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 3.4. Ischemic Heart Disease Ischemic heart disease (IHD) is not common during pregnancy; most publications consider acute coronary syndrome rather than stable ischemic disease. 223 Data from the WHO have shown that the rate of acute infarction is 3.34 events per 100,000 pregnancies, it being most frequent during the third trimester of gestation. 224 The incidence of infarction without ST-segment elevation is higher during gestation. 52 Risk factors for IHD during gestation are maternal age (over 40 years old; for each year of life, there is a 20% increase in the risk of infarction), family history of premature coronary disease, tobacco use, arterial hypertension, dyslipidemia, and diabetes mellitus. 52 Additional risk factors include preeclampsia, thrombophilia, postpartum infection, cocaine use, multiparity, autoimmune diseases, aortic valve stenosis/aortic valve prosthesis thrombosis, mitral stenosis, and PPH. 52 The etiology of IHD during gestation differs from the general population. In a contemporary review, 225 the mechanisms related to infarction were identified with following incidences: spontaneous coronary artery dissection (43%), atherosclerosis (27%), coronary thrombosis (17%), normal arteries on angiography (9%), vasospasm (2%), and Takotsubo syndrome (2%). Spontaneous coronary artery dissection is the most common cause of AMI during gestation and the postpartum period, with a prevalence of around 1.81 events per 100,000 pregnancies, occurring most frequently during the third trimester. The outcome of dissection associated with pregnancy appears to have a worse prognosis than dissection unrelated to pregnancy. 226 Demographic variables and associated comorbidities include the following: black race, chronic hypertension, gestational hypertension, preeclampsia, lipid abnormalities, chronic depression, migraine, advanced maternal age, first delivery, and infertility treatment. 226 The etiology of coronary dissection has yet to be made clear, but it appears to be related to degradation and weakening of arterial walls, as a consequence of the influence of hormones during gestation. The most common maternal complications described are cardiogenic shock (24%), ventricular fibrillation (VF) (16%), and mechanical support (28%), which result in hospital death in 4% of cases. 226 Atherosclerosis: IHD caused by atherosclerosis is linked to the presence of classic risk factors and to those referred to as emerging risk factors, including gestational hypertensive disease, gestational diabetes, history of premature delivery, autoimmune diseases (lupus erythematosus, rheumatoid arthritis, scleroderma), treatment with thorax radiotherapy/ chemotherapy, and depression/general anxiety. 227 Thrombosis: Coronary thrombosis, in the absence of atherosclerosis, is more probable due to hypercoagulability during pregnancy, and it may result in paradoxical embolization. Normal arteries: Mechanisms of AMI with normal coronary arteries continue to be unclear; they include transitory coronary spasm (increased vascular reactivity and/ or use of ergotamine derivatives) or undetected coronary dissection, reflecting the limitations of the diagnosis. 52 Vasospasm: It may be spontaneous or induced by drugs, hypertensive syndromes during pregnancy, increased vascular reactivity to angiotensin II and norepinephrine, endothelial dysfunction, or renin release by the gravid uterus. Vasospasm may be induced by routine obstetric drugs, such as beta- agonists (terbutaline, salbutamol), inhibition of premature labor, ergot derivatives for labor induction or PPH prevention, and bromocriptine, indicated for inhibiting lactation. 227 Other causes : coronary artery aneurysm related to Kawasaki disease. 52 Diagnosis of AMI is not influenced by the status of pregnancy, and it includes symptoms (dyspnea and chest pain), laboratory examinations (increased troponin), ECG (specific and classic alterations of AMI), and echo (alterations in segmental wall contractility). Differential diagnosis of AMI during pregnancy should be done with pulmonary embolism, amniotic fluid embolism, dissection of the aorta, PPCM, and myocarditis. Additional examinations for diagnosis risk stratification and treatment of AMI include scintigraphy, magnetic resonance, and coronary angiography. Patients with acute coronary syndrome should receive defined diagnosis and treatment before delivery. Therefore, in cases with chest pain or suspected acute ischemic disease, we are in favor of indicating coronary angiography, which, in addition to concluding diagnosis, increases the chance of treating the artery “responsible” for the acute ischemic condition. The risks of angiography are relatively low in relation to the benefits for planning delivery and anesthesia in these patients. Treatment for AMI during pregnancy is similar to that of the general population, including revascularization techniques. In cases of coronary dissection, clinical treatment has been the first choice. Percutaneous or surgical intervention is reserved for cases with left coronary trunk involvement or proximal anterior descending lesion. 226 The most frequent complications are HF and cardiogenic shock (38%), arrhythmias (12%), recurring angina and reinfarction (20%), maternal mortality (7%), and fetal death (7%). 52 Clinical practice for cardiogenic shock and cardiorespiratory arrest follows conventional guidelines, with the strategy of emergency delivery in cases with fetal viability. 52 Pharmacological treatment of AMI is similar to that recommended for the general population. Aspirin is safe in low doses; 92 there is, however, little information regarding P2Y12 inhibitors. 73 Clopidogrel is approved for use, but it should be suspended 7 days before delivery. There is no evidence on the benefits of using this medication for coronary dissection; additionally, glycoprotein IIb/IIIa inhibitors, bivalirudin, prasugrel, and ticagrelor are not recommended. 73 The use of beta-blockers, excluding atenolol, has already been established for acute coronary syndrome. Recombinant tissue plasminogen activator (TPA) does not cross the placenta, but it may induce hemorrhagic complications (subplacental bleeding). 52 Benefits of short-term heparinization probably outweigh the risk of hemorrhagic complications. Patients with previous IHD may receive approval for subsequent pregnancy if there are no residual ischemia 887