11

Valve Disease in Pregnancy

Tanush Gupta, Thomas Boucher, and Anna E. Bortnick

Introduction

Cardiovascular disease complicates ∼1%−3% of all pregnancies and is a leading cause of maternal mortality [1–3]. With advances in cardiovascular medical and surgical care over the last few decades, more women with congenital or acquired heart disease are reaching reproductive age [4,5], with a wide spectrum of congenital and acquired valvular heart disease (VHD) seen in pregnant women (Figure 11.1) [6]. Although VHD due to rheumatic heart disease (RHD) has declined in industrialized countries, it continues to be a major cause of global maternal cardiovascular morbidity and mortality [4,6–10]. Despite the improvements in diagnosis and management, VHD remains associated with adverse maternal and fetal events [11,12]. Many patients with significant VHD are not aware of their diagnosis until pregnancy, when hemodynamic stress precipitates symptoms [12].

Hemodynamic Effects of Valvular Heart Disease in Pregnancy

Hemodynamic changes of pregnancy can lead to clinical decompensation of women with VHD due to increases in cardiac output (CO), intravascular volume expansion, and a drop in systemic vascular resistance (SVR) [2,13,14]. Early in pregnancy, there is a 30%–50% increase in CO largely attributable to rises in circulating blood volume and heart rate [14,15]. During the later stages of pregnancy, increases in heart rate contribute more to increased CO. Pregnancy is also accompanied by physiologic anemia with a greater increase in plasma volume than red blood cell volume, resulting in increased flow and increased gradients across preexisting valvular lesions [16]. In addition, SVR decreases toward the end of the second trimester as placental circulation matures and then slowly rises until term [17]. The gravid uterus may compress the inferior vena cava in the second trimester, decreasing preload to the heart, and increasing afterload by compressing the abdominal aorta. These changes, in turn, modulate CO so that it plateaus between the second and third trimesters [2,12,18].

Clinical Implications: Pregnancy leads to a series of hemostatic changes leading to hypercoagulability and risk of thromboembolism, which is of particular concern in patients with known VHD or prosthetic heart valves (PHVs). Uterine obstruction to vena cava flow may also predispose to increased risk of deep venous thrombosis [19]. Importantly, the pharmacokinetics of cardiac drugs may be altered during pregnancy, necessitating more frequent monitoring and/or dose adjustment in women [20].

During labor and delivery (L&D), maternal hemodynamics are influenced by an array of factors including pain, anxiety, mode of delivery, analgesia, blood loss, and uterine contractions [21]. Abrupt changes can have a significant effect on pregnant women with VHD. CO increases by ∼30% in the first stage of labor and by ∼80% early postpartum [22]. There are catecholamine-induced increases in stroke volume and heart rate, which in turn increase CO. Each uterine contraction is accompanied by autotransfusion of up to 500 mL of blood from the placental to systemic circulation [23,24]. Systemic blood pressure can increase by ∼15–20 mmHg with each contraction. The use of epidural and spinal analgesia can attenuate some of these hemodynamic alterations associated with L&D [25]. Manipulating the intensity and duration of anesthesia for optimal vasodilation, decreasing anxiety/stress to reduce maternal heart rate and afterload, controlled permissive blood loss, and postpartum diuresis are ways to counteract the effects of hemodynamic changes on VHD at the time of L&D.

Cardiac hemodynamics change rapidly in the early postpartum period. Delivery is accompanied by loss of intravascular volume, which can be up to 500 mL with vaginal delivery and up to 1000 mL with cesarean delivery [24]. The relief of caval obstruction by the gravid uterus results in redistribution of blood from the lower limbs and an increase in preload and circulating volume [21]. Also, there is an overall increase in afterload due to loss of the low-resistance placental circulation and mobilization of interstitial fluid. Hemodynamic changes peak within 24–72 hours after delivery, a vulnerable period when women with VHD are most likely to manifest symptomatic heart failure (HF) [10,12].

Stenotic versus Regurgitant Valvular Heart Disease in Pregnancy

In general, stenotic valvular lesions pose a higher risk of maternal and fetal adverse events than regurgitant lesions [26]. With stenotic lesions, the increase in CO associated with pregnancy and labor results in increased transvalvular flows and gradients. Increases in heart rate are poorly tolerated in pregnant women with stenotic valvular lesions such as mitral stenosis (MS), where left ventricular filling is heavily dependent on the duration of the diastolic filling period. The combined effect of increased transvalvular flow and shortened diastolic filling time can result in symptomatic HF, pulmonary edema, and arrhythmias such as atrial fibrillation [27].

Transthoracic echocardiography (TTE) is essential for diagnosis and evaluation of stenotic VHD [28–31]. Tachycardia and increased CO in pregnancy increase transvalvular gradients on TTE but do not affect the calculated valve area by the continuity equation. Direct planimetry is a flow-independent measure of valve area and is likely more accurate than flow-dependent measures such as pressure half time. Despite this, the mean gradient across a valve is likely the best reflection of the hemodynamic significance of valvular stenosis at that particular point in time [27,32].

Left-sided chronic regurgitant lesions (mitral regurgitation [MR] and aortic regurgitation [AR]) are typically well tolerated during pregnancy, as the low-resistance placental circulation decreases SVR, and in turn decreases regurgitant volume [32,33]. However, severe regurgitant lesions in the context of impaired left or right ventricular systolic function or acute valvular regurgitation can result in HF [10]. Table 11.1 provides details on the commonly encountered valvular lesions in pregnant women, their etiology, risk to mother and fetus, management, and preferred mode of delivery.

In general, evaluation of VHD should be performed prior to pregnancy and significant symptomatic VHD should be corrected beforehand, particularly if surgery is required, as bypass increases maternal and fetal risk [34,35]. Treating VHD in the setting of symptomatic HF, arrhythmias, or hemodynamic deterioration is necessary to prevent maternal and fetal adverse events (Table 11.2) [12].

MS is the most common acquired VHD in pregnant women [2,36]. MS is considered clinically important if the valve area is ≤1.5 cm2 (Table 11.3) [18]. The gold standard method of estimating MS severity on TTE is direct planimetry; however, this method can be technically challenging and is dependent on optimal image quality. Doppler-derived pressure half time depends on heart rate, with lower gradients observed at slower heart rates. Estimations of transvalvular mean gradients and pulmonary artery pressures on Doppler echocardiography are informative regarding the hemodynamic effects of MS. The assessment of mitral valve anatomy, specifically, leaflet calcification, thickening, subvalvular apparatus, and concomitant MR, elements captured by the Wilkins score, is important prior to consideration for percutaneous mitral commissurotomy (valvuloplasty) [28,37,38]. For asymptomatic women prior to pregnancy, exercise TTE may be useful in assessing exertional tolerance, changes in Doppler-derived gradients, and prognosis [18]. During pregnancy, clinical and echocardiographic follow-up is recommended monthly or bimonthly with moderate or severe MS [18].

Mild MS is usually well tolerated during pregnancy [32]. HF occurs in up to 1/3 of pregnant women with moderate MS and up to 1/2 with severe MS, even in previously asymptomatic patients, and most often during the second or third trimesters [39]. Sustained AF occurs in up to 10% of pregnant women with moderate/severe MS and can predispose to symptomatic HF and thromboembolism [40]. Maternal mortality from MS is reported to vary from 0%–3% in the West but may be higher in other parts of the world [8,32,39–41]. Fetal morbidity includes intrauterine growth restriction and premature birth, and is directly proportional to the severity of MS, ranging from ∼14% in mild MS to ∼35% in severe MS. Fetal death has been reported in 1%–5% with significant MS [32,39,40].

Management:

1.Exertion should be restricted in patients with symptomatic MS [2].

2.Beta-1 selective blockers are first-line drugs in management of MS during pregnancy.

3.Diuretics are often used to avoid volume overload.

4.Digoxin may be utilized in those with HF and concomitant AF not rate-controlled with beta-blockers.

5.Anticoagulation is recommended for paroxysmal or permanent AF, left atrial thrombus, or history of prior thromboembolism [2,18].

Women with moderate or severe MS should be counseled against pregnancy until the lesion is treated, and intervention should be performed prior to pregnancy, with preference given to percutaneous valvuloplasty if the valve is anatomically favorable for the procedure, and termination may be recommended if currently pregnant [32,37]. During pregnancy, percutaneous mitral valvuloplasty should be considered in women with New York Heart Association (NYHA) class III/IV HF or with estimated pulmonary artery systolic pressures of ≥50 mmHg and preferably delayed until after the 20th week of gestation [18,37]. Surgical mitral valve replacement should be considered only in pregnant women with medically refractory symptoms when percutaneous valvuloplasty fails or is not an option, as open heart surgery is highly morbid for both mother and fetus [42].

Vaginal delivery is often preferred in patients with mild MS and in those with moderate or severe MS in the presence of NYHA class I/II symptoms without significant pulmonary hypertension (PH). Cesarean section is often considered for women with NYHA class III/IV symptoms, severe PH, or in whom percutaneous mitral valvuloplasty has failed or is not possible [18].

Aortic Stenosis

The leading causes of aortic stenosis (AS) in pregnant women are bicuspid aortic valve disease, often associated with dilation of the ascending aorta, followed by RHD [43]. Most with mild or moderate AS can tolerate pregnancy (Table 11.4) [44]. HF is infrequent, with an estimated prevalence of <10% in women with moderate AS who were asymptomatic pre-pregnancy. Even in patients with severe AS, maternal mortality is reported to be <1% in presence of close follow-up and treatment [32,33,45,46]. Maternal and fetal adverse events are directly proportional to the severity of AS. Approximately one-third of women with severe AS require hospitalization during pregnancy. Fetal adverse events including growth restriction, low birth weight, and preterm birth have been reported in 20%–25% of babies of mothers with moderate or severe AS [44,46]. TTE is the gold standard for grading severity of AS (Table 11.4) [28,37,38]. Exercise TTE testing can be considered for women with asymptomatic, severe AS prior to pregnancy. Favorable maternal and fetal outcomes were reported for those who remained asymptomatic on exercise testing even in the presence of severe AS. However, surgery should be considered pre-pregnancy for exercise-induced symptoms (like shortness of breath, chest pain, dizziness), drop in blood pressure, or left ventricular dysfunction [18]. In bicuspid aortic valve disease, ascending aortic diameters should be assessed before, during, and after pregnancy to rule out worsened dilation. In pregnant women with severe AS, monthly or bimonthly clinical and echocardiographic follow-up is recommended [18].

Stay updated, free articles. Join our Telegram channel

Join