Maggie NielsenPGY-2

CARDIAC DISEASE IN PREGNANCY

MARCH 22, 2017

Heart disease complicates more than one percent of all pregnancies.1

It is the leading cause of indirect maternal deaths-accounting for 20 percent of all cases.1

Many studies have shown an increasing prevalence, as opposed to other top mortality factors (eg. Hemorrhage, hypertensive disorders).2

Cardiovascular diseases are the leading cause of obstetrical intensive care unit admissions.1

MORBIDITY AND MORTALITY

INCREASING PREVALENCE OF RISK

43% increase in Cardiac Output1

Half of this increase occurs by 8 weeksMaximal increase by mid-pregnancy

17% increase in HR1

4% increase in MAP1

21% decrease in systemic vascular resistance1

34% decrease in pulmonary vascular resistance

PHYSIOLOGY

PHYSIOLOGY

Blood volume increases up to 40% during pregnancy.2

The renin-angiotensin-aldosterone axis is affected. Renin is produced by both maternal kidney and the uteroplacental unit, angiotensinogen is produced by both maternal and fetal liver and its production increases with increasing estrogen levels.1

PHYSIOLOGY

Increased production of prostaglandins in pregnancy plays a central role in control of vascular tone, blood pressure, and sodium balance (eg. PGE2 produced in the medulla).1

Prostacyclin (PGI2), in the endothelium, is increased in late pregnancy. The ratio of PGI2 to thromboxane is maternal urine and blood have been considered and important feature in the pathogenesis of preeclampsia.1

Endothelin-1 acts as a vasoconstrictor and is additionally increased in pregnancy.1

Increased cutaneous blood flow in pregnancy serves to dissipate excess heat generated by increased metabolism.1

PHYSIOLOGY

Bounding pulsesWidened pulse pressure Hyperkinetic, displaced

and enlarged PMI Loud S1, prominent S2

splitting Systolic flow murmurs Normal JVP or mild JVD Peripheral edema,

varicose veins

PHYSICAL FINDINGS

Class I – Uncompromised

Class II – Slight limitation of physical activityOrdinary physical activity results in fatigue,

palpitation, dyspnea

Class III – Marked limitationLess then ordinary activity causes fatigue,

palpitation, dyspnea

Class IV – Severely compromised Inability to preform any physical activity without

discomfort

NYHA CLASSIFICATION

Group I (0-1%) ASD, VSD PDA Pulmonic or tricuspid disease Corrected fallot tetralogy Bioprosthetic valve Artificial Valve is class 2B

Mitral stenosis, NYHA I or II

RISK FOR MATERNAL MORTALITY

Group II (5-15%) Mitral Stenosis, NYHA III and

IVWith atrial fibrillation 2B

Aortic stenosis Aortic coarctation Uncorrected fallot tetralogy Previous MI Marfan syndrome, normal

aorta Group III (25-50%) Pulmonary hypertension Aortic coarctation with valvular involvement Marfan syndrome with aortic involvement

1-Risk not increased Mild pulm stenosis, VSD, PDA, MVP Repaired ASD, VSD, PDA, total anomalous pulm venous

drainage

2. Small increased risk Unoperated ASD, Repaired Fallot tertralogy, Most arrhythmias

2/3. Depends on individual case Mild left ventricular impairment Hypertrophic cardiomyopathy Native or tissue valvular heart disease Marfan syndrome without aortic dilation Heart transplantation

WHO CLASSIFICATION

3. Significant increased risk Mechanical valve Systemic right ventricle-congenitally corrected transposition Post-Fontan operation Cyanotic heart disease Other complex congenital heart disease

4. Very high risk(pregnancy contraindication/termination) Pulmonary arterial HTN Severe systemic ventricular dysfunction (NYHA III/IV) Previous peripartum cardiomyopathy with residual impairment Severe left heart obstruction Marfan syndrome with aorta dilated > 40 mm

WHO CLASSIFICAION

The onset of heart failure is generally gradual, the first warning sign is persistent basilar rales and a cough.3

Infection with sepsis syndrome is an important factor precipitating cardiac failure.1

Bacterial endocarditis is a deadly complication of valvular heart disease. 1

COMPLICATING FACTORS

A number of serious complications can result with mechanical valves, related to the need for continued anticoagulation.Both thromboembolisms involving the

prosthesis and hemorrhage from anticoagulation are of extreme concern.1

Overall the maternal mortality rate is 3 to 4 percent with mechanical valves and fetal loss is common.3

VALVE REPLACEMENT

A number of serious complications can result with mechanical valves, related to the need for continued anticoagulation.Both thromboembolisms involving the

prosthesis and hemorrhage from anticoagulation are of extreme concern.Overall the maternal mortality rate is 3 to 4

percent with mechanical valves and fetal loss is common.

VALVULAR REPLACEMENT

Women with valvular heart disease have higher risk1:CHF (35 %), Arrhythmias (15%), initiation/increase in

cardiac meds (41%), hospitalizations (35%)

Fetuses have higher risk: preterm delivery, IUGR, stillbirth. (Compromised uteroplacental flow).3

Most adverse outcomes occur in women with moderate and severe mitral and aortic stenosis.

VALVULAR DISEASE

Most likely due to congenital lesion if present in young women (1%). 3

Increased complication rate of valve <1.5 cm.1

Decreased preload is a risk due to fixed CO in these patients.1

Vena caval occlusionRegional anesthesiaHemorrhage

May consider surgery if persistently symptomatic (valve replacement/valvotomy via cardiopulmonary bypass).1

AORTIC STENOSIS

MITRAL STENOSIS

Rheumatic endocarditis remains most common cause. Symptoms develop when stenosis narrows surface area to

<2.5 cm2

LA dilation may lead to atrial fibrillation.1

Predisposed to thrombosis formation.1

Limit activity, consider BB with symptoms, anticoagulation with arrhythmias.2

May present as anxiety, palpitations, atypical chest pain, dyspnea with exertion and syncope.1

Associated with myoxmatous degeneration, idiopathic.

Beta blocking drugs will decrease sympathetic tone, relieve chest pain and palpitations, and reduced risk of arrhythmias.3

Decrease SVR leads to decreased L sided regurgitation. Medical management includes diuretics, and vasodilators IF hypertensive (Hydralazine, Nitrates, Nifedepine).1

MITRAL VALVE PROLAPSE

ASD 3% of all congenital cardiac

malformations High risk than VSD Thrombus risk, L>R shunt

VSD Heal in childhood 90%Well tolerated in pregnancy If pulmonary arterial

pressures reach systemic levels, left to right shunts may results in EisenmengerSyndrome.1

SEPTAL DEFECTS

Divided into groups based on etiology. Primary pulmonary hypertension in arterioles vs pulmonary venous hypertension caused by left sided heart disorders.1

Beware of primary disease in scleroderma, SLE, SCD, thyrotoxicosis

Vague symptoms of dyspnea, orthopnea and nocturnal dyspnea are also usually present3

Diuretics, supplemental oxygen, and vasodilator drugs are standard therapy for symptoms. Some recommend anticoagulation. May consider inhaled nitrous oxide.1

Need to avoid hypotension, epidural anesthesia is controversial.

PULMONARY HYPERTENSION

Women at greatest risk are those with congenital heart lesions, IV drug use, degenerative valve disease and intracardiac devices. 1

Usually due to low-virulence bacterial infections (staphylococcus or enterococcus) superimposed on underlying structural lesion. Think Staph aureus in an intravenous user.

Symptoms are “flulike” and diagnosis is made using the Duke criteria (2 major, 1 major and 1 minor, 5 minor).1

High risk lesions: periprocedural antibiotic prophylaxis is recommended for dental procedures but NOT indicated for either vaginal or cesarean deliveries in the absence of pelvic infection.1

ENDOCARDITIS

Increased incidence of new onset of worsening pre-existing arrhythmias encountered in pregnancy. ‘

Pulmonary edema is most common complication at 14%1

Proxysmal supraventricular tachycardia is the most common arrhythmia seen in reproductive-aged women. (Includes atrial fibrillation and atrial flutter). 1

Treatment with vagal maneuvers, adenosine if unresponsive. Electrical cardioversion NOT contraindicatedWPW, may present during pregnancy. Ablation of pathway as

needed Vtach-precipitated by exercise or stress. BB recommended.

Prolonged QT BB recommended, at highest risk for events postpartum Avoid azithromycin, erythromycin and clarithromycin especially

ARRHYTHMIAS

Aortic coarctation Hypertension in upper extremities but normal or reduced pressures in

lower extremities CHF, severe hypertension are most common pregnancy risks

Marfan’s syndrome1

Abnormal fibrillin, FBN1 gene on chromosome 15q21 Associated with joint laxity and scoliosis Progressive aortic dilation causes aortic valve insufficiency Normal aortic root 2 cm, if dilation reaches 5-6 cm surgery should

occur Treatment with prophylactic BB

Aortic dissection1

Presents with severe chest pain Ddx MI, PE, pneumothorax, aortic valve rupture, abruption, rupture CXR will show abnromalities, angiography most definitive. Treatment is to lower BP and treat surgically as indicated.

AORTIC DISEASE

Hypertrophic cardiomyopathy is most common. Inheritance is autosomal dominant an left ventricular hypertrophy can lead to complex arrhythmias which may progress to sudden death.1

Management similar to aortic stenosis-limit exercise, abrupt changes. Avoid decreased preload and diminished vascular resistance.

Dilated cardiomyopathy is characterized by ventricular enlargement and reduced systolic function.3

Peripartum cardiomyopathy-Characterized by cardiac failure in last month of pregnancy or within 5 months of delivery. Systolic dysfunction characteristic.1

CARDIOMYOPATHY

Classic risk factors are the same: diabetes, smoking, hypertension, hyperlipidemia, obesity, deconditioning.

Diagnosis in pregnancy remains the same, Troponin 1* levels are stil l used.3

The mortality rate (35%) with myocardial infarction in pregnancy is increased compared with age-matched nonpregnant women.1

Treatment is similar to that for nonpregnant patients-oxygen, nitroglycerin, low-dose aspirin, heparin, and beta blocking drugs with close blood pressure monitoring. Percutaneous angioplasty/stent placement has several documented successes.

ISCHEMIC HEART DISEASE

Cunningham, F. Gary,, et al. Williams Obstetrics. 24th edition. New York: McGraw-Hill Education, 2014.

Feinber, Loryn. Heart Disease in Pregnancy a PowerPoint presentation Retrieved from http://www.acog.org/-/media/Sections/MA/MembersOnly/20130724Feinberg.pdf. 2013

Yeon, Susan B.Acquired Heart Disease in Pregnancy. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on March 19, 2017.)

REFERENCES