Cardiac Disease in Pregnancy

Etiology

The etiology of cardiovascular diseases in pregnancy varies according to the specific underlying pathology. Various cardiovascular conditions may be encountered during pregnancy. Cardiomyopathy during pregnancy has multiple proposed mechanisms. Commonly cited theories include viral myocarditis, autoimmune processes, hemodynamic instability, and microchimerism, among others.[3] Risk factors associated with cardiomyopathy in nonpregnant individuals persist throughout pregnancy and the postpartum period, with potential for increased myocardial susceptibility during these phases. Relevant contributors include alcohol abuse, doxorubicin exposure, and substance misuse, eg, cocaine and methamphetamines.[4]

Coronary artery disease in pregnancy shares a similar etiology with ischemic heart disease in nonpregnant women. Major risk factors include hypertension, hyperlipidemia, hypertriglyceridemia, diabetes mellitus, obesity, smoking, and immobility.[5] These factors collectively increase the likelihood of atherosclerotic disease and subsequent ischemic events during pregnancy.

Pregnancy-associated myocardial infarction shares the same traditional risk factors as coronary artery disease.[6] Additional hypothesized contributors include pregnancy-related conditions (eg, preeclampsia and eclampsia), which may further predispose affected individuals to myocardial infarction. Valvular disease during pregnancy often worsens due to pregnancy-related hemodynamic changes, although a direct causal role of pregnancy in newly diagnosed valvular disorders remains uncertain.

Epidemiology

The frequency of cardiac disease in women remains incompletely defined, and current evidence does not clearly determine whether incidence differs between developed and underdeveloped countries. Available data suggest that at least 0.2% of pregnancies are complicated by cardiac disease.[7] Reported estimates rise as high as 4% in some studies.[8] Inclusion of hypertensive disorders further increases this proportion, given that hypertensive conditions occur in up to 8% of pregnancies.[8]

Pathophysiology

Physiologic changes during pregnancy play a central role in the development and progression of several cardiac disease processes. These adaptations may begin as early as 5 weeks of gestation, and their magnitude and trajectory vary among individuals.[9] Placental attachment to the uterine wall triggers hormonal release and subsequent maternal physiologic changes. These changes are predominantly hemodynamic and counter-regulatory, while preserving vascular homeostasis and maintaining the new mean arterial pressure of pregnancy.[10]

Cardiac output increases by approximately 20% to 50%, with changes detectable within the first 5 weeks of gestation and progressive elevation through late pregnancy. Increased stroke volume of approximately 25% during the first trimester contributes substantially to this rise, making pregnancy particularly challenging for individuals with preexisting cardiac disease. Patients with conditions, eg, cardiomyopathy, may fail to adequately compensate for this increased hemodynamic load and may develop complications, including pulmonary edema and volume overload states.[11] Heart rate increases by approximately 15% to 30% during the first trimester, further augmenting cardiac output.

Systemic vascular resistance decreases by up to approximately 30% during pregnancy. This reduction reflects decreased vascular responsiveness to angiotensin II and norepinephrine, along with increased release of vasodilatory mediators, eg, prostaglandins and nitric oxide.[12][13][12] Blood pressure demonstrates a mild early decline, with diastolic values decreasing more prominently than systolic values in early pregnancy. Blood pressure commonly normalizes or increases later in gestation.

Collectively, these physiologic and hormonal adaptations are hypothesized to contribute to decompensated cardiac states in pregnancy, including cardiomyopathy, congenital heart disease, and valvular disorders. In addition, structural cardiac remodeling occurs during pregnancy, with enlargement of both atria and both ventricles by the end of gestation.[14] Left ventricular mass increases by up to 50% by the third trimester, accompanied by eccentric hypertrophy and increased septal thickness.[15] Many of these structural and functional changes partially reverse within 6 to 8 months postpartum.[16] In conditions such as peripartum cardiomyopathy, these profound adaptations likely contribute to disease exacerbation, although no definitive mechanism explains the increased vulnerability in affected individuals.[17] Proposed explanations include concurrent myocarditis, autoimmune mechanisms, and familial predisposition. Animal models also suggest a potential role for VEGF dysregulation and impaired angiogenesis.[18]

Preexisting valvular disorders, including mitral stenosis, mitral regurgitation, and aortic stenosis, may worsen during pregnancy due to chamber enlargement, valvular dilation, and increased intravascular volume. These changes contribute to a volume-overloaded state that increases the risk of morbidity and mortality, including respiratory compromise and impaired tissue perfusion.

History and Physical

Careful differentiation between normal physiologic cardiovascular adaptations of pregnancy and pathologic cardiac changes remains essential to avoid misinterpretation of symptoms and examination findings. Accurate distinction ensures timely diagnostic evaluation and appropriate management of true cardiac disease while preventing unnecessary workup for expected pregnancy-related changes. Please see StatPearls' companion resource, "Physiology, Pregnancy," for further information.  

Clinical History

Accurate history taking remains essential for diagnosing cardiac conditions during pregnancy. Clinical features that raise suspicion for cardiac disease include:

• Fatigue
• Shortness of breath
• Dyspnea on exertion
• Paroxysmal nocturnal dyspnea
• Orthopnea
• Increasing edema
• Chest pain or angina
• Lightheadedness
• Syncope
• Personal or familial history of heart disease, especially in pregnancy

Physical Examination 

Physical examination findings that may support cardiac pathology include:

• Tachypnea
• Tachycardia
• Hypotension
• Cyanosis
• Clubbing
• Jugular venous distension
• Rales
• Ascites
• Hepatomegaly
• Peripheral edema
• S3 and S4 
• Hepatojugular reflux
• Prominent a and v waves
• Shifted apical impulse laterally to the midclavicular line
• Gallop rhythm

Many of these clinical findings may also occur in normal pregnancy, creating diagnostic complexity for clinicians attempting to differentiate physiologic adaptations from pathologic cardiac disease.[19] Careful integration of both history and physical examination findings remains critical for accurately distinguishing normal pregnancy-related changes from underlying cardiac conditions.

Evaluation

Evaluation of cardiac disease during pregnancy often requires an advanced diagnostic approach. Initial laboratory assessment typically includes a complete blood count (CBC), a comprehensive metabolic panel (CMP), and a urinalysis, which may provide important clues to underlying pathophysiologic processes. An elevated white blood cell count may support evaluation for inflammatory cardiac conditions (eg, myocarditis or myocardial infarction). Serum creatinine measurement may indicate recent or ongoing hypoperfusion. Liver enzyme abnormalities may suggest congestive hepatopathy, similar to nonpregnant populations. Urinalysis findings of proteinuria may assist in identifying preeclampsia. Additional laboratory testing, including brain natriuretic peptide (BNP), may provide diagnostic value, with reported physiologic increases of up to 2-fold during pregnancy.[20] Patients with overt peripartum cardiomyopathy typically demonstrate higher BNP levels compared with those without this condition.

Electrocardiography may demonstrate findings comparable to cardiovascular disease in nonpregnant individuals. Normal physiologic cardiac changes during pregnancy include leftward cardiac rotation with mild left axis deviation. Pregnancy-related chamber dilation increases susceptibility to dysrhythmias, including atrial premature beats, supraventricular tachycardias, and ventricular premature beats, while ventricular tachyarrhythmias occur less commonly.[21][22] Ischemic processes may produce ST-segment elevation or depression, T-wave inversion, or Q-wave formation. Nonspecific ST-segment and T-wave changes occur in up to 14% of pregnancies.[23]

Echocardiography plays a central role in evaluating suspected cardiac disease during pregnancy. Physiologic findings may include chamber enlargement, mild physiologic aortic, mitral, and tricuspid regurgitation, and valvular dilation.[24] Clinical significance depends on the correlation between echocardiographic findings and patient presentation, as no definitive thresholds distinguish normal from abnormal pregnancy-related changes. Cardiomyopathy may demonstrate exaggerated septal thickening, increased end-diastolic posterior wall thickness, and eccentric hypertrophy.[25] Peripartum cardiomyopathy diagnosis may be supported by an ejection fraction below 45% and/or M-mode fractional shortening below 30%, along with an end-diastolic dimension greater than 2.7 cm/m².[26] Myocardial ischemia or infarction may present with regional wall motion abnormalities. Pericardial effusion may occur during pregnancy and remain physiologic in small volumes; however, findings, eg, hypotension, jugular venous distension, or pulsus paradoxus, warrant prompt echocardiographic evaluation for cardiac tamponade.

Treatment / Management

No empiric regimens exist for the prevention of cardiac disease in pregnancy. Individuals with a prior history of cardiac disease require heightened vigilance and continuation of their prepregnancy therapeutic regimen. When existing regimens include teratogenic agents, replacement with safer alternatives under the guidance of a qualified clinician becomes necessary. Management of cardiac disease in pregnancy varies according to the underlying condition and requires an individualized treatment approach. The following outlines common cardiac disorders in pregnancy and corresponding recommended therapeutic strategies.

Ventricular Dysfunction 

Ventricular dysfunction in pregnancy frequently involves patients with pre-existing heart failure, whether previously recognized or undiagnosed before pregnancy, depending on functional status. Physiologic adaptations of pregnancy, including increased heart rate and expanded circulating volume, may overwhelm compensatory mechanisms, particularly during the second trimester when hemodynamic demands peak. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, commonly used in heart failure with reduced ejection fraction, remain contraindicated due to teratogenic effects, including renal dysplasia, renal failure, oligohydramnios, and intrauterine growth restriction.[27] Alternative therapy with hydralazine and nitrates provides a comparable hemodynamic effect. Beta-blockers may be continued, with preference for cardioselective agents (eg, metoprolol). Diuretics may also be used when clinically indicated.[28](B3)

Peripartum Cardiomyopathy

Peripartum cardiomyopathy, defined as dilated cardiomyopathy occurring during the last 4 weeks of pregnancy or up to 5 months postpartum, follows a treatment approach similar to ventricular dysfunction in pregnancy.[29] After delivery, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker therapy may be reintroduced.

Mitral Stenosis

Mitral stenosis carries substantial morbidity and mortality risk during pregnancy due to its obstructive physiology.[30] No pharmacologic agents reverse the underlying lesion; however, beta-blockers remain the primary medical therapy, reducing transmitral gradient.[31] Diuretics provide symptomatic relief in heart failure manifestations.(B2)

Aortic Stenosis 

Although aortic stenosis in pregnancy is less common, this condition is often more challenging to treat, presenting a more complex management challenge during pregnancy. No medications modify disease progression or serve as definitive therapy. Beta-blockers demonstrate limited efficacy in reducing transvalvular gradients compared with their effect in mitral stenosis. Angiotensin-converting enzyme inhibitors remain contraindicated. Diuretic use requires caution due to the potential for reduced diastolic filling and a further decline in cardiac output.

Tachyarrhythmias

Tachyarrhythmias require individualized management based on maternal and fetal considerations. Agents considered relatively safe during pregnancy include adenosine, verapamil, digoxin, flecainide, and beta-blockers.[32] Amiodarone should be avoided due to its association with fetal hypothyroidism.[33]

Spontaneous Coronary Artery Dissection

Spontaneous coronary artery dissection represents an uncommon cause of acute myocardial infarction, with increased incidence during pregnancy. Clinical suspicion should remain high in pregnant patients presenting with acute coronary syndrome symptoms.[34] Dissection most commonly involves the left main or left anterior descending artery.[35] Proposed mechanisms include hormonal influences, pregnancy-related hemodynamic stress that weakens the arterial wall, and inflammatory infiltrates.[36][37][36](B3)

Diagnosis relies on coronary angiography. Management lacks standardization due to rarity, with reported approaches including medical therapy, coronary artery bypass grafting, and heart transplantation.[38][39][38] Coronary artery bypass grafting may represent the preferred strategy in cases involving multiple-vessel dissection, left main involvement, or failure of percutaneous coronary intervention.[40]

Acute Coronary Syndrome

Acute coronary syndrome and myocardial infarction remain uncommon in pregnancy but demonstrate increasing incidence with rising maternal age at conception. Advancing age contributes to the accumulation of risk factors, eg, diabetes mellitus, hyperlipidemia, and hypertension. Although fluoroscopic exposure during pregnancy presents risks, percutaneous coronary intervention remains indicated, given the high mortality associated with untreated acute coronary syndromes, with maternal shielding using lead protection. Thrombolytic therapy remains an alternative but requires close monitoring due to reported complications, including maternal hemorrhage, spontaneous abortion, subchorionic hematomas, and uterine bleeding.[41][42][41] Drug-eluting stents should be avoided when possible due to prolonged dual antiplatelet therapy requirements, which complicate obstetric management, particularly in cesarean delivery.[43](A1)

Commonly used cardiovascular medications and pregnancy risk categories include morphine (Category C), beta-blockers (metoprolol Category B; atenolol Category C), calcium channel blockers (Category C), angiotensin-converting enzyme inhibitors and angiotensin receptor blockers (Category C in first trimester and Category D in second and third trimesters), statins (Category X), unfractionated heparin (Category C), low-molecular-weight heparin (Category B), aspirin (Category C), and glycoprotein IIb/IIIa inhibitors (eptifibatide and tirofiban Category B; abciximab Category C).[43]

Patients presenting with blood pressure greater than 160/100 require antihypertensive therapy with close outpatient or inpatient monitoring, depending on severity.[44] Agents demonstrated to be safe in pregnancy include oral methyldopa, oral or intravenous labetalol, oral nifedipine, oral or intravenous hydralazine, and intravenous nicardipine.

Differential Diagnosis

Cardiac diseases of pregnancy need evaluation as new processes or exacerbations of previous disease processes. With any cardiac disease process detected in pregnancy, the preexisting pathology must be ruled out, including prior dilated cardiomyopathy, restrictive cardiomyopathy, hypertensive obstructive cardiomyopathy, ischemic heart disease, or previous valvular disorders.

Prognosis

The World Health Organization (WHO) has established a modified classification of maternal cardiovascular risk, which is used as a tool to evaluate risk status for pregnant females with various cardiovascular conditions (see Table. World Health Organization Classification of Maternal Cardiovascular Risk). The risk classifications are as follows:

• I: No Identifiable elevated risk of maternal morbidity and mortality
• II: Mildly elevated maternal mortality; moderate elevation of morbidity
• III: Substantially elevated risk in maternal mortality; severe elevation of morbidity. For these patients, close follow-up is recommended to be initiated with cardiac specialists. Cardiac monitoring should continue regularly throughout pregnancy and should also continue after pregnancy.[45]
• IV: Extremely elevated risk of maternal mortality; severe elevation of morbidity. Pregnancy is contraindicated for these individuals. If pregnancy is to occur, termination should be recommended. However, if the individual chooses to pursue pregnancy, she should be monitored closely as a class III individual.[45]

Table. World Health Organization Classification of Maternal Cardiovascular Risk

Heart disease during pregnancy represents a high-risk clinical condition; however, favorable outcomes frequently occur when patients receive consistent monitoring and regular follow-up. Prognosis varies according to the specific cardiac disorder, with certain conditions carrying substantially greater morbidity and mortality than others. Peripartum cardiomyopathy occurs in approximately 1 in 2,289 live births. Approximately 75% of affected women experience complete recovery of normal ventricular function.[46] Despite the potential severity of this condition, recovery of cardiac function remains common with appropriate management and follow-up.

Among patients with congenital heart disease, regurgitant valvular lesions generally carry lower morbidity than stenotic lesions.[47] Overall maternal mortality remains very low in this population. One study evaluating 90 individuals with congenital heart disease reported no maternal deaths.[48] However, the same analysis identified pulmonary edema in 17% of patients and cardiac events, predominantly nonsustained tachyarrhythmias, in 12%. A meta-analysis involving more than 2,000 pregnancies reported a spontaneous abortion rate of 15% and an 8% incidence of congenital heart disease among offspring.[49]

Acute coronary syndrome and myocardial infarction remain uncommon during pregnancy, with reported estimates ranging from 1 to 2 cases per 35,000 deliveries.[43] In one study evaluating pregnancy outcomes among patients with coronary artery disease or acute coronary syndromes, adverse obstetric events occurred in 16% of pregnancies, while adverse neonatal outcomes occurred in 30%.[50] Reported maternal mortality reached 7.3%, with the greatest risk observed among patients presenting with acute coronary syndrome during the third trimester.[51]

Complications

Complications related to cardiac disease in pregnancy include:

• Excess weight gain during pregnancy
• Preeclampsia
• Preterm birth
• Intrauterine growth restriction
• Hemorrhage
• Placental abruption
• Gestational diabetes
• Progressive heart failure
• Maternal or fetal death