Cardiac disease in pregnancy and peripartum cardiomyopathy

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Special Scenarios: I. Pre-existing Cardiac Disease: Congenital Heart Disease Repaired Congenital Heart Disease Pulmonary Hypertension Rheumatic Heart Disease Connective Tissue Disorders II. Valvular Heart Disease: Mitral Stenosis Mitral Regurgitation Aortic Insufficiency Aortic Stenosis Mechanical Prosthetic Valves Tissue Prosthetic Valves III. Cardiomyopathy: Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Peripartum Cardiomyopathy IV. Cardiac diseases that may develop During Pregnancy: Arrhythmias Acute Myocardial Infarction Hypertension
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief:Anjan K. Chakrabarti, M.D. [2]

Synonyms and Keywords: PPCM; PPCMP

Overview

Peripartum cardiomyopathy (PPCM) is a form of dilated cardiomyopathy that is defined as a deterioration in cardiac function presenting between the last month of gestation and up to six months post-partum. The etiology of postpartum cardiomyopathy is unknown. Reported prevalence of postpartum cardiomyopathy in United States is estimated to be 1 case per 1300-15,000 live births. Treatment for the disease is similar to treatment for congestive heart failure. Delivery is the recommeded overall treatment to decrease the volume load, improve ventricular function and simplify the medical management of these patients.

Definition

Peripartum cardiomyopathy is defined as:

• Heart failure within last month of pregnancy or five months postpartum
• Absence of prior heart disease
• No determinable cause
• Strict echocardiographic indication of left ventricular dysfunction:

• Ejection fraction <45% and/or
• Fractional shortening <30%
• End-diastolic dimension >2.7 cm/m2 BSA (body surface area)

Pathophysiology

The etiology of postpartum cardiomyopathy is largely unknown. It has been postulated that a defective antioxidant mechanism may contribute. There are elevated levels of cathepsin D and an increase in total prolactin and angiostatic 16kDa prolactin. These molecules promote:

• Apoptosis
• Inhibit endothelial cell proliferation
• Increase vasoconstriction
• Impair myocyte function

The potential role of prolactin forms the molecular basis of treatment with bromocriptine in the mouse.

As with other forms of dilated cardiomyopathy, PPCM involves decrease of the left ventricular ejection fraction with associated congestive heart failure and increased risk of atrial and ventricular arrhythmias and even sudden cardiac death.

Differentiating Peripartum Cardiomyopathy from Other Disorders

• Accelerated HTN
• Infection/sepsis
• Diastolic dysfunction
• High output state of pregnancy

Epidemiology and Demographics

• Estimates of incidence 1/1300-15000. Previous studies likely overestimated

Risk Factors

PPCM is more common among women with:

• Prior PPCM
• Multiple pregnancies
• African decent, Haitian descent
• History of toxemia
• Long-term tocolytic use
• Age >30
• Twin Pregnancy

Diagnosis

History and Symptoms

Signs and symptoms are similar to those of normal pregnancy

Hemodynamic Findings

Chamber	Normal Pregnancy	Peripartum cardiomyopathy
Right atrium	2	11 (2-34)
Pulmonary artery	11	39 (18-62)
Pulmonary capillary wedge pressure	6	18 (5-32)
Cardiac output (L/min)	7	6 (5-9)
Heart rate	83	104 (76-142)

Treatment

• Delivery is the recommeded overall treatment to decrease the volume load, improve ventricular function and simplify the medical management of these patients.

Pharmacotherapy:

• Bromocriptine
• Digoxin and diuretics are Class C recommendation.
• ACE inhibitors absolutely contraindicated prepartum (hydralazine drug of choice).
• Anticoagulation recommended (heparin prepartum and coumadin postpartum).

Prognosis

• Mortality 25-50% (half deaths in first 3 months).
• Remainder stable/recover within 6 months.
• Can recur with subsequent pregnancies.
• Favorable outcomes with cardiac transplantation.

References

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