Peripartum Cardiomyopathy and Cardiogenic Shock Supported with Percutaneous Left Ventricular Assist Device
- Volume 20 - Issue 7 - July 2012
- Posted on: 7/3/12
- 0 Comments
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Peripartum cardiomyopathy is a rare but potentially devastating cause of heart failure. We report the case of a 32-year-old female who developed cardiogenic shock seven days post-delivery secondary to peripartum cardiomyopathy that was successfully treated with supportive care, including a percutaneous left ventricular assist device.
A 32-year old female with no past medical history, except for the delivery of a healthy child seven days prior to presentation, developed syncope while at home. The patient was complaining of chest pain immediately prior to the event and her fiancé provided cardiopulmonary resuscitation when he found her collapsed until EMS arrived few minutes later. She was noted to be in ventricular fibrillation and was successfully cardioverted to sinus rhythm. Post-cardioversion, she had significant ST-segment elevations in V3-V6. Lab work done upon ER arrival revealed a troponin-I of 1.0 ng/mL and a CPK of 319 IU/L.
Due to concern about acute myocardial infarction, emergent coronary angiography was performed, which demonstrated only a 50% mid left anterior descending coronary artery (LAD) stenosis (Figure 1). Left ventricular (LV) end-diastolic pressure was elevated at 35 mmHg and ventriculography revealed an LV ejection fraction of 15% with severe hypokinesis of the mid and apical myocardial segments (Figure 2), and severely reduced cardiac output. An Impella percutaneous LV assist device (Abiomed Inc.) was placed (Figure 3) for hemodynamic support due to severely reduced cardiac output at a setting of P-8, improving the augmented cardiac output to 2.2 L/min/m².
Echocardiography post-catheterization confirmed the finding of severe LV dysfunction with moderate basal hypokinesis, and severe mid and apical segment hypokinesis. Attempts to wean the level of Impella support during the next 24 hours were unsuccessful; however, by 48 hours post-implantation, the device was successfully weaned and removed. On day four of the hospitalization, the patient was successfully extubated. Neurological and respiratory status were stable and follow-up echocardiogram showed improvement of ejection fraction to 25%. The patient was discharged home seven days after her initial presentation with a LifeVest external defibrillator (Zoll Corporation), and optimized heart failure medications, including beta blocker and ACE inhibitor.
Peripartum cardiomyopathy (PPCM is a rare and potentially life-threatening form of dilated cardiomyopathy with LV dysfunction that affects women in late pregnancy or early after delivery1 and is often an idiopathic cause of cardiogenic shock.2
Heart failure (HF) associated with pregnancy was first described as a definitive form of cardiomyopathy in 1937.3 The term PPCM was later coined to define a class of patients that developed HF within the last month of pregnancy or within 5 months of delivery; with absence of a determinable etiology of HF; and absence of demonstrable heart disease prior to the last month of pregnancy.4 An additional criterion of LV dysfunction documented by EF < 45% by echocardiography5 was subsequently added to the formal definition of PPCM.6
The etiology of PPCM is still unknown, and many potential causes have been proposed including viral myocarditis, abnormal immune response to pregnancy, increased hemodynamic burden of pregnancy, hormonal abnormalities, malnutrition, inflammation, and apoptosis, but none have been proven.7
Physical examination often reveals tachycardia and tachypnea, elevated or reduced blood pressure, increased jugular venous pressure, displaced apical impulse, right ventricular heave, murmurs of mitral and tricuspid regurgitation, third heart sound, pulmonary rales, and peripheral edema.7 Electrocardiography usually shows sinus tachycardia with nonspecific ST-T wave changes, and occasionally LV hypertrophy, left atrial enlargement, and left bundle branch block.8 Chest radiography typically reveals cardiomegaly and pulmonary venous congestion or pulmonary edema, with or without pleural effusion.8 Echocardiography often confirms moderate to severe depression of LV systolic function, with occasional right ventricular and biatrial enlargement, as well as moderate to severe mitral and tricuspid regurgitation.5
The treatment of PPCM primarily includes standard drug therapy for acute and chronic HF with the use of diuretics, intravenous and oral vasodilators, intravenous inotropes, ACE inhibitors or ARBs, beta-blockers, spironolactone, and digoxin.9
Rarely, the presentation of patients with PPCM is related to a severe form of myocarditis10, stress-induced CM11, toxic shock syndrome12, or acute ST-segment elevation myocardial infarction13, resulting in cardiogenic shock. In these subsets of patients demonstrating rapid deterioration, intra-aortic balloon pumps, extracorporeal membrane oxygenation, and LV assist devices have been successfully used as a bridge to recovery before referral for cardiac transplantation.14