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Peripartum Cardiomyopathy (Risk Factors (obesity, hx of cardiac disorders,…
Peripartum Cardiomyopathy
Medical Management
Medications
Angiotensin converting enzyme, or ACE, inhibitors – Help the heart work more efficiently
Beta blockers – Cause the heart to beat more slowly so it has recovery time
Diuretics – Reduce fluid retention
Digitalis – Derived from the foxglove plant, it has been used for more than 200 years to treat heart failure. Digitalis strengthens the pumping ability of the heart
Anticoagulants – To help thin the blood. Patients with PPCM are at increased risk of developing blood clots, especially if the EF is very low.
Bromocryptine- inhibits the pituitary secretion of prolactin. (Studies suggest it helps treat PPCM, but more research is needed)
Surgery/Procedures
Heart transplant
if waiting for donor, (L)(R)VAD can be placed in the mean time
Cardiac resynchronization therapy
VAD
left ventricular assist device — a surgically implanted, electrically (battery) powered pump
Needed because the patient is waiting for a heart transplant. Therefore she needs LVAD to keep heart pumping
functions to that help failing heart's left ventricle pump adequate amounts of blood to the body.
Medications necessary to keep R side of heart pumping
Pt stays in cardiac ICU for 1-2 weeks
Complications of LVAD's include:
right heart faiulre
infection
preoperative hemorrhage
device failure
haemolysis
thromboembolism
Defibrillator
Pacemaker
Cardioverter
intravenous γ-globulin and immunoabsorption (treatments that later the immune system) ~not proven yet
Education on Lifestyle Changes
Healthy diet
less salt
heart healthy diet
Physical activity
Smoking cessation
Weight loss
Limit alcohol intake
Stress reduction
Pathophysiology
Idiopathic etiology
possible explanations
Prolonged Tocolysis
Potential association between tocolytic therapies and pulmonary edema
Abnormal Hemodynamic Response
During pregnancy 40-50% increase in blood volume and cardiac output
LV remodeling and hypertrophy
Decreased LV systolic function in women
Hemodynamic stress of gestational hypertension
Development of HF
Viral Myocarditis
viral infection
inflammation and injury to myocardium
decreased myocardial contractility
heart enlarges
increased LV EDV
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increased LAP
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scarring (fibrosis)
dysarhythmias
chronic heart failure
Abnormal Immune Response
Fetal cells may escape into the maternal circulation
cells remain their due to weak immunogenicity of the paternal haplotype of the chimeric cells
If these cells lodge in the cardiac tissue, they can trigger a pathologic autoimmune response
Apoptosis and inflammation
increase in Inflammatory cytokines
increase in tumor necrosis factor (TNF)-alpha and interleukin-6
Selenium Deficiencies and Malnutrition
increases cardiovascular susceptibility to viral infections, hypertension, hypocalcemia.
increase in prolactin levels
decreased STAT3 levels
increased levels of oxidative stress
up-regulates the activity of proteolytic Cardiac Cathepsin which is responsible for cleavage of prolactin hormone (PRL) into 16 kDa.
16 kDa fragment is anti-angiogenic which reduces capillary angiogenesis
and is also responsible for apoptosis causing vascular remodelling and regression of blood vessel
Angiogenic Imbalance
lack cardiac PGC-1α
unable to regulate pro-angiogenic factors such as VEGF
Considered a dilated cardiomyopathy
Heart chambers enlarge
myocardial mm weakens
decrease in contractility
decreased ejection fracture (<45%)
decrease stroke volume
decrease blood flow to the body (cardiac output)
no longer meeting the body's organs oxygen demand
decreased renal perfusion
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Sympathetic Compensation
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increase filling pressure (after load)
pulmonary & systemic congestion
peripheral edema
increase/enlarged radius
mitral/tricuspid regurgitation
increased systolic diastolic tension
diastolic dysfunction
decreased subendocardial coronary flow
Physical Findings
Fatigue with activity
Palpitations
Nocturia
SOB
Swelling in the ankles/feet
Swollen neck veins
Low blood pressure
worsening of pre-existing cardiac conditions
Angina
Diagnostic Testing
Diagnostic Criteria
Heart failure develops in the last month of pregnancy or within 5 months of delivery.
Absence of determinable cause of cardiac failure.
Absence of demonstrable heart disease before the last month of pregnancy
Echocardiographic evidence of new left ventricular systolic dysfunction that occurs in the peripartum period.
Tests
Chest X-ray
ECG
CT
Nuclear heart scan
Lab Tests
CBC
BUN/CR
Electrolytes
Troponins
BNP
Urea
Thyroid stimulating hormone
Liver function
Cardiac MRI
Cardiac catheterization
Differential Diagnosis
Pre-existing dilated cardiomyopathy
Pre-existing other form cardiomyopathy
Pre-existing valvular heart disease, particularly valvular stenosis
Pre-existing congenital heart disease
Hypertensive heart disease including preeclamspia and eclampsia
Acute myocarditis
Acute PE
Acute coronary spasm, dissection, thrombosis, MI
Tyrotoxicosis
Maternal Sepsis
Severity of Symptoms Classification
Class I - Disease with no symptoms
Class II - Mild symptoms/effect on function or symptoms only with extreme exertion
Class III - Symptoms with minimal exertion
Class IV - Symptoms at rest
Risk Factors
obesity
hx of cardiac disorders
smoking
alcoholism
multiple pregnancies
African-American decent
poor nourishment
hx of preeclampsia, eclampsia, or postpartum hypertension
age over 30
maternal cocaine use
Long-term (>4 weeks) oral tocolytic therapy with beta adrenergic agonists such as terbutaline
Mental stress and depression
Metabolic syndrome (DM, low HDL-cholestrol, elevated blood glucose and triglycerides, high blood pressure)
Complications with pregnancy (pre-eclampsia and gestational DM)
Rheumatologic diseases such as rheumatoid arthritis or lupus
Cardiotropic viral infections
