ABC | Volume 114, Nº5, May 2020

Statement Brazilian Cardiology Society Statement for Management of Pregnancy and Family Planning in Women with Heart Disease – 2020 Arq Bras Cardiol. 2020; 114(5):849-942 prolactin 16kDa, with apoptotic and proinflammatory properties. The 16kDa prolactin in endothelial cells suppresses vasodilation depends on nitric oxide (ON) and angiogenesis. In addition, the endothelial cell secretes microparticle exosomes (microRNAs), specifically miRNA (miRNA), which, when absorbed by cardiomyocytes, interferes with their cellular metabolism and, consequently, leads to cellular apoptosis. 205,206 MicroRNA-146a is a highly specific marker for the diagnosis of CMPP 207 Prolactin blockade by bromocriptine or cabergoline, a dopamine-D2 receptor agonist, has shown promising results in therapy and recovery of myocardial function in PPCM. 207-211 The main risk factors for PPCM are hypertensive pregnancy syndromes 212 (gestational hypertension, preeclampsia, eclampsia or HELLP syndrome), chronic hypertension, multiple pregnancies, obesity, smoking, pre-diabetes and diabetes mellitus, advanced age or adolescence and prolonged use of beta agonists. 213 Mortality rates may be lower than 5%, or they may be as high as 50% of cases. The causes of maternal death are HF, ventricular arrhythmia, and thromboembolism, which mainly occur during the first 6 months of the disease until the first postpartum year (late maternal death), which may lead to underreporting of the disease. 214,215 The main clinical manifestations are progressive or sudden dyspnea with acute pulmonary edema or cardiogenic shock. Cardiac arrest, severe arrhythmias or thromboembolic events [stroke, mesenteric ischemia or acute myocardial infarction (AMI)] and cardiogenic shock as the first manifestation of the disease are not uncommon. 216 The diagnosis of PPCM should always be considered when cardiac decompensation occurs in the last months of pregnancy or the months following delivery in previously healthy women. 201 The diagnosis of PPCM is by exclusion and should have differential diagnosis with myocarditis, acute myocardial infarction, pulmonary thromboembolism (PTE), severe preeclampsia, amniotic fluid embolism, pre-existing cardiomyopathies, Takotsubo syndrome, congenital or valvular preexisting disease, and systemic infections. Do not value the symptoms, such as exertion, chest pain, or fatigue, which usually occur in late pregnancy and postpartum, contribute to delay in the diagnosis of PPMC , and consequently, a worse prognosis and less chance of recovery of myocardial systolic function. 201,215,217,222 Complementary examinations include the following: 201 • ECG: in most cases presents nonspecific changes in ventricular repolarization, sinus tachycardia or ventricular arrhythmias. Normal ECG does not exclude the diagnosis of PPCM; • Chest X-ray: The most frequent alterations are cardiomegaly, redistribution of blood flow the pulmonary apices, and “butterfly” pattern; • Biomarkers: Natriuretic peptides (B-type natriuretic peptide [BNP] / or NT-proBNP) are valid markers in HF investigation because, when elevated, they help establish the diagnosis and, when normal, exclude the diagnosis. BNP level is not significantly elevated in pregnancy and postpartum, the significant increase in BNP or NT-proBNP levels in pregnancy can diagnose PPCM; reference values for HF diagnosis are NT-proBNP > 300 pg/ml and BNP > 100 pg/ml; BNP has a good predictive value for persistent left ventricular systolic dysfunction after delivery and is correlated with left ventricle echocardiographic parameters; • Troponins: Troponin may be slightly elevated in PPCM; have predictive value for persistence of ventricular dysfunction 6 months after the onset of the disease; • Transthoracic Doppler echocardiography is the “gold standard” examination for diagnosing PPCM. Left ventricular hypokinesis findings predominate, with LVEF below45% andmay present with regurgitation of the atrioventricular valves and pericardial effusion. LVEF below 30% and final left ventricular diastolic diameter > 60 mm are correlated with worse maternal prognosis; • CMR provides information on the degree of myocardial involvement and should be considered for estimation of prognosis and treatment in the late course of the disease; • Coronary cineangiography and myocardial biopsy are not indicated for diagnosing PPCM. Time to diagnose PPCM is crucial for patient survival. The immediate goals in acute treatment are to stabilize the hemodynamic state, providing symptomatic relief and ensuring maternal and fetal well-being. Emergency physicians should be aware of PPCM in the differential diagnosis of dyspnea in pregnancy-related emergencies and play a role in early diagnosis. Care should be provided by a multidisciplinary team including cardiologists, intensivists, obstetricians, neonatologists, anesthetists and cardiac surgeons. For rapid diagnosis and decision making in all pregnant women with acute heart failure, a pre-specified management algorithm and the establishment of a multidisciplinary team is crucial. 221,222 The pharmacological treatment of PPCM 218,219 follows the guidelines of HF with reduced echocardiographic ejection fraction (EF). Beta-blockers, preferably β 1-selective (carvedilol, bisoprolol, and metoprolol), are initiation with low doses associated with loop diuretics; digoxin may be considered in heart rate control indicated at initially low doses associated with loop diuretics; digoxin may be considered in heart rate control. It is important emphasis that ACEI, ARB, sacubitril/valsartan, ivabradine, spironolactone, and warfarin are contraindicated during gestation, but they may be considered during lactation. Is recommend anticoagulation with heparin to avoid cardio‑embolic complications in patients with LVEF ≤35%with LMWH or oral anticoagulation at least in prophylactic dose. The use of bromocriptine (ergot alkaloid) and cabergoline (dopamine D2 receptor agonist) has shown satisfactory results in the immediate response and late recovery of PPCM ventricular dysfunction. 208-211 The eventual contraindication to the use of these medications should also be weighed. If bromocriptine is not available, cabergoline may be used as an alternative to bromocriptine. As thromboembolic events have been reported during the use of bromocriptine (albeit mostly at higher dosages), bromocriptine treatment should always be accompanied by anticoagulation at least in prophylactic dosages heparin; full doses of heparin (fractional/ unfractionated) is mandatory in the presence of intracardiac 885