During pregnancy, the maternal circulatory system undergoes significant changes characterized by increased total blood volume, elevated cardiac output, higher heart rate, and reduced systemic vascular resistance. These hemodynamic alterations can exacerbate diastolic dysfunction in patients with valvular heart disease. The coexistence of pregnancy and cardiovascular disease represents a major contributor to maternal morbidity and mortality, ranking as the second leading cause of maternal death in China and the most common non-direct obstetric cause of death. Cardiovascular diseases complicate 1%−3% of pregnancies and account for 10%−15% of maternal deaths (12). In recent years, with the advancement of medical technology, an increasing number of reproductive-aged women with congenital or acquired heart disease are achieving pregnancy viability. This demographic shift presents substantial clinical management challenges (3).

In developing countries, rheumatic heart disease tends to occur at a younger age compared to developed regions. The European Registry of Pregnancy and Heart Disease reported that mitral stenosis and/or regurgitation is the most common site of valvular lesion (63%), followed by the aortic valve involvement (23%). Maternal mortality rates are substantially higher in pregnancies complicated by valvular heart disease vs. congenital cardiac conditions (13). A clinical study from Africa documented 50% mortality among women with severe symptomatic mitral stenosis during pregnancy, predominantly occurring in the postpartum period (14).

Patients with valvular heart disease must undergo a comprehensive evaluation before pregnancy. Those with severe valvular heart disease may undergo replacement surgery with a prosthetic mechanical valve. Prosthetic valve thrombosis is a rare complication in non-pregnant patients, with an incidence rate of approximately 0.1%–5.7% (15). In pregnancy, the risk of thrombosis increases due to the hypercoagulable state, raising the risk to about 10% (15). Compared to open-heart surgery, low-dose thrombolytic therapy guided by transesophageal echocardiography has a definite therapeutic effect on pregnant women with mechanical mitral valve thrombosis (16). It results in fewer maternal and infant complications, and there have been no reported cases of maternal mortality (17). The neonatal mortality rate is 20% (18). Once valve replacement is accepted, anticoagulation therapy is crucial. When formulating an anticoagulation treatment plan, it is necessary to consider comprehensively factors such as the type and location of the valve, history of thromboembolism, presence of atrial fibrillation, and the patient's compliance.

Warfarin remains the most effective anticoagulant for mechanical heart valves in non-pregnant patients. However, during pregnancy, its transplacental passage poses significant fetal risks. In the first trimester, warfarin exposure has been associated with dose-dependent embryotoxic effects, including skeletal malformations (e.g., nasal hypoplasia, facial anomalies) and severe central nervous system defects (e.g., intraventricular hemorrhage, cerebral edema) (19, 20). In the late stages of pregnancy, warfarin use may result in neonatal intracranial hemorrhage, including subarachnoid hemorrhage and periventricular necrosis (21–23). A 2023 meta-analysis quantified this dose-response relationship: live birth rates were 83.6% for daily warfarin doses ≤5 mg vs. 43.9% for >5 mg, while congenital malformation rates increased from 2.3%–12.4% (24). Notably, these observational data face inherent limitations: warfarin is predominantly used in high-risk pregnancies (e.g., mechanical valve recipients), where underlying maternal pathology itself contributes to adverse outcomes. Interspecies differences in warfarin teratogenicity and ethical considerations regarding maternal-fetal safety have also limited the availability of high-quality evidence on its use during pregnancy, leaving warfarin's safety profile inadequately characterized despite clinical urgency. In contrast, LMWH demonstrates superior fetal safety, with a 92% live birth rate in pregnancies managed exclusively with LMWH (24). Nevertheless, its variable thromboprophylactic efficacy perpetuate clinical equipoise. This therapeutic dilemma underscores a critical gap: no anticoagulant optimally balances maternal and fetal safety throughout all gestational stages.

The 2014 American College of Cardiology and American Heart Association (ACC/AHA) guidelines (4) and the 2018 European Society of Cardiology (ESC) guidelines (21) recommend that patients with mechanical valve replacement continue low-dose warfarin anticoagulation (≤5 mg/day) during early pregnancy. When the daily dose exceeds 5 mg, transitioning to LMWH or unfractionated heparin (UFH) is advised, with dose adjustments guided by anti-Xa level monitoring. Notably, the ESC guidelines demonstrate a critical divergence: given to the increased risk of thrombosis during pregnancy, they do not recommend LMWH use at any gestational stage and consider warfarin to be the safest option, particularly when the daily dose remain below5 mg (25, 26). In summary, regardless of the anticoagulant chosen in early pregnancy, warfarin therapy is generally recommended during mid to late pregnancy. It is advised to discontinue warfarin and switch to LMWH or UFH prior to a planned vaginal delivery. In cases requiring urgent delivery during late pregnancy (e.g., acute valve dysfunction or hemodynamic instability), cesarean section is recommended when inadequate time exists for safe anticoagulant transition from warfarin to LMWH or UFH, thereby minimizing peripartum hemorrhagic risks associated with traumatic delivery (27). A meta-analysis published in 2023, which included 15 studies with 722 pregnancy events (87.2% mechanical valves, 12.5% biological valves), reported a maternal mortality rate of 1.33% and an overall bleeding risk of 6.9%. The risks of thromboembolism and miscarriage after mechanical valve replacement during pregnancy were 4.71% and 29.29%, respectively. Additionally, a warfarin dose >5 mg/day was associated with an increased incidence of adverse fetal events (28).

During pregnancy, the occurrence of mechanical valve dysfunction, regardless of the cause, poses a serious threat to both maternal and fetal safety. When maternal mechanical valve dysfunction is combined with heart failure, the pathophysiological mechanisms leading to impaired uterine-placental blood flow are multifaceted, directly threatening fetal oxygen supply and nutrient exchange. Firstly, mechanical valve dysfunction (such as thrombosis or valve leaflet dysfunction) leads to increased right ventricular afterload, reduced right heart output, and systemic venous congestion, significantly decreasing maternal cardiac output. During late pregnancy, maternal cardiac output needs to increase by 30%–50% compared to the non-pregnant state to maintain high placental perfusion (29). However, in right heart failure patients, this demand cannot be met, resulting in reduced uterine artery blood flow, which is reflected in increased pulsatility index (PI) and resistance index (RI) (30). Studies have shown that for every 0.1 increase in uterine artery PI, fetal birth weight decreases by approximately 200 g on average (31), which aligns with the phenomenon observed in this case, where the preterm infant (1880g) is below the average birth weight of a full-term infant despite being appropriate for gestational age.

The indirect effects of right heart failure further exacerbate placental underperfusion. Elevated central venous pressure impedes uterine venous return, increasing placental interstitial pressure and reducing maternal-fetal exchange efficiency. Meanwhile, sympathetic nervous activation and overactivation of the renin-angiotensin-aldosterone system (RAAS) counteract the vasodilatory effects of pregnancy hormones (such as estrogen), thereby aggravating uterine artery vasoconstriction. Furthermore, the additive effect of pulmonary arterial hypertension (PAH) limits blood volume redistribution, prioritizing perfusion to vital organs like the brain and kidneys. In contrast, placental perfusion is sacrificed, potentially leading to fetal hypoxic vascular remodeling (32). While this compensatory mechanism may maintain fetal survival in the short term, it may increase the risk of cardiovascular diseases during childhood in the long term (33, 34).

Coagulation abnormalities play a dual role in this process. On the one hand, anticoagulant imbalance (such as coagulopathy due to hepatic congestion) increases the risk of microthrombi in the placenta (35). On the other hand, the choice between warfarin or LMWH directly affects fetal safety (36). In this case, the use of low-dose warfarin (target INR 2.5–3.0) during early pregnancy may have minimized embryotoxicity, with reported teratogenic rates of 2.3% for low doses compared to 12.4% for higher doses. Transitioning to LMWH in late pregnancy helped reduce the risk of fetal intracranial hemorrhage. This case highlights the critical role of pharmacological interventions as key environmental factors influencing fetal outcomes.

While prolonging gestational age can improve neonatal short- and long-term outcomes and quality of life, patient conditions must be thoroughly evaluated, and gestational age extension should be carefully timed under multidisciplinary management. The management of pregnancy complicated by maternal mechanical valve dysfunction demands a nuanced approach to safeguard fetal health, as exemplified by this case; central to fetal protection is the optimization of maternal hemodynamics and placental perfusion, emphasizing the need for vigilant monitoring of uterine and umbilical artery Doppler parameters to detect placental insufficiency early.

Anticoagulation strategy is pivotal in balancing maternal thrombotic risks and fetal safety. Transitioning from warfarin (INR 2.5–3.0) to LMWH at appropriate gestational weeks mitigated fetal intracranial hemorrhage risk while addressing maternal hypercoagulability. Currently, there is a lack of specialized guidelines and large-scale clinical studies to inform decision-making, necessitating comprehensive evaluations to integrate NYHA class and PAH severity based on the patient's medical history, physical examination, and relevant diagnostic tests.

For patients with poor cardiac function and high suspicion of mechanical valve dysfunction, an active strategy of concurrent cesarean section and cardiac surgery should be pursued to ensure maternal and fetal safety, provided the institution is equipped for cardiopulmonary bypass. Multidisciplinary collaboration remains the cornerstone of care. Intraoperative echocardiography and postpartum valve replacement exemplified coordinated cardiac-obstetric interventions and anesthesiology to reduce maternal and neonatal mortality and optimize perinatal outcomes.