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Inherited Cardiac Conditions reference

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Pregnancy in inherited cardiac conditions

mWHO Classification of Cardiovascular Risk in Pregnancy
ClassRiskManagement
mWHO INo detectable increased maternal mortality; no/mild morbidity increaseLocal obstetric care; annual or once per pregnancy cardiology review
mWHO IISmall increased risk of maternal mortality; moderate morbiditySpecialist centre; cardiology review each trimester
mWHO IIISignificantly increased risk; expert counselling essentialExpert multidisciplinary Pregnancy Heart Team; monthly or more frequent review; delivery in tertiary centre
mWHO IVExtremely high maternal riskDetailed individualized counselling before conception; if pregnancy has already occurred, the Pregnancy Heart Team should discuss all options, including continuation with expert care and termination, with the decision led by the patient

The class shown for each condition below is a general starting point, not a fixed assignment. Per the 2025 ESC pregnancy guideline, actual risk should be individualized by a Pregnancy Heart Team using the specific risk modifiers listed for that condition (ventricular function, arrhythmia history, aortic dimensions, genotype, etc.), and can move within or across mWHO classes accordingly. All women with an inherited cardiac condition should have pre-pregnancy counselling from this team.[1][14]

Cardiomyopathies

Condition mWHO Class Key Risks Medications: Continue Medications: STOP / Avoid Delivery / Monitoring
HCM II–III
  • LVOTO
  • LVEF
  • Symptoms
 LVOTO can worsen with reduced preload; higher risk with reduced LVEF, symptomatic obstruction or prior arrhythmia, but risk should be individualized by a Pregnancy Heart Team rather than assigned to a fixed class.[1][2][14]
  • Beta-blockers (bisoprolol/metoprolol preferred)
  • Verapamil if beta-blocker intolerant
  • Disopyramide (1st trimester, uterotonic)
  • Vasodilators
  • Mavacamten (no data)
  • Echo every trimester, ± more if obstructive
  • Vaginal delivery preferred; shortened 2nd stage
  • Avoid hypovolaemia
  • Epidural preferred
DCM III–IV
  • LVEF
  • Functional class
 Risk rises with lower LVEF and worse functional class, and a history of peripartum cardiomyopathy carries a recognised risk of recurrence, but there is no single validated LVEF cut-off that makes pregnancy universally contraindicated; risk should be assessed individually by a Pregnancy Heart Team.[1][3][14]
  • Beta-blocker
  • Diuretic (furosemide) if pulmonary oedema
  • LMWH if LVEF <30%
  • Digoxin for rate control
  • ACEi/ARB/ARNI (teratogenic, stop pre-conception)
  • Spironolactone (antiandrogenic)
  • SGLT2i (limited data)
  • Amiodarone (last resort)
  • Echo monitoring individualized to severity (more frequent if reduced LVEF)
  • Mode/timing of delivery and any need for invasive monitoring decided by the Pregnancy Heart Team based on haemodynamic status at the time, not a fixed LVEF-based rule
ACM / ARVC II–III Pregnancy raises sympathetic tone and volume load, which can increase arrhythmic risk, particularly with a history of ventricular arrhythmia or significant RV/LV dysfunction; risk should be assessed individually using baseline function, arrhythmia history and genotype where known, rather than assigned to a fixed class.[1][2][4][14]
  • Beta-blockers (continue, max tolerated)
  • Sotalol if required (monitor QTc)
  • Flecainide (limited safety data, use only if essential)
  • Amiodarone (last resort)
  • Echo + Holter surveillance individualized to risk (typically each trimester or more often)
  • Epidural generally preferred (minimises catecholamines)
  • Mode and timing of delivery decided by the Pregnancy Heart Team based on functional status and arrhythmia history, not a fixed rule
  • Defibrillator available at delivery
Cardiac Amyloidosis III–IV Restrictive physiology can worsen in pregnancy and systemic disease involvement adds risk; ATTR amyloidosis in women of childbearing age is rare, and management should be individualized by an expert Pregnancy Heart Team given the limited evidence base.[1][14]
  • Diuretics (careful)
  • Rate control
  • Tafamidis (no safety data, stop pre-conception)
  • Diflunisal
  • Patisiran/inotersen (no data)
 Expert MDT, individual assessment; very rare scenario.

Channelopathies

Condition mWHO Class Key Risks Medications: Continue Medications: STOP / Avoid Delivery / Monitoring
LQTS I–II Generally well tolerated. Postpartum risk is meaningfully higher, LQT2 in particular (within 9 months).[5][6] Risk increases with QTc >500ms or prior arrest; individualize surveillance intensity accordingly.[1][14]
  • Beta-blockers, essential; do not stop
  • Nadolol or propranolol preferred
  • Continue into postpartum (increased risk)
  • Monitor neonate for bradycardia/hypoglycaemia
 Check any QT-prolonging drug against a current resource (e.g. crediblemeds.org) and the BNF/SmPC, with pharmacy or anaesthetic input where available, rather than assuming a simple substitution is safe:
  • Ondansetron (recognised QT-prolongation risk)
  • Metoclopramide/cyclizine (not established as electrically neutral either)
  • Erythromycin, azithromycin
  • Some antifungals
  • Droperidol
  • Continuous ECG monitoring in labour
  • Avoid hypokalaemia (IV K⁺ supplementation)
  • Epidural preferred (reduces catecholamines)
  • Defibrillator immediately available
Brugada II–III Fever (common peripartum) can precipitate VF. Vagal predominance in labour may unmask a Brugada pattern. Higher risk if prior cardiac arrest or spontaneous type 1 ECG; individualize monitoring accordingly.[1][4][14]
  • Treat all fever aggressively with paracetamol
  • ICD if high-risk, should be implanted pre-pregnancy
  • Sodium channel blockers (bupivacaine; use ropivacaine instead)
  • Propofol (avoid as sole anaesthetic)
  • Check drugs at brugadadrugs.org
  • Continuous ECG monitoring
  • Defibrillator available
  • Epidural with ropivacaine preferred
  • Temperature monitoring throughout labour and postpartum
CPVT II–III Labour pain/catecholamine surges may trigger VT/VF. Sympathetic activation should be minimised where possible. Beta-blocker adherence is important throughout.[1][4][14]
  • Beta-blockers (nadolol/propranolol), do not stop; maximise dose
  • Flecainide if already established add-on therapy
  • Avoid catecholamine-releasing GA agents (ketamine, ephedrine)
  • Avoid adrenaline-containing dental/local anaesthetics
  • Epidural analgesia strongly recommended, primary strategy to blunt sympathetic response
  • Continuous ECG + defibrillator
  • Avoid 2nd stage prolongation
Short QT Syndrome Not established
  • Very limited evidence
 Data are too limited to assign a reliable risk class; arrhythmia risk is possible during labour/postpartum given the condition's rarity, so care should be individualized by an expert team.[4][14]
  • Quinidine if established
  • Avoid drugs shortening QT
 Drugs shortening QT interval
  • Continuous ECG
  • Defibrillator available
  • Expert MDT (very limited evidence base)

Aortopathies & Connective Tissue Disorders

Condition mWHO Class Aortic Thresholds Medications Delivery Key Points
Marfan syndrome III–IV
  • Root diameter
  • Growth rate
  • Dissection history
 Risk rises substantially with a larger or growing aortic root or prior dissection; there is no single universal diameter cut-off, and the decision (including consideration of prophylactic surgery before conception) should be individualized by an aortopathy/Pregnancy Heart Team.[1][7][8]
  • Continue: beta-blocker (bisoprolol/atenolol/propranolol)
  • Stop pre-conception: losartan/ACEi (teratogenic)
  • Echo every 4–6 weeks
  • Vaginal delivery with epidural + shortened 2nd stage (avoid Valsalva) if stable
  • Caesarean if root >40mm or rapid growth
  • Postpartum aortic imaging at 6 weeks and 6 months
  • Dissection risk persists postpartum
  • Breastfeeding: beta-blockers acceptable (monitor infant)
Loeys-Dietz syndrome Generally high risk
  • Gene-specific
  • Patient-specific
 Dissection can occur at smaller diameters than in Marfan, and elsewhere in the arterial tree, not just the aortic root. Risk is gene- and patient-specific rather than defined by a single diameter cut-off; older case series quoting maternal mortality of 25-50% should not be presented as a general estimate for all LDS pregnancies. Decision individualized by an aortopathy/Pregnancy Heart Team.[1][9]
  • Continue: beta-blocker
  • Stop pre-conception: losartan/ACEi
  • ARB beneficial (TGF-β suppression) but teratogenic
  • Tertiary expert centre only
  • Delivery mode individual; avoid Valsalva
  • Full MDT including aortic surgery on standby
  • Higher-risk pregnancy requiring detailed individualized counselling
  • Even with prophylactic surgery pre-pregnancy, residual risk from non-root dissections persists
  • Pan-arterial imaging post-delivery
Vascular Ehlers-Danlos syndrome (vEDS) Generally high risk
  • Variant-specific
  • Vascular history
 Risk of arterial, uterine or bowel rupture is genuinely elevated but not universal or automatically prohibitive; published mortality estimates per pregnancy vary considerably across cohorts, and risk depends on the specific COL3A1 variant and prior vascular history (a previous dissection or rupture confers materially higher risk than no prior vascular event). Decision individualized by a vascular-genetics Pregnancy Heart Team.[14]
  • Continue: beta-blocker (celiprolol where already established)
  • Stop pre-conception: losartan/ACEi/ARB
  • Mode and timing individualized: weighs tissue-injury risk from labour/vaginal delivery against surgical haemorrhage/organ-injury risk at caesarean in fragile tissue; caesarean is not automatically safer
  • Rupture risk continues postpartum, so specialist access and urgent-symptom education continue for several weeks after delivery
  • Pre-pregnancy counselling: non-coercive, patient-led, variant-informed; covers the realistic range of outcomes and all family-building options (continuing pregnancy with surveillance, deferring pregnancy, surrogacy, adoption)
  • No validated fixed review schedule or blood-pressure target; monitoring intensity set by the MDT based on individual risk
Bicuspid aortic valve (BAV) I–III
  • Depends on severity
 Pre-pregnancy aortic surgery is recommended in BAV at root diameter ≥50mm (2022 ACC/AHA); 45–50mm individualised with expert MDT. Caesarean is reasonable if root ≥45mm; vaginal delivery if <40mm and stable.[7]
  • Beta-blocker if aortopathy
  • Stop ACEi/ARB pre-conception if used
  • Echo each trimester
  • If severe AS or AR: discuss valve intervention pre-pregnancy
  • Vaginal delivery possible in mild-moderate disease
  • Screen for coarctation (increased BP in pregnancy if coarctation present)
  • FBN1/SMAD3 testing if family history
Turner syndrome III–IV
  • If aortic disease
 BAV in ~30%; coarctation ~10%; aortic dilatation, use aortic size index (ASI >2.5 cm/m² = high risk). ASI >2.5 cm/m²: high risk, pregnancy generally not advised. Assess pre-pregnancy with CMR or CT and weigh other risk modifiers (BAV, coarctation, hypertension).[1]
  • Antihypertensives
  • Avoid ACEi/ARB
  • Aortic imaging pre-pregnancy and each trimester
  • If ASI >2 cm/m²: tertiary centre delivery
  • Pregnancy usually via oocyte donation
  • Obstetric complications high (hypertension, pre-eclampsia)
  • Postpartum aortic monitoring

Storage & Infiltrative Conditions

Condition mWHO Class Key Risks Medications Monitoring & Delivery
Fabry disease II
  • If stable cardiac/renal function
 Generally well tolerated if no significant cardiac or renal involvement. CKD increases obstetric risk. Neuropathic pain may worsen.[12]
  • Continue: ERT (agalsidase alfa 0.2mg/kg q2wks or agalsidase beta 1mg/kg q2wks); continuation may be considered where clinically indicated after specialist discussion, evidence reassuring but limited to case series[12]
  • Avoid: migalastat (inadequate safety data)
  • Stop ACEi/ARB pre-conception
  • Echo + renal function each trimester
  • Vaginal delivery generally possible
  • Monitor neonate if ERT continued (no known neonatal effects)
Pompe disease II–III Respiratory involvement may compromise pregnancy, assess FVC. Cardiac involvement usually mild in late-onset forms.
  • Alglucosidase alfa (ERT), limited data; generally continued in specialist centres
  • Respiratory support if needed
  • Respiratory function assessment essential
  • May require assisted ventilation
  • MDT including respiratory medicine

Neuromuscular Conditions

Condition mWHO Class Key Risks Medications Monitoring & Delivery
DMD/BMD female carriers II–III
  • If LV dysfunction
 ~30% of female DMD carriers have LV dysfunction, often subclinical.[10] Pregnancy can unmask or worsen cardiomyopathy; risk should be assessed individually by a Pregnancy Heart Team using baseline LV function, and obstetric complications may be higher if skeletal muscle involvement is present.[1][14]
  • Continue: beta-blocker if LV dysfunction present
  • Stop pre-conception: ACEi/ARB/eplerenone
  • SGLT2i: avoid (limited data)
  • Echo at booking + each trimester
  • Vaginal delivery generally possible; epidural preferred
  • Monitor respiratory function if skeletal myopathy present
Myotonic dystrophy type 1 (DM1) II–III Cardiac arrhythmias (AV block, VT), uterine atony (prolonged labour), respiratory compromise.[11] Maternal and congenital myotonic dystrophy risk in infant (anticipation, maternal transmission worse).[1]
  • ICD/pacemaker if indicated pre-pregnancy
  • Avoid drugs worsening myotonia
  • ECG/Holter each trimester
  • Anaesthetic risk, detailed assessment essential
  • Oxytocin for uterine atony; PPH risk
  • Neonatal assessment for congenital DM1
Friedreich ataxia II–III Hypertrophic or dilated cardiomyopathy; arrhythmias. Neurological disease affects mobility and labour management.[1]
  • Continue cardiac medications (beta-blocker if LV dysfunction)
  • Omaveloxolone: stop pre-conception (no safety data)
  • Cardiology + neurology MDT
  • Echo each trimester
  • Regional anaesthesia may be limited by scoliosis; anaesthetic assessment essential

Cardiac Drug Safety in Pregnancy: Quick Reference[1][14]

Drug / Class ICC Indications Pregnancy Safety Recommendation
Beta-blockers (bisoprolol, metoprolol, propranolol, nadolol, atenolol) HCM, DCM, ARVC, LQTS, CPVT, Marfan, DCM Generally considered compatible, and usually continued where indicated. They cross the placenta, so monitor fetal growth and the neonate for bradycardia and hypoglycaemia. Atenolol associated with IUGR (avoid in 1st trimester).[1] Bisoprolol/metoprolol/propranolol preferred. Continue, do not stop
Verapamil HCM (if beta-blocker intolerant) Generally acceptable. May cause neonatal bradycardia/hypotension near term. Avoid high doses. Acceptable if beta-blocker not tolerated; lowest effective dose
Sotalol ARVC Acceptable safety profile in pregnancy. Monitor foetal HR. QTc monitoring required. Acceptable, monitor foetal and maternal QTc
Diuretics (furosemide) DCM, HF Generally acceptable if used judiciously. Avoid excessive dose, which may reduce uteroplacental perfusion. Acceptable for pulmonary oedema; use minimum effective dose
LMWH (enoxaparin, dalteparin) DCM, AF, mechanical valves Drug of choice for anticoagulation in pregnancy, does not cross placenta Preferred anticoagulant throughout pregnancy; does not cross the placenta. Requires dose adjustment and monitoring
Disopyramide HCM Uterotonic, may stimulate contractions (especially 1st trimester). Limited data overall. Avoid in 1st trimester; use only if benefit > risk with expert advice
Flecainide ARVC, CPVT Limited human data. Used for foetal arrhythmias, some foetal safety data. Avoid unless essential. Use only if essential; specialist advice required
Spironolactone DCM Antiandrogenic, animal studies show feminisation of male foetus at high doses Avoid; switch to eplerenone (less antiandrogenic) or stop if safe
SGLT2 inhibitors (dapagliflozin, empagliflozin) DCM No adequate human data; animal embryotoxicity concerns Stop pre-conception or as soon as pregnancy confirmed
Migalastat (Galafold) Fabry disease No human data Stop pre-conception; switch to ERT if treatment required
Warfarin Mechanical heart valves, AF Warfarin embryopathy <12 weeks; foetal intracranial haemorrhage risk. Acceptable weeks 14–34 for mechanical valves if dose ≤5mg/day. Mechanical valve specific use only; avoid <12 weeks and near term; switch to LMWH peripartum
ACE inhibitors (ramipril, lisinopril, perindopril) DCM, Duchenne Teratogenic, renal agenesis, oligohydramnios, neonatal renal failure, skull ossification defects (2nd/3rd trimester).[1] STOP pre-conception; switch to alternative
ARBs (losartan, candesartan, valsartan) Marfan, DCM, Fabry Same fetotoxicity as ACEi, contraindicated from conception.[1] STOP pre-conception
Sacubitril/valsartan (ARNI) DCM Valsartan component fetotoxic; sacubitril, no human data STOP pre-conception; switch to beta-blocker ± diuretic
Amiodarone ARVC, DCM Foetal hypothyroidism, goitre, IUGR, premature birth, neonatal bradycardia. High iodine content. Last resort only.[1] Avoid, use only for life-threatening arrhythmia uncontrolled by other agents
Mavacamten HCM (obstructive) No human data; animal reproductive toxicity.[2] Stop pre-conception; effective contraception required (CYP2C19 metabolism, drug holidays)
DOACs (apixaban, rivaroxaban, edoxaban, dabigatran) AF in various conditions Foetal and embryo toxicity in animal studies; no human safety data; cross placenta.[1] Contraindicated in pregnancy, switch to LMWH pre-conception

Pre-Pregnancy Genetic Counselling

Key Principles
  • Genetic counselling should be offered to all patients with an ICC and their partners before conception.[1][13]
  • Ideally initiated at diagnosis, not at point of pregnancy planning (allows time for family decisions)
  • Involves: inheritance pattern, risk to offspring, available reproductive options, implications for family members
  • Refer to regional clinical genetics service; joint cardiac-genetics clinic optimal

Inheritance Patterns & Offspring Risk by Condition

Condition Inheritance Risk to Offspring Penetrance Notes
HCM (MYBPC3, MYH7) Autosomal dominant 50% per child Variable, MYBPC3 ~65% by age 50; MYH7 >95%.[2] De novo mutations ~5%. Cascade testing of 1st-degree relatives.
DCM (LMNA, TTN, FLNC etc.) Autosomal dominant (most) 50% per child LMNA >90%; TTN 30–40%; variable by gene.[2] Early cardiac surveillance in gene-positive offspring. LMNA/FLNC, higher arrhythmic risk that may justify ICD consideration earlier than conventional thresholds, individualised by risk model/phenotype.
ACM / ARVC (PKP2, DSP etc.) Autosomal dominant (most); AR (Naxos/Carvajal) 50% per child (AD); 25% (AR) 30–50% (PKP2); >90% males (TMEM43) Exercise restriction advice for gene-positive offspring. Clinical screening from childhood.
LQTS (KCNQ1, KCNH2, SCN5A) Autosomal dominant (Romano-Ward); AR (Jervell-Lange-Nielsen, deaf) 50% per child 25–75% (AD); ~100% (AR) Neonatal ECG ± genetic testing. Beta-blocker started promptly if QTc prolonged. JLN: if both parents carry KCNQ1/KCNE1 variants, 25% risk of severe phenotype in offspring.
Brugada (SCN5A) Autosomal dominant; incomplete penetrance 50% per child 15–35%; male-predominant expression ~70% genetically elusive. Cascade ECG ± genetic testing in family. Fever protocols for gene-positive children.
CPVT (RYR2, CASQ2) RYR2: autosomal dominant; CASQ2: autosomal recessive 50% (RYR2); 25% affected, 50% carrier (CASQ2) >80% (RYR2) Exercise stress test in gene-positive children. Start beta-blocker immediately if symptomatic.
Fabry disease (GLA) X-linked (GLA on Xq22) Sons: 100% unaffected (receive Y chr); daughters: 100% obligate carriers. If mother affected: 50% sons affected, 50% daughters carriers. Males: near 100%. Females: variable (lyonisation). Female carriers have variable expression, many develop significant disease. Neonatal/early testing recommended for male carriers.
Marfan (FBN1) Autosomal dominant 50% per child Near 100% (high penetrance, variable expressivity).[8] ~25% de novo. Clinical assessment of offspring at birth and periodically. Early beta-blocker if aortic dilation.[8]
Loeys-Dietz (TGFBR1/2, SMAD3, TGFB2/3) Autosomal dominant 50% per child High but variable by gene and variant Full aortic imaging of gene-positive offspring from early childhood. More aggressive than Marfan.
Duchenne (DMD) X-linked recessive Female carrier: 50% of sons affected, 50% of daughters carrier Males: ~100%. Females: carriers may have cardiac involvement (~30%). Carrier females: cardiac surveillance. PGT-M available. Pre-implantation or prenatal diagnosis (CVS/amniocentesis) important option.

Reproductive Options for Couples with ICC

Option Description Considerations
Natural conception + postnatal testing Conceive naturally; test child after birth (or at appropriate age) Simple; no intervention. Child will require surveillance if gene-positive. Discuss age of testing (respect child autonomy for adult-onset conditions).
Prenatal diagnosis (PND): CVS or amniocentesis Chorionic villus sampling (10–13 wks) or amniocentesis (15–20 wks) for foetal genetic testing Enables decision whether to continue pregnancy. Risk of miscarriage ~0.5–1%. Available on NHS. Psychological impact of result significant.
Preimplantation genetic testing, monogenic (PGT-M) IVF with embryo biopsy + genetic testing before transfer; only unaffected embryos implanted.[13] Avoids pregnancy termination decision. Requires IVF (cycles, cost, success rate ~25–40%/cycle). HFEA licensed centre required. Lead time ~12 months. NHS-funded in some regions for high-penetrance conditions.
Donor gametes (sperm or egg donation) Use unaffected donor, removes genetic transmission risk from one parent Eliminates transmission from carrier parent. Requires donor services; legal and psychological counselling. Not suitable if both parents carry pathogenic variants.
Adoption / fostering Parenting without genetic transmission Valid option, discuss without bias. Process can be lengthy. No medical contraindication from ICC itself.

PGT-M requires identification of the familial pathogenic variant in advance. Couples should be referred to clinical genetics and reproductive medicine well before planned conception. NHS funding criteria vary by region and condition penetrance.

References & Review Date

Last reviewed: July 2026

  1. Regitz-Zagrosek V, et al. 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy. Eur Heart J. 2018;39(34):3165–3241. DOI: 10.1093/eurheartj/ehy340
  2. Arbelo E, et al. 2023 ESC Guidelines for the management of cardiomyopathies. Eur Heart J. 2023;44(37):3503–3626. DOI: 10.1093/eurheartj/ehad194
  3. McDonagh TA, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599–3726. DOI: 10.1093/eurheartj/ehab368
  4. Zeppenfeld K, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022;43(40):3997–4126. DOI: 10.1093/eurheartj/ehac262
  5. Seth R, et al. Long QT syndrome and pregnancy. J Am Coll Cardiol. 2007;49(10):1092–1098. DOI: 10.1016/j.jacc.2006.09.054
  6. Rashba EJ, et al. Influence of pregnancy on the risk for cardiac events in patients with hereditary long QT syndrome. Circulation. 1998;97(5):451–456. DOI: 10.1161/01.CIR.97.5.451
  7. Erbel R, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. Eur Heart J. 2014;35(41):2873–2926. DOI: 10.1093/eurheartj/ehu281
  8. Loeys BL, et al. The revised Ghent nosology for the Marfan syndrome. J Med Genet. 2010;47(7):476–485. DOI: 10.1136/jmg.2009.072785
  9. MacCarrick G, et al. Loeys-Dietz syndrome: a primer for diagnosis and management. Genet Med. 2014;16(8):576–587. DOI: 10.1038/gim.2014.11
  10. McNally EM, et al. Contemporary Cardiac Issues in Duchenne Muscular Dystrophy. Circulation. 2015;131(18):1590–1598. DOI: 10.1161/CIRCULATIONAHA.114.015151
  11. Groh WJ, et al. Electrocardiographic abnormalities and sudden death in myotonic dystrophy type 1. N Engl J Med. 2008;358(25):2688–2697. DOI: 10.1056/NEJMoa062800
  12. Germain DP. Fabry disease. Orphanet J Rare Dis. 2010;5:30. DOI: 10.1186/1750-1172-5-30
  13. Musunuru K, et al. Genetic Testing for Inherited Cardiovascular Diseases: A Scientific Statement From the American Heart Association. Circ Genom Precis Med. 2020;13(4):e000067. DOI: 10.1161/HCG.0000000000000067
  14. 2025 ESC Guidelines for the management of cardiovascular disease during pregnancy. Eur Heart J. 2025. DOI: 10.1093/eurheartj/ehaf193