertension during pregnancy is considered severe when SBP values are ≥ 160 to 170 mmHg and DBP are ≥ 110 mmHg. 72 Thus, hypertension may precede (in this case, chronic hypertension) or develop during the course of pregnancy (preeclampsia/eclampsia/gestational hypertension), characterizing four different categories of hypertension: 70-72 1. Chronic hypertension begins before pregnancy or is diagnosed before the 20th week of gestation. Only 20 to 25% of the cases of chronic hypertension in pregnancy progress to preeclampsia. 2. Gestational hypertension is the most common disorder (10% of the cases occur in primiparous women; 20 to 25% of the cases overlap chronic hypertension). It develops after the 20 th gestational week and is not accompanied by proteinuria. BP returns to normal values 1 to 2 weeks after delivery. Progresses with a favorable maternal and fetal prognosis. 3. Preeclampsia/eclampsia. Preeclampsia (PE), a process specific of pregnancy, is defined by hypertension that appears after the 20 th gestational week and presents with proteinuria (> 300 mg/24 hours or protein/creatinine ratio > 300 mg/g), edema, and sometimes abnormal coagulation and liver function. Preeclampsia can progress rapidly to eclampsia, a clinical condition characterized by tonic-clonic seizures preceded by severe hypertension, headache, and hyperreflexia. Cerebral hemorrhage is the most serious complication, with a high rate of maternal mortality. Proteinuria and elevated BP should return to normal within 12 weeks after delivery. 4. Chronic hypertension with preeclampsia/overlapping eclampsia. This condition should be suspected in the presence of microalbuminuria (30 to 300 mg in 24-hour urine or 30 to 300 mg/g albumin/creatinine ratio in spot 745