Pregnancy and HTN

Cindy M. Martin, M.D.

Section Head - Advanced Heart Failure, Transplantation, and Mechanical Circulatory Support Director - Adult Congenital and Cardiovascular Genetics Center Associate Professor of Medicine, University of Minnesota Disclosures

• I have no financial disclosures • I am not pregnant • I have never been pregnant • I have >400 reasons not to become pregnant and most have nothing to do with anything discussed in this talk Objectives

• Discuss the hemodynamic changes during pregnancy • Review the definitions and treatment of pregnancy associated HTN conditions • Review CVD risk associated with pregnancy complications Pregnancy and the Heart • 2-4% of pregnancies in women without preexisting cardiac abnormalities are complicated by maternal CV disease • The risk of CVD in pregnancy is increasing – In the United States, the rate of pregnancy-relate maternal mortality increased from 7.2 deaths per 100000 live births (1987) to 17.8 deaths per 100000 live births (2011) • Increased women with CHD – In 2000, there were an estimated 1 million adult patients in the US with congenital heart disease (CHD), with the number increasing by 5% yearly – Deliveries in women with CHD increased more than 63% compared to women without CHD (34.5% vs 21.3%; 1998-2007) • Advancing maternal age • Increased incidence of risk factors, including diabetes mellitus, hypertension, pre-eclampsia, and multifetal pregnancies Hemodynamic Changes during Pregnancy

• Blood Volume – increases 40-50% • Heart rate – increases 10-15 bpm • SVR and PVR – decreases • Blood Pressure – decreases 10mmHg • Cardiac Output – increases 30-50% – Peaks at end of second trimester and plateaus until delivery • These changes are usually well tolerated Physiologic Changes in Pregnancy CV Exam During Pregnancy

• Brisk and full carotid upstroke • JVP normal or mildly increased • Displaced and enlarged apical impulse • 96% will have SEM (usually not loud) • 88% will have wide loud split S1 • 84% will have a loud S3 • Not normal to have S4, DM, or fixed split S2 Proposed CHD Pregnancy Risk Assessment Models

• CARPREG (2001) • ZAHARA (2010) • WHO CLASSIFICATION (2014) • CARPREG II (2018) Who IV - 27% event risk

• Moderate LV impairment (EF 30–45%) • Previous PPCM with nrl LVEF (>50% • Mechanical valve • Systemic right ventricle nrl or mildly decreased EF • Fontan circulation uncomplicated. • Unrepaired cyanotic heart disease • Other complex CHD • Moderate mitral stenosis • Severe asymptomatic aortic stenosis • Moderate aortic dilatation – (40–45 mm in Marfan syndrome or other HTAD; 45–50 mm in bicuspid aortic valve, Turner syndrome ASI 20–25 mm/m2, tetralogy of Fallot <50 mm) • Ventricular tachycardia Who V - 39% event risk Pregnancy Contraindicated • Pulmonary arterial hypertension • Severe systemic ventricular dysfunction (EF <30% or NYHA class III–IV) • Previous peripartum cardiomyopathy with any residual LV impairment • Severe mitral stenosis • Severe symptomatic aortic stenosis • Systemic right ventricle with mod or sev decreased ventricular function • Severe aortic dilatation – (>45 mm in Marfan syndrome or other HTAD, >50 mm in bicuspid aortic valve, Turner syndrome ASI >25 mm/m2, tetralogy of Fallot >50 mm) • Vascular Ehlers–Danlos • Severe (re)coarctation • Fontan with any complication Pregnancy Outcomes in Women With Heart Disease The CARPREG II Study

• Candice K. Silversides, MD, MS, Jasmine Grewal, MD, Jennifer Mason, RN, Mathew Sermer, MD, Marla Kiess, MD, Valerie Rychel, MD, Rachel M. Wald, MD, Jack M. Colman, MD,, Samuel C. Siu, MD, SM, MBA • JACC (2018) 71; 2419-30 CARPREG II

Silversides , C et al. JACC (2018) 71; 2419-30

HTN in Pregnancy • Chronic HTN/essential HTN – BP ≥140/90 mmHg known to predate conception or detected before 20 wk of gestation, with no underlying cause • Gestational HTN – New-onset elevations of BP after 20 wk of gestation, often near term, in the absence of accompanying proteinuria • Preeclampsia/eclampsia – HTN as defined above, associated with proteinuria (24-h excretion ≥300 mg), dx after 20 wk of gestation up to 2 wk postpartum – In the absence of proteinuria, new-onset HTN with new onset of any of the following • Platelet count <100,000/μl, serum creatinine >1.1 mg/dl, or doubling of concentration in absence of other renal disease,Transaminitis to twice normal concentration,Pulmonary edema,Cerebral/visual symptoms HTN in Pregnancy • Treatment Initiation – All guidelines support initiating treatment when BP > 160/105 – Most recommend starting treatment when BP > 140-150/90-105 in patients with co-morbid conditions • DM • Target organ damage – LVH – Microalbuminuria – Retinopathy • Dyslipidemia • Maternal age < 40 • h/o CVA • Previous perinatal loss • Secondary HTN HTN in Pregnancy • Treatment goals – BP 120-160/80-105 – In patients with comorbid conditions or preeclampsia BP <140-150/90-100 • First-line medications – Methyldopa – Labetalol – Nifedipine – Hydralazine • Medications to AVOID – ACE-I, ARBs – Mineralocorticoid Receptor Antagonists • Spironolactone and Eplerenone

Timing for Delivery • Preexisting hypertension without superimposed intrauterine growth restriction or a history of or current signs of abruption – ≥38-39 weeks of gestation for women not requiring medication – ≥37-39 weeks for women with hypertension controlled with medication – Late preterm delivery (34 to 36+6 weeks) for women with severe hypertension difficult to control • Superimposed preeclampsia or other pregnancy complications (eg, fetal growth restriction, previous stillbirth, abruption in the current or past pregnancy) – Timing of delivery should be decided on a case-by-case basis based on the type and severity of these complications

Preeclampsia Prevention • Low-dose aspirin (81-150mg/day) prophylaxis – Recommended for high risk factor for preeclampsia – Should be considered for >1 moderate risk factors for preeclampsia – Should be initiated btwn 12-16 weeks and continued until delivery

Preeclampsia Risk Factors • High risk factors • Moderate risk factors – h/o preeclampsia – Nulliparity – Multifetal gestation – BMI > 30 – Chronic HTN – Age >35 – Type 1 or 2 Diabetes – Family h/o preeclampsia – Renal disease – AA race, low – SLE or APL syndrome socioecononmic status – h/o low birthweight, SGA, adverse preg outcome, >10yr preg interval Pregnancy complications & CVD

Hauspurg, A. et al. Clinical Cardiology 2018:41:239-246 Ying, W. et al. JAHA 2018;7:e009382 Pregnancy complications & CVD

Hauspurg, A. et al. Clinical Cardiology 2018:41:239-246 Pregnancy complications & CVD

Hauspurg, A. et al. Clinical Cardiology 2018:41:239-246 CARPREG also predicts adverse cardiac events late after pregnancy

Balint O H et al. Heart 2010;96:1656-1661 Silversides , C et al. JACC (2018) 71; 2419-30

Pregnancy and the Heart

• Pregnancy usually well tolerated but there are conditions in which pregnancy poses high risk • Physiologic changes of pregnancy peak at end of second trimester • Not normal to have S4, DM or fixed split S2 • Several tools for CVD risk stratification • Pregnancy related BP optimization reduces maternal morbidity and mortality • Pregnancy complications increase risk for future CVD CPR in late pregnancy