Cardiovascular disease in pregnancy

This page follows a woman with heart disease from the decision to conceive, through each trimester and delivery, to the months after birth. Recommendations are taken from the 2025 ESC pregnancy guideline unless another document is named. Aortopathy, congenital heart disease, pulmonary arterial hypertension, venous thromboembolism, heart transplantation and cardio-oncology in pregnancy are outside this page. ESC 2025 recommends a staged approach from pre-conception and pregnancy through labour, delivery and post-partum care.^[1]

Why pregnancy unmasks heart disease

Start with the numbers. From 6 weeks of gestation, stroke volume and cardiac output rise by 30%–50% and heart rate rises by 10–20 beats per minute.^[1] Peripheral vascular resistance falls by 20%–50%.^[1] Both atria and both ventricles enlarge while ventricular function is preserved.^[1]

^[1]

Blood pressure and cardiac output increase during labour.^[1] After delivery, the uterus contracts and cardiac output drops rapidly to about 15%–25% above normal, then falls gradually over 3–4 weeks to pre-pregnancy levels at about 6 weeks post-partum.^[1]

The question is whether a diseased heart can follow. In women with heart disease, left and right ventricular adaptation can be suboptimal and can lead to HF and atrial and ventricular tachyarrhythmias.^[1] Atrial arrhythmias may develop in response to cardiac stretch and hormonal changes and may not be well tolerated in women with CVD.^[1]

• Thrombosis: pregnancy is a hypercoagulable state associated with an increased risk of thromboembolism.^[1]
• Aorta: the haemodynamic and hormonal changes of pregnancy are risk factors for aortic dissection in women with aortopathy.^[1]
• Drugs: increased gastrointestinal–hepatic metabolism, liver enzyme activity, glomerular filtration and plasma volume, altered protein binding and lower serum albumin all change the pharmacokinetics of many drugs.^[1]

^[1]

How common, and how dangerous

• Globally, up to 4% of pregnancies are complicated by CVD, rising to 10% when hypertensive disorders are included.^[1]
• Maternal CVD is now the leading cause of non-obstetric mortality in pregnant women, accounting for 33% of pregnancy-related deaths worldwide.^[1]
• ESC 2025 notes that 68% of pregnancy-related deaths caused by CVD are preventable.^[1]
• In women with pre-existing CVD, up to 16% of pregnancies are complicated by CVD.^[1]
• In pregnancies of women with CVD, adverse neonatal outcomes occur in about 25%, with high rates of obstetric complications (17%) and maternal mortality or morbidity (11%).^[1]
• In high-income countries the numbers are growing, a trend that ESC 2025 says originates from higher maternal age at first pregnancy, more women with congenital heart disease reaching childbearing age, and a rising prevalence of cardiovascular comorbidities.^[1]

Risk assessment: the mWHO 2.0 classification

ESC 2025 recommends a risk assessment in all women with CVD of childbearing age using the mWHO 2.0 classification (Class I, Level C).^[1] mWHO 2.0 updates the modified WHO classification of the 2018 ESC pregnancy guideline.^[1]

Various scoring systems are available to assess maternal and foetal risk, but ESC 2025 says they do not fully explore the interaction with non-cardiac risk factors, only focus on maternal cardiac events, and have mainly been validated in higher-income countries.^[1] Despite these limitations, it says disease-specific risks can be effectively assessed with the mWHO classification, validated as the best-available risk assessment model.^[1] The original classification was oriented towards adult congenital heart disease, so mWHO 2.0 adds other CVDs and integrates the CARPREG II study.^[1]

ESC 2025 Table 6: risk and event rates by mWHO 2.0 class

^[1]

Cardiac events in these rates are cardiac arrest, cardiac death, arrhythmia requiring treatment, left or right HF, thromboembolism, aortic dissection, ACS or hospitalisation for a cardiac reason; endocarditis was counted only by van Hagen.^[1]

ESC 2025 Table 6: who counsels, who cares and where to deliver

^[1]

Table 6 also lists the diagnoses in each class; this page gives a class only where the guideline text states it.^[1] Mechanical heart valves carry a high risk of complications (mWHO 2.0 class III or higher).^[1] Worse than mild ventricular dysfunction (mWHO 2.0 class above II) needs expert Pregnancy Heart Team care, with input from the advanced HF team.^[1] Pre-existing severe HF (LVEF below 30%) is mWHO 2.0 class IV and accounts for up to 15% of maternal deaths globally.^[1] Adverse obstetric and foetal outcomes are more frequent with a higher mWHO 2.0 class.^[1]

^[1]

The Pregnancy Heart Team

Pregnancy Heart Team care starts before pregnancy and continues through the post-partum period.^[1] ESC 2025 reports that management by such a team is associated with favourable maternal, foetal and healthcare outcomes, including lower maternal mortality and readmission rates.^[1] The team's responsibilities are risk assessment, a collaborative care plan, continuous monitoring, coordination, patient education and psychological counselling.^[1]

Patient selection is best done by an mWHO 2.0 risk assessment.^[1] Specific expertise and collaborative management by the team are mandatory for every woman with a condition of mWHO 2.0 class II–III or above.^[1] Not every hospital needs its own team, but each hospital should establish communication and collaboration with nearby expert teams.^[1]

Counselling, contraception, reproduction and team rows

^{[1] [3]}

Before conception: counselling and planning

ESC 2025 says women should receive pre-pregnancy counselling and education about maternal, foetal and transmission risks.^[1] In adolescents with congenital or inherited heart disease, discussions about reproductive health should start early, ideally from menarche, and rates of unintended pregnancy of up to 45% have been reported in adolescents with congenital heart disease.^[1]

• The assessment is personal: diagnosis, functional status and medication, plus non-cardiac factors such as maternal age, smoking, comorbidities, BMI, obstetric history, logistics, ethnicity and socioeconomic status.^[1]
• Cardiopulmonary exercise testing can be useful for pre-pregnancy risk stratification.^[1]
• Genetics: most heritable CVDs show autosomal dominant inheritance with a 50% transmission risk.^[1]
• Drugs: HF drug regimens should be modified before pregnancy as part of risk stratification, with reassessment after at least 3 months.^[1]
• Contraception: accurate counselling should be provided to all girls and women of childbearing age with CVD, starting from menarche, to prevent unplanned pregnancies.^[1]
• Assisted reproduction adds risk above that of pregnancy alone: superovulation is pro-thrombotic and can be complicated by ovarian hyperstimulation syndrome, with marked fluid shifts and a high thrombosis risk.^[1]
• Transferring a single embryo is strongly advised in women with CVD, as carrying multiple gestations is associated with greater cardiovascular changes and more maternal and foetal complications.^[1]
• Fertility treatment should be avoided in women with mWHO 2.0 class IV conditions.^[1]
• Termination: ESC 2025 strongly recommends considering and discussing termination with women in mWHO 2.0 class IV, because of the exceptionally elevated risk of maternal and foetal mortality or severe morbidity (text; the class IV row above is Class I, Level C).^[1]
• Surgical methods of termination are often preferred, but pharmacological methods remain an option until the ninth week of pregnancy.^[1]

Normal pregnancy or heart disease?

Pregnancy changes the ECG and the echo, and its symptoms overlap with those of heart disease.^[1] ESC 2025 warns that the symptoms and signs of acute HF can be misinterpreted as changes due to pregnancy, and that mild to moderate PPCM is often mistaken for physiological change, especially post-partum.^[1]

^[1]

Natriuretic peptides help here: values within the normal range throughout pregnancy and early post-partum have a strong negative predictive value for HF.^[1] The specificity of D-dimer is reduced during pregnancy, and women should not undergo chest CT based solely on D-dimer levels.^[1]

Investigations in pregnancy

Recommendation Table 2: diagnostic methods in pregnancy

^[1]

• Agitated saline contrast should not be used during pregnancy, because of the risk of placental infarction from microbubble embolism causing foetal distress.^[1]
• If new CVD is suspected, submaximal exercise testing (at 80% of predicted maximal heart rate) can be useful; pharmacological stress agents such as dobutamine should be avoided.^[1]
• With syncope or palpitations, long-term Holter monitoring or implantable loop recorders should be considered as additional diagnostic tools.^[1]
• Foetal echocardiography should routinely be offered at 18–22 weeks when a parent has congenital heart disease, and detects up to 80% of significant congenital cardiac defects.^[1]

Native valve disease

Stenotic and regurgitant lesions behave differently in pregnancy.^[1] ESC 2025 says valve regurgitation is generally better tolerated than valve stenosis.^[1] When reading serial echoes, remember that valve gradients usually rise by up to 50% because of the normal increase in cardiac output.^[1]

Mitral stenosis

• Mild stenosis is usually well tolerated, but symptoms may occur if the valve area is below 1.5 cm².^[1]
• Maternal mortality is higher with NYHA class above II, systolic pulmonary arterial pressure above 30 mmHg, severe stenosis, older age and in low-income countries.^[1]
• Valve area by 2D planimetry is thought to be more reliable than flow-dependent measures in pregnancy, because higher stroke volume and tachycardia increase the measured gradient.^[1]
• Therapeutic anticoagulation with full therapeutic-dose LMWH or VKA is indicated with AF, left atrial clot or previous embolism; ESC 2025 says anticoagulation should be considered with significant mitral stenosis, spontaneous echo contrast in the left atrium, a dilated left atrium with a left atrial volume index above 60 (unit printed as mL/mL²) or HF (text; no class or level given).^[1]
• Before and during pregnancy, percutaneous mitral balloon commissurotomy is the primary intervention for women who remain in NYHA III/IV or have severe pulmonary arterial pressure elevation despite medical therapy (text; for pregnant women with severe symptoms or systolic pulmonary artery pressure above 50 mmHg despite medical therapy, the formal row below says percutaneous mitral commissurotomy should be considered, Class IIa, Level C; before pregnancy, the formal row below recommends intervention in women with mitral stenosis and a valve area below 1.5 cm², Class I, Level C).^[1]
• Vaginal delivery is the preferred option; caesarean section is preferred in severe mitral stenosis and in women with refractory HF.^[1]

Aortic stenosis

• Women with severe stenosis, and those with symptoms before pregnancy, have a 1 in 4 risk of developing HF during pregnancy.^[1]
• Cardiac surgery with cardiopulmonary bypass is associated with at least a 20% risk of foetal loss.^[1]
• If the foetus is at a viable gestation, taking account of comorbidities and the available level of neonatal care, delivery should occur before valve intervention.^[1]
• Caesarean delivery should be considered in severe symptomatic aortic stenosis.^[1]

Regurgitant lesions

With valve regurgitation and either symptoms or LV dysfunction, HF occurs in 20%–25% of women with at least moderate regurgitation.^[1]

Recommendation Table 18: native valve disease and pregnancy

^[1]

The ESC/EACTS 2025 valve guideline adds a row for clinically severe mitral stenosis (Class IIa, Level C).^[10] Percutaneous mitral commissurotomy should be considered in asymptomatic patients without unfavourable clinical and anatomical characteristics for it who have a high thromboembolic risk and/or a high risk of haemodynamic decompensation.^[10] High thromboembolic risk means previous systemic embolism, dense left atrial spontaneous contrast, or new or paroxysmal AF.^[10] High risk of decompensation means systolic pulmonary artery pressure above 50 mmHg at rest, need for major non-cardiac surgery, or pregnancy or a desire for pregnancy.^[10]

Mechanical valves and anticoagulation, trimester by trimester

Mechanical heart valves expose pregnant women to a high risk of complications (mWHO 2.0 class III or higher).^[1] In women with a mechanical valve, the chance of an event-free pregnancy with a live birth was only 58% in the initial ROPAC II study and did not improve after 8 years in ROPAC III (54%).^[1] In ROPAC III the figure with a tissue valve was 79%.^[1] ESC 2025 cites thrombotic complications in 9%–24% and bleeding complications in 20%–30% of cases in the ROPAC III and a United Kingdom study, respectively, and says women with a mechanical mitral valve are especially at risk of adverse outcomes, including mortality.^[1]

ESC 2025 asks for an individualised shared decision with careful consideration of maternal thrombosis risk against foetopathy.^[1] Continuous VKA use is the most effective regimen for preventing maternal thrombotic complications, but VKAs cross the placenta and carry embryopathy and foetopathy risk even at low doses.^[1] The embryopathy risk is highest in the first trimester (0.6%–12%), with a lower but persisting foetopathy risk later (0.7%–2%).^[1] First-trimester embryopathy depends on the VKA dose: two systematic reviews found 0.45%–0.9% with low-dose warfarin.^[1] Low dose means the dose that maintains the appropriate INR, given as 5 mg or less of warfarin, 2 mg/day or less of acenocoumarol or 3 mg/day or less of phenprocoumon.^[1] Embryopathy or foetopathy has not been reported with LMWH, even at therapeutic doses, but thromboembolic complications in women with mechanical valves are higher than with VKAs (8.7% with LMWH, 5.8% with UFH and 2.7% with VKA).^[1] Data from ROPAC III indicated a higher risk of miscarriage in VKA users.^[1]

Anticoagulation for mechanical valves (Table 10, Recommendation Tables 3 and 19)

^[1]

On valve choice, the same-season ESC/EACTS 2025 valve guideline says a biological valve should be considered in women contemplating pregnancy (Class IIa, Level C).^[10] For anticoagulation it refers readers to the pregnancy guideline.^[10] The valve guideline text says warfarin throughout pregnancy, changing to UFH before delivery, is advocated when 5 mg/day or less is needed (no class or level given).^[10] For higher doses, it recommends switching to dose-adjusted LMWH at least twice daily with strict anti-Xa monitoring in the first trimester (no class or level given).^[10]

Why do most women end up on a VKA later in pregnancy? ESC 2025 says that in most cases VKAs will be the favoured therapy in the second and third trimesters, to minimise maternal risk after embryogenesis, although some women choose to stay on therapeutic-dose LMWH throughout.^[1] In women with a very high thrombotic risk, adding low-dose aspirin should be considered.^[1]

Monitoring and dosing

Monitoring anticoagulation with a mechanical valve

^[1]

ESC 2025 does not recommend DOACs during pregnancy (Class III, Level C) and says they should only be used in the absence of any other option, with the Pregnancy Heart Team and haematology team.^[1] Accidental exposure is not an absolute indication to interrupt pregnancy on current data.^[1] In pregnant women with AF who need anticoagulation, the presence of a mechanical valve or moderate to severe mitral stenosis requires a VKA.^[1]

^[1]

Cardiomyopathies

Before pregnancy, women with cardiomyopathy should be evaluated to optimise treatment, avoid contraindicated drugs and assess the risk of HF and arrhythmias, and indicated procedures such as ICD implantation should be performed first.^[1] In DCM and non-dilated LV cardiomyopathy, pre-pregnancy risk stratification should include temporary withdrawal of contraindicated medication with close monitoring.^[1]

• Dilated and non-dilated LV cardiomyopathy: severe systolic LV dysfunction, NYHA class III/IV, RV failure, sustained ventricular arrhythmias, AF and/or severe mitral regurgitation are high-risk criteria; mild LV dysfunction, good functional status, no arrhythmias and no previous cardiac events make an uncomplicated pregnancy likely.^[1]
• ACE inhibitors, ARBs, MRAs, sacubitril/valsartan and SGLT2 inhibitors are all contraindicated during pregnancy.^[1]
• Arrhythmogenic RV cardiomyopathy: sustained ventricular arrhythmias were reported in 5% of pregnancies and HF in 13%.^[1]
• Hypertrophic cardiomyopathy (HCM): absolute maternal mortality is low (0.5%) and confined to women at particularly high risk, although in the ROPAC registry 23% developed major cardiac events, including VT (10%) and AF (1.7%), mostly in women already identified as high risk.^[1]
• In obstructive HCM, ESC 2025 recommends evaluating the gradient at rest, with exercise and with the Valsalva manoeuvre before pregnancy, on only the drugs allowed in pregnancy, to identify women needing septal reduction therapy before pregnancy (text; no class or level given).^[1]
• Myosin inhibitor treatment should be stopped at least 6 months before planning pregnancy.^[1]
• In HCM with severe LVOT obstruction, peripheral vasodilatation is poorly tolerated, so epidural and spinal anaesthesia should be applied cautiously.^[1]

Recommendation Table 5: cardiomyopathies and pregnancy (selected rows)

^[1]

Peripartum cardiomyopathy

Picture a woman a few weeks after delivery who cannot lie flat. ESC 2025 defines PPCM as HF with LVEF below 45%, without any other cause of HF, occurring mainly during the peripartum period or in the months after delivery, termination or miscarriage.^[1] PPCM is essentially a diagnosis of exclusion and requires urgent management.^[1]

^[1]

• Incidence varies by region, ethnicity and socioeconomic factors: 1–4 per 1000 births in the United States and 10 per 1000 births in north-western Nigeria.^[1]
• Data from 49 countries show that most women present post-partum.^[1]
• Genetics: variants in TTN, FLNC, BAG3 and DSP are found in up to 15% of women with PPCM, TTN truncating variants being the most common.^[1]
• Mechanism: ESC 2025 describes growing evidence that several mechanisms converge on a common pathway of inflammation, unbalanced oxidative stress and generation of the anti-angiogenic 16 kDa prolactin, which causes endothelial dysfunction and damage and then HF; blocking prolactin with the dopamine D2 agonist bromocriptine has emerged as a potential disease-specific therapy.^[1]
• Other anti-angiogenic factors, such as soluble fms-like tyrosine kinase-1 (sFlt-1), contribute to local and widespread vascular dysfunction.^[1]

Presentation and diagnosis

• PPCM may present subtly, but most women present with acute HF and severe symptoms (NYHA III/IV); milder cases are often mistaken for physiological changes, especially post-partum.^[1]
• Diagnostic measures should include ECG, natriuretic peptides and echocardiography.^[1]
• Myocarditis is a differential diagnosis and should be excluded by CMR.^[1]
• New VT in the last 6 weeks of pregnancy or the first month post-partum should prompt exclusion of underlying PPCM.^[1]
• PPCM with pre-eclampsia carried a higher risk of adverse neonatal outcome but also a higher likelihood of LV recovery (LVEF 50% or more).^[1]

Treatment

Treatment of acute HF caused by PPCM follows the main principles of acute HF management during and after pregnancy.^[1] Most HF drugs are foetotoxic and contraindicated during pregnancy (ACE inhibitors, ARBs, MRAs and SGLT2 inhibitors).^[1] In the post-partum period, full HF treatment can be initiated, except that ARBs and SGLT2 inhibitors should be avoided if lactation and breastfeeding are necessary for nutritional reasons.^[1] Mechanical circulatory support should be considered for persistent cardiogenic shock despite medical treatment.^[1]

Bromocriptine has emerged as a potential disease-specific therapy.^[1] Stopping lactation is a secondary effect, which allows full HF treatment in a mother who is not breastfeeding; ESC 2025 names women with moderate and severe HF as the preferred candidates.^[1] ESC 2025 reports a multicentre randomised study in women with severe PPCM that compared 2.5 mg daily for 1 week with 5 mg daily for 2 weeks followed by 2.5 mg daily for 6 weeks.^[1] LV recovery at 6 months was high, with no significant difference between 1 week and 8 weeks of treatment.^[1] ESC 2025 says this suggests that a 1-week addition of bromocriptine to standard HF treatment would be beneficial.^[1] Figure 22 of ESC 2025 gives a starting dose of 2.5 mg twice daily, up-titrated if needed.^[1]

Recommendation Table 7: peripartum cardiomyopathy

^[1]

Outlook and the next pregnancy

• Markers of complications include LVEF below 30%, LV end-diastolic diameter above 60 mm, biventricular dysfunction, QT prolongation, delayed diagnosis and Middle Eastern or African ethnicity and/or geography.^[1]
• PPCM may cause ventricular tachyarrhythmias, so patients should be monitored; because about 50% recover within a year, a wearable defibrillator may be considered as a bridge to recovery with LVEF below 35% and risk of sudden death.^[1]
• In the EORP PPCM registry, all-cause death at 1 year was 8%, varying by region (Europe 5%, Africa 6%, Asia–Pacific 9%, Middle East 19%).^[1]
• Stepwise withdrawal of HF therapy may be considered after 1 year if recovery is complete and no genetic predisposition has been identified, but recent data indicated a higher risk of LVEF relapse in subsequent pregnancies in women who had stopped their HF medication.^[1]
• More than mild LV dysfunction before a new pregnancy increases the risk of LVEF deterioration, and women with recovered LV function remain at risk of relapse.^[1]
• If a new pregnancy is planned after PPCM, stopping beta-blockers may not be advisable, and restarting them may be beneficial in the subsequent pregnancy, irrespective of baseline LV systolic function.^[1]

^[1]

Heart failure in pregnancy

HF complicates 11% of pregnancies in women with pre-existing heart disease, with an in-hospital maternal mortality of 9%.^[1] ESC 2025 describes two peaks of deterioration: at 23–30 weeks and around delivery.^[1]

• Pregnant women with acute HF need urgent hospital admission and referral to an expert centre with advanced HF care, including on-site surgery and mechanical circulatory support, or even a transplant programme as backup.^[1]
• Cardiogenic shock: levosimendan is given as a continuous infusion without a loading dose; dobutamine is an option, whereas adrenaline should be avoided.^[1]
• Mechanical circulatory support, preferably veno-arterial ECMO, should be considered in severe refractory cardiogenic shock.^[1]
• Milder acute HF can be treated with oral diuretics, beta-1-selective blockers (bisoprolol, metoprolol succinate), hydralazine and oral nitrates.^[1]
• Post-partum, ivabradine may be considered to control heart rate in addition to beta-blockers, or if beta-blockers are contraindicated.^[1]

Heart failure rows: ESC 2025 Recommendation Table 20 and ESC 2026 HF Recommendation Table 27

^{[1] [3]}

ESC 2026 HF repeats the ESC 2025 beta-blocker and drug-avoidance rows, adding the purpose of the beta-blocker switch, so its wording is given above.^[1][3] ESC 2026 HF itself refers readers to the 2025 ESC pregnancy guideline for comprehensive guidance.^[3]

Arrhythmias

ESC 2025 says arrhythmia may have serious effects on the health of both mother and foetus and should be treated similarly to arrhythmias in non-pregnant women.^[1] The incidence of arrhythmias in pregnancy is increasing, AF being the most clinically relevant, and AF in pregnancy is associated with increased maternal death.^[1] Compared with women under 25, the odds ratio of AF episodes was 5.2 in women aged 40 or more, and higher in the third than the first trimester.^[1]

Narrow QRS tachycardia, AF and flutter

• With haemodynamic instability caused by any SVT, including AF and flutter, synchronised direct current cardioversion is indicated, and the foetal heart rate should be closely monitored after cardioversion.^[1]
• Electrical cardioversion is safe and effective in all phases of pregnancy, and shock energies should be the same as in non-pregnant patients.^[1]
• If vagal manoeuvres fail, i.v. adenosine (6–18 mg bolus) is recommended for terminating AV re-entrant or AV nodal re-entrant tachycardia (AV(N)RT).^[1]
• Figure 14 doses: metoprolol 2.5–15 mg; verapamil 2.5–10 mg bolus over 5 min; atenolol is contraindicated.^[1]
• The Figure 15 legend printed verapamil as 2.5–1 mg; the February 2026 correction changed it to 2.5–10 mg.^[2]
• Rhythm control is the preferred AF strategy in pregnancy.^[1]
• Anticoagulation with LMWH before cardioversion, and the need for transoesophageal echo, are judged as in non-pregnant women, and anticoagulation is maintained for at least 4 weeks after cardioversion.^[1]
• In persistent or permanent AF, the decision to anticoagulate is the same as outside pregnancy and uses the CHA2DS2-VA score, although its threshold of 2 or more has not been validated in pregnancy.^[1]
• WPW: AV nodal blockers increase the risk of rapid ventricular rates if AF occurs, but long-term AV blockade is acceptable for prevention in women without documented AF, with known orthodromic AVRT and intermittent pre-excitation.^[1]

Recommendation Table 14: SVT, AF and pregnancy

^[1]

ESC 2024 AF, published before the pregnancy guideline, preferred unfractionated heparin or LMWH for AF anticoagulation in pregnancy, which do not cross the placenta.^[6] It said VKAs should be avoided in the first trimester (risk of miscarriage, teratogenicity) and from week 36 onwards (risk of foetal intracranial bleeding if early unexpected delivery).^[6] ESC 2025 now recommends therapeutic LMWH for persistent or permanent AF at elevated thromboembolic risk (Class I, Level C), and says that in AF the presence of a mechanical valve or moderate to severe mitral stenosis requires a VKA.^[1] The ESC 2024 AF text also recommends electrical cardioversion with haemodynamic instability, considerable risk to mother or foetus, or concomitant HCM (text; its pregnancy recommendation table is an image in the held HTML and is not quoted).^[6]

Ventricular arrhythmias

• New VT and VF in pregnancy are rare (18 per 100 000 pregnancy-related hospitalisations); the most common type is idiopathic VT from the RV outflow tract.^[1]
• New VT in the last 6 weeks of pregnancy or the first month post-partum should prompt exclusion of PPCM.^[1]
• Amiodarone is not recommended in pregnancy and should be limited to refractory or life-threatening arrhythmias that no other anti-arrhythmic can control.^[1]
• Catheter ablation should preferably be performed after the first trimester, in a centre with experience in non-fluoroscopic electro-anatomical mapping and catheter navigation systems.^[1]
• Device implantation is not associated with more major complications and can be performed safely, particularly after 8 weeks of gestation; most data show maternal ICD shocks have no major foetal adverse effects.^[1]

Recommendation Table 15: VT, devices, ablation and pregnancy

^[1]

Bradycardia

• Mobitz type I AV block is common in pregnant women and rarely progresses during pregnancy.^[1]
• Pacing indications, temporary and permanent, do not differ between pregnant and non-pregnant women.^[1]
• A prophylactic temporary pacemaker during delivery is not recommended in women with asymptomatic congenital AV block, normal cardiac anatomy and function, a narrow QRS and a ventricular rate of 50 b.p.m. or more (Class III, Level C).^[1]

Cardiac arrest

Haemorrhage and anaesthetic complications are the most common overall causes; HF, ACS, arrhythmias, aortic dissection and PE are the most common cardiovascular causes.^[1]

Recommendation Table 16: cardiac arrest and pregnancy

^[1]

One pregnancy-specific step is easy to forget: in a woman on a magnesium infusion for pre-eclampsia, stop the infusion and give calcium gluconate.^[1]

Chest pain, ACS and SCAD

Chest pain in pregnancy is evaluated with the same protocol as outside pregnancy, including examination, ECG, biomarkers and echocardiography.^[1] ESC 2025 recommends excluding life-threatening causes, including PE, ACS (including SCAD) and acute aortic syndrome (Class I, Level C).^[1] With a suspected acute aortic syndrome, there should be a low threshold for aortic CT and for consultation with the aortic team in emergencies.^[1]

• ACS accounts for 20% of cardiovascular maternal deaths in developed countries; its risk is three to four times higher in pregnant than non-pregnant women of reproductive age, and mortality is estimated at 5%.^[1]
• ACS can occur at any stage but is more common in the third trimester or post-partum.^[1]
• Classic ASCVD risk factors are associated with ACS in pregnancy, and ESC 2025 adds pre-eclampsia, thrombophilia, transfusion, post-partum infection, multiparity and post-partum haemorrhage as additional risk factors.^[1]
• Causes: SCAD 43%, atherosclerosis 27%, coronary embolism 17% and vasospasm 2%; vasospasm has been associated with ergot derivatives used for lactation suppression or post-partum haemorrhage.^[1]
• ACS should be suspected with cardiac arrest, acute chest pain, dyspnoea, ischaemic ECG changes or raised cardiac biomarkers; presentation is the same as outside pregnancy, but SCAD tends to present more severely than non-SCAD ACS.^[1]
• STEMI in pregnancy involves the anterior wall in 70%–80% of cases.^[1]
• MINOCA should be treated as a working diagnosis that warrants further investigation.^[1]

Pregnancy-associated SCAD

Pregnancy-associated SCAD affects 1.81 per 100 000 pregnancies and may occur at any time during or after pregnancy, but more than 70% occur early post-partum, most commonly within the first week.^[1] Pregnancy-associated SCAD predominantly involves the left-sided coronaries, with multivessel involvement.^[1] The Fifth Universal Definition of MI (2026) says SCAD should be considered particularly in women under 50 and in pregnancy or the post-partum period.^[8] The Fifth Universal Definition classes SCAD among the acute coronary pathologies of primary myocardial infarction, with or without ST elevation.^[8]

• ESC 2025: PCI in SCAD carries more complications, particularly iatrogenic dissection and haematoma extension, so a conservative approach to revascularisation is advised in clinically stable women without active or ongoing ischaemia.^[1]
• ESC 2023 ACS (not specific to pregnancy): in SCAD, PCI is recommended only for patients with symptoms and signs of ongoing myocardial ischaemia, a large area of myocardium in jeopardy and reduced antegrade flow (Class I, Level C).^[9]
• ESC 2025: with left main or proximal vessel involvement, CABG may be considered depending on technical considerations and local expertise.^[1]
• ESC 2025: limited observational data suggest that beta-blockers (for example labetalol) and avoiding hypertension may be associated with a lower risk of recurrent SCAD; evidence favours single antiplatelet therapy with aspirin in conservatively managed SCAD.^[1]
• ESC 2025: women with previous SCAD should be carefully counselled about the risk of recurrence in a subsequent pregnancy.^[1]
• ESC 2026 cardiac rehabilitation: tailoring rehabilitation to women should be considered for women with ACS, chronic coronary syndromes, SCAD and HF, to improve enrolment and adherence (Class IIa, Level B1).^[12]

Revascularisation, antiplatelets and delivery after ACS

• ESC 2025 text: with high or very high-risk ACS, immediate coronary angiography and PCI, if indicated, are recommended (no class or level given in this sentence).^[1]
• Stent choice should not differ from that for non-pregnant women.^[1]
• Systemic thrombolysis may be an alternative if timely PCI is not available; recombinant tissue plasminogen activator does not cross the placenta but can cause bleeding, including subplacental bleeding.^[1]
• Figure 11 dosing for DAPT: clopidogrel 300–600 mg orally as a loading dose, then 75 mg once daily; aspirin 150–300 mg orally, or 75–250 mg i.v. if oral ingestion is not possible, as a loading dose, then 75–100 mg orally once daily.^[1]
• All pregnant women with ACS, and their foetus, should be monitored in an intensive cardiac care unit.^[1]
• Clopidogrel must be withheld for at least 5 days before neuraxial anaesthesia to reduce the risk of epidural haematoma.^[1]
• ESC 2025 gives an arbitrary minimum time to delivery in stable women of 2 weeks after ACS.^[1]
• Chronic coronary syndromes carry high risk (32% cardiovascular complications and 2% maternal mortality); pregnancy can preferably be considered when there is no residual ischaemia or LV dysfunction 12 months after the index event.^[1]

Recommendation Table 12: coronary artery disease and pregnancy

^[1]

ESC 2025 revised its ACS row: 2018 said an invasive strategy should be considered for NSTE ACS with high-risk criteria (Class IIa, Level C), and 2025 recommends managing ACS as in non-pregnant women (Class I, Level C).^[1]

Drugs in pregnancy and lactation

In pregnancy, increased gastrointestinal–hepatic metabolism, liver enzyme activity, glomerular filtration and plasma volume, changes in protein binding and lower serum albumin all contribute to changes in the pharmacokinetics of many drugs.^[1] For lactation, ESC 2025 uses the relative infant dose, and a value below 5%–10% is generally considered safe.^[1]

Cardiovascular drugs in pregnancy and lactation (ESC 2025 Section 5)

^[1]

US rows on lipid-lowering in pregnancy and lactation

^[11]

• Statin history: contraindicated in pregnancy since 1987, statins now remain contraindicated only during lactation; in July 2021 the US FDA said evidence was insufficient to conclude that statins increase miscarriage risk and requested removal of the contraindication.^[1]
• Nifedipine: a meta-analysis of 22 randomised trials (2595 hypertensive participants) found it significantly more effective at lowering BP than labetalol, hydralazine or methyldopa.^[1]
• Beta-blockers in ROPAC: small-for-gestational-age rates were higher with beta-blocker exposure (15.3% vs 9.3%); against metoprolol, labetalol was the least likely to cause it (0.2, 95% CI 0.1–0.4) and atenolol the most likely (2.3, 95% CI 1.1–4.9).^[1]
• Anti-arrhythmics: in women without structural heart disease, anti-arrhythmic drugs such as flecainide, sotalol and ibutilide can be used to prevent or terminate AF and flutter.^[1]

Hypertensive disorders of pregnancy

Hypertensive disorders affect 5%–15% of pregnancies worldwide and are the second most common medical complication of pregnancy after post-partum haemorrhage.^[1] Maternal risks include placental abruption, stroke, multiple organ failure and disseminated intravascular coagulation.^[1] In pre-eclampsia, the foetus faces IUGR in 25%, prematurity in 27% and intrauterine death in 4%.^[1]

ESC 2025 typically defines hypertension in pregnancy as systolic BP of 140 mmHg or more and/or diastolic BP of 90 mmHg or more.^[1] The readings are repeated office or hospital measurements on two separate occasions, or 15 min or more apart in severe hypertension (160/110 mmHg or more).^[1] The 2025 AHA/ACC guideline cites the ACOG definition: systolic BP of 140 mmHg or more or diastolic BP of 90 mmHg or more on 2 occasions at least 4 hours apart, with severe-range hypertension verified within 15 minutes to avoid treatment delays.^[5]

ESC 2025 Table 14: hypertensive disorders of pregnancy

^[1]

Eclampsia is new seizures or coma in a woman with pre-eclampsia, and HELLP syndrome (haemolysis, thrombocytopenia and raised transaminases) is usually considered a variant of pre-eclampsia.^[1]

Measurement and tests

• Measure BP at each encounter, sitting (or left lateral during labour), with a correctly sized cuff at heart level, using Korotkoff V for diastolic BP; only automatic devices validated for pregnancy should be used.^[1]
• Diagnosis by ambulatory BP monitoring is superior to office or home readings for predicting pregnancy outcomes.^[1]
• An sFlt-1/PlGF ratio below 38 can be used to reliably exclude pre-eclampsia over the next 7 days when it is clinically suspected.^[1]

Treatment

ESC 2025 says management depends on BP, gestational age and associated maternal and foetal risk factors.^[1] At 140–159/90–99 mmHg, BP control is mandatory with a target below 140/90 mmHg, and above 160/110 mmHg hospital admission is recommended.^[1] ESC 2025 reports that in two large trials, tight diastolic control (below 85–90 mmHg) in women with pre-existing hypertension was superior to less tight control (below 100–105 mmHg) and caused no harm.^[1] In mild gestational hypertension it seems reasonable to start treatment at 140/90 mmHg, but lowering diastolic BP below 80 mmHg is not recommended.^[1]

Recommendation Table 13: hypertensive disorders and pregnancy

^[1]

• Aspirin in practice: ESC 2025 says women with at least one high-risk or two moderate-risk factors for pre-eclampsia should be advised to take 75–150 mg daily at bedtime from week 12 to week 36/37, and advises stopping low-dose aspirin at week 36/37 when the indication is pre-eclampsia.^[1]
• Calcium supplements are recommended to prevent pre-eclampsia in women with low dietary calcium intake (below 600 mg/day).^[1]
• Salt restriction is not advised to reduce hypertensive disorders, although continuing a low-sodium diet is reasonable in pre-existing hypertension.^[1]
• ACE inhibitors, ARBs and direct renin inhibitors are strictly contraindicated; diuretics are not advised in gestational hypertension and pre-eclampsia because they reduce intravascular volume and uteroplacental perfusion.^[1]
• Figure 12C oral doses: labetalol 100 mg twice daily; metoprolol 100 mg twice daily; methyldopa 250 mg two or three times daily; nifedipine 5–10 mg, or 10 mg if BP is above 160/110 mmHg.^[1]
• In severe hypertension, gradual reduction to below 160/110 mmHg in hospital is mandatory, with continuous cardiotocographic monitoring.^[1]
• Hydralazine is a second-line option only if other drugs are not available, and sodium nitroprusside is the drug of last resort because prolonged treatment is associated with an increased risk of foetal cyanide poisoning.^[1]
• Pulmonary oedema with pre-eclampsia: the drug of choice is nitroglycerine by i.v. infusion at 5 μg/min, increased every 3–5 min to a maximum of 100 μg/min, with diuretics.^[1]
• Pre-eclampsia with severe features should be managed with a magnesium sulfate infusion to prevent eclampsia, in addition to early delivery.^[1]
• Magnesium toxicity can present with cardiac effects, including prolonged PR, QRS and QT intervals at 2.5–5 mmol/L, and can progress to AV block, bradycardia, hypotension and cardiac arrest at 6–10 mmol/L; if toxicity is suspected, stop the infusion and give 30 mL i.v. calcium gluconate.^[1]

Delivery and after

• ESC 2025 reports a UK randomised trial in late preterm pre-eclampsia (34–37 weeks): planned delivery within 48 h of diagnosis lowered maternal morbidity and severe maternal hypertension, but more neonates were admitted to neonatal intensive care.^[1]
• With well-managed hypertension alone, delivery should be planned around 39 weeks.^[1]
• Women with severe pre-eclampsia benefit from neuraxial anaesthesia to reduce the hypertensive response to pain.^[1]
• After delivery, methyldopa should be avoided because of the risk of post-partum depression; stop it within 2 days and change to an alternative.^[1]
• BP should be monitored in hospital, or with equivalent outpatient surveillance, for 72 h after birth and checked again at 7–10 days post-partum.^[1]

Other guidelines on hypertension in pregnancy

AHA/ACC 2025 pregnancy rows, and ESC 2024 rows not restated in full by ESC 2025

^{[5] [4] [1]}

The aspirin dose differs: AHA/ACC 2025 names 81 mg/day for individuals with hypertension who are planning a pregnancy or who become pregnant, while ESC 2025 recommends 75–150 mg daily from weeks 12 to 36/37 in women at moderate or high risk of pre-eclampsia.^[5][1] The AHA/ACC supportive text describes the CHAP trial, which randomised 2,408 women with chronic hypertension to treatment to below 140/90 mm Hg or to no treatment unless SBP reached 160 mm Hg or DBP 105 mm Hg.^[5] Treatment gave an 18% absolute risk reduction in the primary composite of preeclampsia with severe features, preterm birth, placental abruption or fetal or neonatal death, without evidence of more fetal growth restriction.^[5]

ESC 2024 rows that ESC 2025 now restates are dated history. ESC 2024 said systolic BP of 160 mmHg or more or diastolic BP of 110 mmHg or more can indicate an emergency, and that immediate hospitalisation should be considered (Class IIa, Level C).^[4] ESC 2025 calls it an emergency and recommends treatment in hospital (Class I, Level C).^[1] ESC 2024 recommended lowering BP below 140/90 mmHg but not below 80 mmHg diastolic in chronic and gestational hypertension (Class I, Level C).^[4] ESC 2025 now recommends aiming for systolic BP below 140 mmHg and diastolic BP below 90 mmHg in pregnant women (Class I, Level B), and its text on mild gestational hypertension says a diastolic BP reduction to below 80 mmHg is not recommended.^[1] ESC 2024 named dihydropyridine CCBs (preferably extended-release nifedipine), labetalol and methyldopa as first-line drugs (Class I, Level C); ESC 2025 gives methyldopa Class I, Level B and labetalol, metoprolol and dihydropyridine CCBs Class I, Level C.^[4][1] ESC 2024 said RAS blockers are not recommended during pregnancy (Class III, Level B).^[4] The ESC 2025 HF table and ESC 2026 HF say ACE inhibitors, ARBs, ARNIs, MRAs, ivabradine and SGLT2 inhibitors are not recommended during pregnancy (Class III, Level C).^[1][3] The ESC 2025 hypertension text calls ACE inhibitors, ARBs and direct renin inhibitors strictly contraindicated.^[1]

^{[1] [5]}

Planning delivery

ESC 2025 asks for an individualised delivery plan covering induction, labour, delivery and post-partum surveillance, made in shared decision-making with the pregnant woman.^[1] Vaginal delivery is recommended in most women with CVD (Class I, Level B); ESC 2025 notes that it is associated with less blood loss and lower risks of infection and venous thromboembolism.^[1] Planned caesarean section gives no maternal advantage over planned vaginal delivery and may be associated with adverse foetal outcomes.^[1]

• Timing: induction between 39 and 40 weeks reduces emergency caesarean section by 12% and stillbirth by 50% in women without CVD, and ESC 2025 says the benefit is likely to be greater with CVD; routine induction before 39 weeks is not recommended in stable CVD (Class III, Level C).^[1]
• Induction methods considered safe: mechanical methods, misoprostol, slow-release 10 mg dinoprostone, oxytocin and artificial rupture of membranes; a cervical ripening balloon might be preferable when a fall in systemic vascular resistance would be harmful.^[1]
• The correction of February 2026 changed the high-dose misoprostol figure in Section 4.5.2 from 600 mg to 600 µg.^[2]
• In mWHO 2.0 classes III–IV, oxytocin is generally the first-line uterotonic, with misoprostol and carboprost second line.^[1]
• Monitoring: in women with significant CVD, pulse oximetry, BP and continuous ECG monitoring may help detect early decompensation, arrhythmia and ischaemia; arterial lines are reserved for haemodynamic instability or its risk, and a right-heart catheter should be avoided in most cases.^[1]
• Analgesia reduces physical stress in labour, and spinal analgesia suits high-risk CVD when a faster sympathetic block is wanted.^[1]
• Endocarditis prophylaxis: systemic antibiotics may be considered for delivery in women at high risk (prosthetic valves, previous endocarditis, or cardiac transplant with residual valve defects) (Class IIb, Level C); in 2018 prophylaxis was not recommended (Class III, Level C).^[1]

Delivery on anticoagulation

Recommendation Table 3 (timing and mode of delivery): rows for women on anticoagulants

^[1]

• VKAs are stopped well before delivery because of slow VKA metabolism in the foetus.^[1]
• One strategy on therapeutic LMWH is to switch to i.v. UFH at least 36 h before planned delivery, targeting an aPTT of at least twice control; UFH can then be stopped 4–6 h before caesarean section, regional anaesthesia or anticipated vaginal delivery.^[1]
• In women on therapeutic-dose LMWH for non-MHV indications (any indication other than a mechanical heart valve), doses can be omitted for 24 h before caesarean section or anticipated vaginal delivery with no need for bridging.^[1]
• With a mechanical valve on LMWH plus aspirin, stopping aspirin 4 days before delivery should be considered.^[1]
• Urgent delivery after VKA use within the last 2 weeks: caesarean section is recommended to reduce the risk of foetal intracranial bleeding.^[1]
• When urgent delivery is required, i.v. four-factor prothrombin complex concentrate (4F-PCC), dosed by INR (25 U/kg for a therapeutic INR range of 2–4), is the preferred method for rapid INR normalisation, with vitamin K if needed.^[1]
• If 4F-PCC is not available, fresh frozen plasma is an alternative but reverses the INR more slowly and needs a larger fluid challenge; the foetus may stay anticoagulated for 8–10 days after maternal VKAs stop.^[1]
• Delivery soon after heparin (for example within 4–6 h of UFH with an aPTT not normalised, or within 12 h of therapeutic LMWH): give protamine sulfate, 1 mg per 1 mg enoxaparin within 8 h or 0.5 mg per 1 mg after 8 h, and 1 mg per 100 units of UFH.^[1]
• Late obstetric bleeding (after 24 h) is common; in ROPAC III it occurred on mean post-partum day 3.6, and VKAs should only start 7–14 days or later post-partum.^[1]
• Post-partum haemorrhage prevention: a slow i.v. infusion of 2 IU oxytocin over 10 min immediately after birth, then 12 mU/min for 4 h, reduces PPH risk with minimal cardiovascular effect.^[1]

^[1]

After delivery and the long view

The post-partum period brings significant haemodynamic changes and fluid shifts, with a risk of adverse outcomes such as hypertension, HF or stroke.^[1] For women at highest HF risk, or with HF symptoms in pregnancy or delivery, admission to an intensive cardiac care unit for the first 24–48 h should be considered.^[1] Lactation can be inhibited with standard doses of cabergoline in general, or bromocriptine in PPCM.^[1] About 1 in 3 mothers with CVD report post-partum depressive symptoms, against about 10%–20% of new mothers in general.^[1]

Recommendation Table 23: long-term effects of adverse pregnancy outcomes (selected rows)

^[1]

Special populations

• Adolescents with congenital or inherited heart disease: start reproductive health discussions early, ideally from menarche.^[1]
• Assisted reproduction: all women with CVD embarking on fertility treatment should have an individual VTE risk assessment, given the risk associated with these techniques; ovulation-induction drugs are associated with an increased risk of DVT and PE.^[1]
• Older mothers: compared with women under 25, the odds ratio of AF episodes was 5.2 in women aged 40 or more.^[1]
• Lactating women: use the relative infant dose (below 5%–10% generally considered safe), and remember that statins remain contraindicated during lactation.^[1]
• Low-resource settings: for anticoagulation, ESC 2025 says regional differences, including lower availability of anti-factor Xa monitoring in low- and middle-income countries as indicated by ROPAC III, need to be taken into account.^[1]

Guidelines, evidence and regional differences

The ESC guidelines checked for this topic are the 2025 pregnancy guideline with its February 2026 correction, 2026 HF, 2026 cardiac rehabilitation, 2025 valve (ESC/EACTS), 2025 dyslipidaemia focused update (ESC/EAS), 2024 hypertension, 2024 AF, 2023 ACS and 2023 cardiomyopathies. Also checked were the Fifth Universal Definition of MI (2026), the 2025 AHA/ACC BP, 2025 ACC/AHA ACS and 2026 ACC/AHA dyslipidemia guidelines, and the SOMANZ 2023 summary. Other ACC/AHA documents with pregnancy rows, including the 2020 valve, 2023 AF and 2025 adult congenital heart disease guidelines, were not checked for this topic. ESC 2026 HF and the ESC/EACTS 2025 valve guideline both refer readers to the 2025 ESC pregnancy guideline for detailed guidance.^[3][10]

• What changed since 2018 (ESC 2025 Table 5): a bioprosthesis moved from should be considered (Class IIa, Level C) to recommended over a mechanical valve in young women contemplating pregnancy who need a prosthesis (Class I, Level B).^[1]
• ESC 2025 Table 5: in the second and third trimesters, 2018 said LMWH with anti-factor Xa monitoring and dose adjustment may be considered in women needing a high VKA dose, after patient information and consent (Class IIb, Level C); 2025 says continuing VKAs until the 36th week should be considered in women with prosthetic heart valves at higher risk of thrombosis (Class IIa, Level C).^[1]
• ESC 2025 Table 5: in HCM, 2018 recommended continuing beta-blockers in women already taking them (Class I, Level C); 2025 says continuing beta-blockers should be considered in cardiomyopathy, with foetal growth follow-up (Class IIa, Level C).^[1]
• Same-season ESC documents differ on valve choice: ESC/EACTS 2025 valve says a biological valve should be considered in women contemplating pregnancy (Class IIa, Level C), while ESC 2025 pregnancy recommends a bioprosthetic over a mechanical valve in young women contemplating pregnancy who need a prosthesis (Class I, Level B).^[10][1]
• ESC 2024 AF, before the pregnancy guideline, gave verapamil as a rate-control option if beta-blockers fail but said it should be avoided in the first trimester; ESC 2025 calls oral verapamil safe, with no teratogenicity observed.^[6][1]
• Among the ESC 2025 rows on this page, the only Level A row is low-dose aspirin for pre-eclampsia prevention, and most of the others are Level C.^[1]

No NHFA/CSANZ guideline on cardiovascular disease in pregnancy was found in the register used for this topic; the Australian and New Zealand guideline held is the SOMANZ 2023 hypertension summary. SOMANZ presents its recommendations as evidence-based recommendations or practice points.^[7]

Exam pearls

• mWHO 2.0 class II–III or above means Pregnancy Heart Team care from pre-pregnancy to post-partum (ESC 2025, Class I, Level C).^[1]
• The PPCM definition uses LVEF below 45% (HF without any other cause, mainly in the peripartum period or the months after delivery, termination or miscarriage).^[1]
• Bromocriptine in PPCM may be considered in addition to optimal HF treatment (Class IIb, Level B), and adding at least prophylactic LMWH to it should be considered (Class IIa, Level C).^[1]
• Mechanical valve: LMWH is not recommended when anti-factor Xa monitoring is not available (Class III, Level C).^[1]
• If delivery starts on a VKA, or less than 2 weeks after stopping it, caesarean section is recommended for foetal protection (Class I, Level C).^[1]
• SCAD is the most frequent cause of ACS in pregnancy and post-partum (43%), and more than 70% of pregnancy-associated SCAD occurs early post-partum.^[1]
• If DAPT is required, clopidogrel is recommended as the P2Y12 inhibitor of choice in pregnancy (Class I, Level C); ticagrelor is contraindicated because of embryotoxicity.^[1]
• Atenolol is excluded from the beta-blocker rows and is not recommended in pregnancy.^[1]
• Cardiac arrest at 20 weeks or more: continuous manual left uterine displacement during CPR is recommended to relieve aortocaval compression (Class I, Level C).^[1]
• Cardiac arrest: immediate caesarean section at the site of arrest should be considered and immediately prepared if there is no ROSC after 4 min of resuscitative efforts and the foetus is viable, taking gestational age, comorbidities and the available level of medical care into account (Class IIa, Level C).^[1]

References12ShowHide

1. [1]De Backer J, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294
2. [2], et al. Correction to: 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy: Developed by the task force on the management of cardiovascular disease and pregnancy of the European Society of Cardiology (ESC) Endorsed by the European Society of Gynecology (ESG). Eur Heart J, 2026.PMID 41428090
3. [3]Køber L, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J, 2026.PMID 42661420
4. [4]McEvoy JW, et al. 2024 ESC Guidelines for the management of elevated blood pressure and hypertension. Eur Heart J, 2024.PMID 39210715
5. [5]Jones DW, et al. 2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2025.PMID 40815242
6. [6]Van Gelder IC, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J, 2024.PMID 39210723
7. [7]Shanmugalingam R, et al. A summary of the 2023 Society of Obstetric Medicine of Australia and New Zealand (SOMANZ) hypertension in pregnancy guideline. Med J Aust, 2024.PMID 38763516
8. [8]Mills NL, et al. Fifth Universal Definition of Myocardial Infarction (2026): On behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS) and the Society of Thoracic Surgeons (STS) Affirmation of Value by the Society for Cardiovascular Angiography and Interventions (SCAI). Glob Heart, 2026.PMID 42666939
9. [9]Byrne RA, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J, 2023.PMID 37622654
10. [10]Praz F, et al. 2025 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J, 2025.PMID 40878295
11. [11]Blumenthal RS, et al. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2026.PMID 41824590
12. [12]Bäck M, et al. 2026 ESC Guidelines on cardiac rehabilitation. Eur Heart J, 2026.PMID 42661418