Introduction
Prosthetic heart valves have been used since the 1950s for the replacement of both congenital and acquired valvular heart disease; more than 60,000 valve replacement procedures are performed in the United States annually [1]. There are two primary types of prosthetic valves: mechanical heart valves (MHV) and bioprosthetic heart valves (BPV). The former is primarily composed of metal or carbon alloys, the latter is derived from bovine or porcine tissue mounted on a metal support or preserved human valves [1].
The major differences between MHV and BPV are durability and thrombogenicity. Mechanical heart valves are highly durable, lasting 20–30 years whereas up to 30% of BPV will fail in 10–15 years [1]. MHV are more thrombogenic and require ongoing anticoagulation throughout the lifespan of the valve; with adequate anticoagulation, the risk of valve thrombosis with MHV is decreased from 12–22% per patient-year to 0.1–5.7% per patient-year [1,2]. The thrombogenicity of MHV is dependent on valve type: the newer generation bileaflet-tilting disks are less thrombogenic than the older generation single-tilting or caged-ball types [1]. Thrombogenicity is also influenced by valve position (mitral greater than aortic), adequacy of anticoagulation therapy and number of prosthetic heart valves [2].
In comparison to MHV, the risk of valve thrombosis is low with BPV and anticoagulation is not usually required after the initial 3 months following valve replacement, at which point aspirin is recommended [1,2].
Regardless of valve type, patients with prosthetic heart valves (MHV or BPV) may have an increased risk of thromboembolic complications (TEC). If atrial fibrillation, left ventricular dysfunction and previous history of TEC are present in these patients, ongoing antithrombotic agents should independently be considered [2].
Based on the durability of MHV and the fact that anticoagulation therapy may be less well tolerated in the older patients, younger patients (<40 years), such as women of childbearing age, tend to be implanted with MHV, while BPV are used in older individuals [1].
Anticoagulation therapy for patients with MHV in the nonpregnant population
Vitamin K antagonists (VKA), like warfarin, are the mainstay anticoagulant for thromboprophylaxis in patients with MHV [1,2]. For most newer generation MHV (i.e. excluding the caged-ball valves) in the aortic position, a target international normalized ratio (INR) of 2.0–3.0 is recommended while for valves in the mitral position, an INR of 2.5–3.5 is recommended [2]. In patients with concurrent risk factors (such as atrial fibrillation, low ejection fraction, previous TEC, myocardial infarction, left atrial enlargement or endocardial damage), an INR target of 2.5–3.5 and addition of low-dose aspirin (75–100 mg/day) should be considered [2].
For bridging anticoagulation, i.e. in situations where therapeutic anticoagulation with VKA has not yet been achieved or during short periods in which interruption of VKA therapy is required (such as invasive procedures), both intravenous unfractionated heparin (UFH) or full-dose low molecular weight heparin (LMWH) have been used successfully, with minimal risks of TEC during the period of VKA interruption [3,4]. However, the risk of major bleeding in the postprocedure phase is significant with full-dose LMWH or IV heparin and major bleeding can result in interruption of anticoagulation with subsequent TEC. In a multicenter cohort study of 224 patients treated with full-dose LMWH, the postoperative TEC rate was 3.1% and 75% of these occurred in patients who had anticoagulation held due to bleeding [4].
Bacterial endocarditis prophylaxis
Patients with prosthetic heart valves have an increased lifetime risk of developing infective endocarditis (IE) (400 per 100,000 patient-years); antibiotic prophylaxis is recommended for MHV patients who undergo:
- dental procedures involving the manipulation of gingival tissue, periapical region of teeth or perforation of the oral mucosa
- procedures on the respiratory tract
- procedures on infected skin, skin structures or musculoskeletal tissue [5].
Antibiotic prophylaxis is no longer recommended in BPV patients undergoing these procedures unless they have had previous IE, congenital heart disease or cardiac transplant [5].
In previous guidelines, antibiotic prophylaxis could be considered in patients with BPV or MHV undergoing vaginal delivery or cesarean section; however, more recent guidelines do not advocate the use of antibiotic prophylaxis solely for the purpose of preventing bacterial endocarditis for these procedures [5,6] (see also Chapter 5).
Management of valve thrombosis
Valve thrombosis is an infrequent but potentially life-threatening complication in patients with MHV. The presentation of valve thrombosis may be sudden death, acute pulmonary edema, embolic accidents, onset of shortness of breath or heart failure. Currently the best diagnostic studies for the detection of MHV thrombosis are transesophageal echocardiogram or fluoroscopy [6,7]. If valve thrombosis is suspected, a consultation with a cardiologist and/or cardiovascular thoracic surgeon is recommended. Depending on the degree of valve thrombosis, right- or left-sided valve thrombosis and patient factors (e.g. NYHA class symptoms, reviewed in Chapter 5), valve thrombus could be managed medically with intravenous heparin therapy (small clot burden and minimal symptoms) or thrombolysis (right-sided lesions with NYHA class III or IV symptoms or large clot burden), or surgically with valve replacement (left-sided lesions with NYHA class III or IV symptoms or large clot burden) [6].
There is little in the literature to guide the management of valve thrombosis during pregnancy. Case studies of the use of both thrombolytic therapy and surgery in pregnant women with MHV thrombosis have been reported [8,9] but with some complications [10]. In these latter situations, the risks and benefits of these procedures must be weighed carefully against the risk of maternal morbidity and mortality associated with valve thrombosis.
Pregnant women with prosthetic heart valves
Bioprosthetic heart valves
Young patients (16–40 years) implanted with BPV undergo structural valve deterioration in 50% at 10 years, and 90% at 15 years [6,11].
Pregnant women with BPV avoid the need for anticoagulation and the problems associated with the need for VKA therapy (see below), so the pregnancy outcomes, from the fetal point of view, in these patients are mostly favorable [5]. However, in these patients, the risk of structural valve deterioration during pregnancy and shortly after (within 1 year) is high, at about 28% [5]. This rate of valve deterioration is, however, similar to other age-matched patients who do not undertake pregnancy [12–14]. For patients with BPV who require valve reoperation, the mortality rate, although decreasing over the past 20 years, is still significant at 3.5–11.1% [15].
The presentation of valve deterioration in patients with BPV is often the gradual onset of dyspnea and symptoms of heart failure. These symptoms often mimic the normal symptoms associated with physiologic changes with pregnancy [1] so careful auscultation and regular functional assessment with echocardiography may be required.
Mechanical heart valves
Anticoagulation therapy
The major challenge with managing women with MHV during pregnancy is that VKA, which are highly effective in preventing valve thrombosis and TEC in the nonpregnant MHV population [6], are associated with adverse effects on the pregnancy and developing fetus [16]. The use of either UFH or LMWH, which are both “safe” for the developing fetus, is associated with an apparent higher risk of valve thrombosis than VKA and even maternal death [16]. In addition, there are no large clinical trials comparing anticoagulation therapies in pregnant women with MHV to dictate appropriate choice; recommendations are largely based on cohort studies, case series and expert opinion. In this section, an overview of the reported pregnancy experiences in women with MHV with the respective anticoagulant therapy will be presented, as well as the fetal and maternal risks associated with each regimen.
Vitamin K antagonists
Coumarin derivatives (or VKA such as warfarin) depresses synthesis of vitamin K-dependent clotting factors (factors II, VII, IX, and X) by blocking reduction of the epoxide form of vitamin K. Because of their low molecular weight, coumarins cross the placenta, achieving clinically significant levels in the fetus [17]. Fetal exposure to coumarin derivatives leads to congenital anomalies, presumably through inhibition of vitamin K-dependent proteins in bone and brain. A specific pattern of congenital anomalies known as coumarin embryopathy is recognized in children exposed in utero to coumarin derivatives between 6 and 12 weeks of pregnancy [18]. These anomalies consist of nasal hypoplasia (depressed nasal bridge and underdeveloped or absent nasal septum) and chondrodysplasia punctata (radiographic epiphyseal and vertebral stippling). This stippling resolves after the growth plates calcify but it may lead to limb and digit hypoplasia [18]. Beyond the first trimester of pregnancy, coumarin exposure, likely through fetal anticoagulation, has also been associated with central nervous system abnormalities such as intraventricular hemorrhages, microcephaly, hydrocephalus, cerebellar and cerebral atrophy, eye and vision abnormalities (optic atrophy, cataracts, blindness, microphthalmia) seizures, and growth and mental retardation [17,18].
Beyond these CNS side effects diagnosed at birth, recent prospective studies evaluating neurodevelopmental outcomes in children exposed to coumarin in utero
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