ABC | Volume 114, Nº4, April 2020

Statement Luso-Brazilian Position Statement on Hypertensive Emergencies – 2020 Arq Bras Cardiol. 2020; 114(4)736-751 thrombolysis or other reperfusion therapy, BP should be maintained at or below 180/105 mmHg. 40 7.2. Hemorrhagic Stroke Treatment goals in hemorrhagic stroke are controversial. 41-43 Elevation in BP is common during acute intracerebral hemorrhage and is associated with a higher risk of expansion of the hematoma, increased risk of death, and worse recovery prognosis. In this case, immediate (within 6 hours) decrease in BP to values < 140/90 mmHg has shown no benefit in the primary outcome of disability or death at 3 months, despite reducing the expansion of the hematoma and improving functional recovery. 41 In contrast, another study has shown that a more intensive reduction in SBP is not beneficial and is associated with a greater number of adverse renal events. 42 Thus, in individuals with hemorrhagic stroke, European guidelines recommend against immediate BP reduction for patients with SBP < 220 mmHg. 44 In individuals with SBP ≥ 220 mmHg, careful BP reduction with intravenous therapy to achieve SBP < 180 mmHg should be considered 44 . Labetalol, at the aforementioned doses, is the first therapeutic choice, and sodium nitroprusside and nicardipine are the alternative therapies. 1-4,28 8. Acute Coronary Syndromes and Hypertensive Emergency Epidemiological data indicate that acute coronary syndrome (ACS) is the leading cause of death and hospitalization in patients with HE. Additionally, almost 50% of all patients with hypertension admitted to the emergency room die of acute myocardial infarction (AMI) during long-term follow- up. Notably, no differences have been found when other risk factors are present, such as smoking or diabetes mellitus. 11,45 Obviously, hypertension is associated with acute coronary events as a risk, atherogenic, and hemodynamic factor, imposing profound effects on cardiovascular morbidity and mortality. During a HE, increased BP causes mechanical stress and endothelial injury, leading to increased vascular permeability, activation of the coagulation cascade and platelets, fibrin deposition, and thrombosis. This process results in ischemia and release of vasoactive mediators, leading to a vicious cycle of permanent injury. The activation of the renin-angiotensin system leads to increased vasoconstriction and production of proinflammatory cytokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-6, etc.). It also increases NADPH oxidase activity and production of reactive oxygen species, causing oxidative stress. These mechanisms promote hypoperfusion, myocardial ischemia, and endothelial dysfunction, which manifest during the HE. 14,15 Assessment of cardiovascular risk and investigation of comorbidities are essential in the approach to patients presenting with HE and ACS. Electrocardiography is the gold standard for the detection of ischemia or acute coronary events. Also, vital signs (BP, oxygen saturation, and heart rate) should be carefully measured during physical examination in patients with HE. Laboratory analysis includes the quantification of cardiac enzymes and determination of troponin I. In a retrospective study, patients with HC and increased cardiac troponin I (cTn-I) concentration were 2.7 times more likely to present adverse cardiovascular events and stroke at 2 years of follow-up compared with those with normal cTn-I values. 46 Treatment of HE associated with ACS should initiate with nitroglycerin infusion. Nitroglycerin is a venodilator that reduces preload and cardiac oxygen demand. This agent is used mainly in ACS and acute edema along with other antihypertensive regimens. 47-49 An alternative to nitroglycerin intolerance is the administration of dihydropyridine calcium- channel blockers (amlodipine, nicardipine), as they are useful for patients with ACS because of their beneficial effect on coronary blood flow. Alternatively, clevidipine – a short-acting calcium-channel blocker – may be administered intravenously, and since its dosing regimen is not based on weight, it allows for prolonged infusion and successful transition to oral therapy. 50 If available, especially in ST-segment elevation ACS, primary angioplasty is the best choice for reperfusion therapy in patients with HE, as thrombolysis may increase the risk of cerebral bleeding. 47-49,51 Beta-blockers like labetalol (a nonselective alpha-1- adrenergic receptor blocker), which reduces systemic vascular resistance while maintaining cerebral, renal, and coronary blood flow, or esmolol (a short-acting cardioselective beta-1 blocker with fast onset of action) are indicated to attenuate the increase in heart rate, reduce myocardial oxygen consumption without compromising the left ventricular diastolic filling, and improve prognosis. 28 Additionally, BP reduction decreases the risk of pulmonary edema and the size of the infarct zone. 52 Tolerance to higher maintenance doses of esmolol is a good predictor of results with oral beta-blocker therapy. 53 The optimal BP value after ACS remains controversial. Several studies have shown an inverse relationship between DBP and ischemic adverse cardiac events ( i.e. , the lower the DBP, the higher the risk of coronary heart disease and adverse outcomes). This effect is defined as the J-curve phenomenon, which describes the shape of the relationship between BP and the risk of cardiovascular morbidity and mortality. 54 This profile seems to be more pronounced in patients with underlying coronary artery disease. 55 9. Acute Left Ventricular Dysfunction in Hypertensive Emergency Acute left ventricular dysfunction is best known as APE. HE, acute mitral regurgitation (papillary muscle dysfunction secondary to ischemic disease or spontaneous rupture), and ACS are the most common causal factors of cardiogenic APE. 56,57 About 1/3 of the patients admitted with APE and HE have preserved left ventricular function. Patients with HE presenting manifestations of APE should be managed in an intensive care unit, receive parenteral medications and monitoring, and undergo gradual BP decrease. 58 Nitroglycerin and sodium nitroprusside are used to reduce preload and afterload. Administration of loop diuretics also decreases volume overload and helps reduce BP. The use of noninvasive continuous positive airway pressure may help reduce pulmonary edema and venous return. 28,59 744