Hemodynamic Changes of Pregnancy

Pregnancy is associated with major cardiovascular adaptations that are needed to support maternal and fetal demands [11]. Plasma volume and cardiac output progressively increase, nearly doubling, whereas systemic vascular resistance falls [1, 12]. The rise in cardiac output is driven mainly by increased stroke volume early in pregnancy and increased heart rate, with the greatest hemodynamic stress occurring during the peak stress of pregnancy ~ 28–32 weeks, followed by labor and delivery [1, 13]. Within 24–72 h postpartum, there is a increased fluid shift that also puts a significant demand on the cardiovascular system and requires more diligent monitoring in high risk patients [14]. These cardiovascular adaptations have important implications for women with VHD, and their effects depend on lesion type and severity. Women with limited cardiac reserve, particularly those with left-sided stenotic lesions, may not tolerate the increased volume and flow of pregnancy, and therefore require close monitoring [5, 9].

Pregnancy also creates a hypercoagulable state, which is particularly relevant in women with mechanical prosthetic valves because of the increased risk of valve thrombosis. Later in gestation, compression of the inferior vena cava (IVC) by the enlarging uterus may further impair venous return and potentially worsen thrombosis risk and valve gradients [11, 15].

Labor, delivery, and the early postpartum period are especially vulnerable times because of abrupt shifts in preload, afterload, heart rate, and oxygen demand [9, 13]. Uterine contractions transfer blood into the systemic circulation, and after delivery, relief of the IVC compression together with mobilization of extravascular fluid produces a sudden increase in preload [9, 13].These rapid changes may precipitate decompensation, so women with high-risk lesions require additional monitoring during labor and in the first few days postpartum [9]. Large delivery datasets reflect this physiology: in the United States National Inpatient Sample analysis (2016–2018), women with VHD had markedly higher adjusted odds of pulmonary edema, arrhythmias, acute ischemic heart disease, peripartum cardiomyopathy and obstetric complications than women without VHD, highlighting labor and delivery as important periods of risk amplification [16].

Risk Scores and Guideline-based Classification

Risk stratification in women with VHD begins before conception and continue throughout pregnancy [8]. The modified World Health Organization classification remains the principal guideline-based framework, linking lesion type and severity to expected maternal risk and to the level of specialist care required. In the 2025 European Society of Cardiology (ESC) guidelines for the management of cardiovascular disease and pregnancy, the revised mWHO 2.0 model is recommended as the primary organizing tool, and women in mWHO 2.0 class II–III or higher should be managed with Pregnancy Heart Team involvement. Within VHD, severe mitral stenosis and severe symptomatic aortic stenosis are classified as mWHO 2.0 class IV, reflecting extremely high maternal risk, whereas moderate mitral stenosis, uncomplicated mechanical valves with stable INR control, severe asymptomatic aortic stenosis, and severe left-sided regurgitation fall into lower but still clinically important higher-risk categories. mWHO Risk IV is the highest maternal risk and recommendations against pregnancy and even pregnancy termination are recommended from a medical standpoint if the lesion cannot be treated [8, 17].

Adjunctive risk models may further refine individualized risk estimates. CARPREG II is a more broadly applicable, integrates clnical status, lesion type, management factors across both acquired and congenital heart disease; could even specify some of the factors like ventricular dysfunction, NYHA class or cyanosis, PHTN, aortopathy, anticoagulation use [18]. In contrast, ZAHARA was derived more specifically from congenital heart disease populations and uses weighted lesion-specific variables, making it most useful in selected women with congenital lesions [7]. Emerging valve-specific models such as DEVI may offer additional value in rheumatic or valve-predominant populations, although they are not yet widely used in routine clinical practice [19, 20]. In summary, while mWHO 2.0 is best used as the primary framework for counselling and care planning, CARPREG II, ZAHARA, and emerging valve-specific models may be used as adjuncts to refine individualized risk estimates [8, 19]. A quick-reference summary of mWHO 2.0 lesion categories and the CARPREG II modifiers most relevant to VHD is provided in Table 1.

Table 1 Summary of pregnancy risk stratification in valvular heart diseaseLesion-Specific Management in Pregnancy

Key lesion-specific maternal risks, management principles, and delivery considerations are summarized in Table 2.

Table 2 Lesion-specific maternal risks, management principles, and delivery considerations in native valvular heart diseaseLeft-Sided Stenotic Lesions (Mitral, Aortic)

Left-sided stenotic lesions are among the highest-risk native valve lesions in pregnancy due to the physiological increases in plasma volume, heart rate, and cardiac output which can markedly increase transvalvular flow and filling pressures. As a result, women with MS or AS may decompensate with heart failure, arrhythmia, pulmonary hypertension, or reduced exercise tolerance as pregnancy progresses [8, 9, 11, 21]. These hemodynamic changes also increase Doppler-derived gradients, so imaging findings must be interpreted in the context of pregnancy physiology [21, 22].

In women of childbearing age, AS is most often related to congenital bicuspid aortic valve disease, frequently with associated aortopathy. Mild or moderate obstruction is often tolerated, but severe symptomatic AS remains high risk, particularly when ventricular dysfunction or associated aortopathy are present [5, 21]. In the multinational ROPAC analysis of pregnancies complicated by at least moderate AS, maternal death was not observed, but cardiac hospitalization occurred in 20.8%, and women with severe or symptomatic disease had substantially greater morbidity [23]. Medical therapy has a limited role; activity restriction and cautious diuresis may help selected symptomatic patients, whereas persistent symptoms despite medical therapy may necessitate balloon valvuloplasty as the preferred first-line intervention and, rarely, aortic valve replacement in expert centers. Because bicuspid aortic valve disease may coexist with ascending aortic dilation, coarctation, or aneurysmal disease, pre-pregnancy imaging of the thoracic aorta is essential [5, 8, 21].

MS, which is most often rheumatic in origin, is usually less well tolerated than AS because pregnancy-related increases in preload, heart rate, and cardiac output can markedly increase transmitral gradients, left atrial pressure, and pulmonary pressures [9, 22].These changes may lead to progressive dyspnea, atrial arrhythmias, pulmonary edema, and heart failure as pregnancy advances [9, 11]. Recent data further highlight the vulnerability of women with significant MS during pregnancy, demonstrating progressive worsening in functional class, a 16% rate of percutaneous balloon mitral commissurotomy, and a persistently hig burden of maternal and fetal complications [24]. These findings are consistent with earlier data showing that pregnancy-related increases in mitral gradients and pulmonary pressures are associated with adverse cardiac events in women with isolated MS [22]. Accordingly, women with moderate-to-severe MS should ideally undergo evaluation and, when appropriate, intervention before conception [8, 9]. During pregnancy, management is centered on activity restriction, beta-1 selective blockade, cautious diuresis, and anticoagulation when indicated, while women with persistent severe symptoms despite medical therapy may require percutaneous balloon mitral commissurotomy in experienced centers [8, 9, 24].

Left-Sided Regurgitant Lesions (Mitral, Aortic) and Aortopathy

Compared to stenotic lesions, mitral regurgitation (MR) and aortic regurgitation (AR) are usually better tolerated in pregnancy. This is due to the hemodynamic and physiologic changes of pregnancy, which reduce afterload and systemic vascular resistance, thereby lowering regurgitant burden [21, 25]. For this reason, regurgitant lesions have traditionally been viewed as lower risk than obstructive lesions. However, this relative tolerance should not be interpreted as benign, since women with severe regurgitation, symptoms, left ventricular dysfunction, or concomitant aortic disease remain at meaningful risk for heart failure and other complications [8, 9, 11, 21].

The most common causes of MR in pregnancy include rheumatic heart disease and mitral valve prolapse, whereas AR is more often associated with bicuspid aortic valve disease or aortic root pathology [9, 13]. Although many women with even severe chronic MR or AR can complete pregnancy successfully, risk rises substantially when symptoms or ventricular dysfunction are present. The 2025 ESC guideline notes that heart failure occurs in roughly 20% to 25% of women with at least moderate regurgitation when symptoms or left ventricular dysfunction are present [8]. Similarly, in a 2021 analysis of valvular regurgitation during pregnancy, adverse cardiac events occurred in 13% overall and were more common in women with MR, TR, or multivalve disease than in those with isolated AR or PR, suggesting that lesion type alone is insufficient and that ventricular function and associated hemodynamic burden also matter [26].

Management is broadly guided by the same pathophysiologic principles as in nonpregnant patients, but treatment in pregnancy is more conservative and must account for fetal safety and perfusion. Diuretics may be used for congestion, and hydralazine or nitrate-based regimens can be considered when afterload reduction is required. Beta-blockers and selected antihypertensive agents (labetalol, methyldopa, nifedipine) may also be used when clinically indicated. These medications are safe for pregnancy and require additional fetal growth monitoring. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are contraindicated during pregnancy because of fetal teratogenicity. Surgery for isolated regurgitant lesions is rarely required during gestation and is generally reserved for refractory deterioration or life-threatening decompensation [9, 11, 27].

When AR is associated with bicuspid aortic valve disease or heritable aortopathy, management must extend beyond the valve itself to the size and behavior of the ascending aorta. In such patients, preconception imaging and risk assessment are essential, and surveillance during gestation should be individualized according to aortic dimensions, symptoms, and underlying genetic substrate, with strict blood pressure control to reduce the risk of progressive aortic dilation or dissection [8, 21].

Right Sided and Multivalve/Complex Valve Disease

Right-sided lesions are generally better tolerated than left-sided obstructive lesions when right ventricular function is preserved. Isolated tricuspid regurgitation (TR) usually does not require specific intervention during pregnancy, although diuretics and rhythm management may be necessary in symptomatic women or those with associated atrial arrhythmias. Tricuspid stenosis is rare and is usually rheumatic in origin; when hemodynamically significant, it may exacerbate systemic venous congestion during pregnancy and is generally managed conservatively with diuretics, while intervention is best considered before pregnancy in severe symptomatic disease [5, 27, 28]. Although uncommon, pulmonic stenosis, even when severe, is typically managed conservatively with clinical and echocardiographic surveillance, with intervention (e.g., balloon valvuloplasty) reserved for rare cases with refractory symptoms or right heart failure. Pulmonic regurgitation, often seen in repaired congenital heart disease, is usually tolerated unless associated with significant right ventricular dilation or dysfunction, in which case closer monitoring is warranted. In women with severe right-sided valve disease, particularly when symptoms, right ventricular dysfunction, or significant hemodynamic burden are present, intervention and medical optimization should be considered before pregnancy [5, 8, 13].

Multivalve disease is common in RHD and warrants caution because the coexistence of more than one abnormal valve can amplify hemodynamic stress and maternal risk. Across contemporary cohorts, multivalve disease and impaired functional status consistently emerge as key predictors of adverse cardiac events, with additional risk conferred by lesion severity, left ventricular systolic dysfunction, prosthetic valves, pulmonary hypertension, and delayed diagnosis [22]. These findings reinforce the need for individualized risk assessment and close cardio-obstetric follow-up in women with right-sided or multivalve disease, especially when pulmonary hypertension, ventricular dysfunction, or rheumatic disease is present.