The incidence of CAD in women of childbearing age is unclear and varies between countries.Although acute MI (AMI)/acute coronary syndromes (ACS) complicating pregnancy is relatively uncommon (1.7–6.2/100 000 deliveries),CAD accounts for >20% of all maternal cardiac deaths.
Pregnancy is associated with a three- to four-fold increase in AMI risk compared with age-matched non-pregnant women.Risk factors include smoking,maternal age, hypertension, diabetes, obesity, and dyslipidaemia . Additional risk factors include (pre-)eclampsia, thrombophilia, transfusion, post-partum infection, cocaine use, multiparity, and post-partum haemor rhage . As the birth rate in women >40 years increases, ACS complicating pregnancy will become more common, as for every year increase in maternal age there is a 20% increase in MI risk. The aetiology of CAD in pregnancy differs from the general population; the majority of CAD has non-atherosclerotic mechanisms, including pregnancy-related spontaneous coronary artery dissection (P-SCAD) (43%), angiographically normal coronary arteries (18%), and coronary thrombosis(17%).
Pregnancy-related spontaneous coronary artery dissection (P-SCAD)-related AMI occurs most commonly in late pregnancy/ early post-partum, and predominantly involves the left-sided coronaries, frequently with multivessel involvement. Potential pregnancy-related precipitating factors include fluctuating oestrogen/ progesterone levels resulting in structural changes in coronary vasculature, in background of fibromuscular dysplasia or connective tissue disease, and increased coronary shear stresses associated with labour.
The mechanisms of AMI with angiographically normal coronary arteries remains unclear and include transient coronary sp-as-m (increased vascular reactivity and/or use of ergot derivatives), rather reflecting the limitations of this diagnostic technique. Coronary thrombosis in the absence of atherosclerosis is most likely due to the hypercoagulability of pregnancy and can result from paradoxical embolization.
Increasing survival in Kawasaki disease (in the USA it is predicted that by 2030, one in every 1600 adults will have suffered from Kawasaki disease) presents an additional challenge.Relevant Kawasaki disease manifestations include aneurysms, coronary blood flow alteration, coronary stenoses, myocardial ischaemia/fibrosis, congestive cardiac failure, and valvular abnormalities.Coronary thrombosis in the absence of atherosclerosis is most likely due to the hypercoagulability of pregnancy and can result from paradoxical embolization.
The aetiology of pregnancy-associated cardiomyopathy includes acquired and inherited diseases, such PPCM（peripartum cardiomyopathy）, toxic cardiomyopathy, HCM(hypertrophic cardiomyopathy), dilated cardiomyopathy (DCM), Takotsubo cardiomyopathy, and storage diseases.Although rare,they may cause severe complications in pregnancy.HF with preserved EF(Ejection Fraction)an important cause of HF in older patients, does not appear to be a major clinical problem in pregnancy; however,it maybe underdiagnosed.
8.1 PPCM presents with HF secondary to LV systolic dysfunction towards the end of pregnancy and in the months following delivery, with the majority diagnosed post-partum. Careful history taking is necessary to identify and exclude other causes of HF.The LV may be non-dilated, but the EF is usually <45%.Symptoms and signs are often typical for HF with numerous phenotypes reported. Patients frequently present with acute HF, but also with ventricular arrhythmias and/or cardiac arrest. Echocardiography is the imaging modality of choice. Initial LVEF(Left Ventricular Ejection Fraction )<30%, marked LV dilatation(LV end-diastolic diameter> _6.0cm),and RV involvement are associated with adverse outcomes.
DCM encompasses a number of conditions resulting in LV dilatation and dysfunction including prior viral infection, drugs, and ischaemia. Some 50% of cases are idiopathic, of which 20–35% are heredi- tary.Around 40% of the genetic causes of DCM have been identified, with >50 gene mutations described.The prevalence of idiopathic DCM is 1:2500; however,this is likely an underestimate.
Patients may already be known to have DCM, or may present de novo during pregnancy. Distinguishing symptoms and signs of normal pregnancy from HF demands careful attention. Although PPCM and DCM are distinct disease entities, patients may share a genetic predispo- sition ,and differentiation during pregnancy may be impossible.
The true prevalence of HCM in different populations is a topic of debate, but a number of methodologically diverse studies in North America, Europe, Asia, and Africa have reported a prevalence of unexplained increase in LV thickness in the range of 0.02–0.23% in adults.The observed incidence of HCM in pregnancy is <1:1000.
Women with HCM usually tolerate pregnancy well. In a recent meta-analysis, maternal mortality was 0.5%, and complication or worsening of symptoms occurred in 29% of cases. Foetal mortality by spontaneous abortion (15%), therapeutic abortion (5%), or stillbirth (2%) is comparable to the general population; however, the risk of premature birth is increased (26%).Risk is increased where women are symptomatic pre-pregnancy or exhibit a high-risk profile, including diastolic dysfunction, severe LV outflow tract obstruction, and arrhythmia.Medication in the pre-pregnancy period, and a CARPREG or ZAHARA score > _1, are risk factors for pregnancy/ post-partum cardiac events.Symptoms are typical for HF with pulmonary congestion and echocardiography is usually diagnostic。
8.5Recommendations for the management of cardiomyopathies and heart failure
1.Anticoagulation is recommended in patients with intracardiac thrombus detected by imaging or with evidence of systemic embolism.
2.It is recommended to treat women with HF during pregnancy according to current guidelines for non-pregnant patients, respecting contraindications for some drugs in pregnancy.
3.It is recommended to inform women with HFrEF about the risk of deterioration of the condition during gestation and peripartum. 4.Therapeutic anticoagulation with LMWH or vitamin K antagonists according to the stage of pregnancy is recommended for patients with atrial fibrillation.
5.In HFrEF, it is recommended that beta- blockers are continued in women who used them before pregnancy or are installed with caution, if clinically indicated.
6.In patients with PPCM and DCM, counselling for recurrence risk during subsequent pregnancy is recommended in all cases, even after recovery of LV function.