Cardiomyopathy during pregnancy has substantial implications for the mother and fetus. Peripartum cardiomyopathy describes a rare form of idiopathic left ventricular (LV) failure afflicting patients without antecedent heart disease during the last month of pregnancy or within 5 months after delivery.1 Although cardiac function may partially or completely recover, symptoms can recur with subsequent pregnancies. There is controversy as to whether all forms of cardiomyopathy diagnosed during pregnancy are peripartum cardiomyopathy.2 We report the obstetrical, anesthetic, and intensive care unit (ICU) management of peripartum eclampsia-related reverse apical ballooning (reverse takotsubo) cardiomyopathy.
The patient provided written consent to publish this case report.
A previously healthy 19-year-old primigravida was admitted to the ICU after recurrent preterm eclamptic seizures at 29 weeks' gestation. She had not sought prenatal care during the pregnancy. Per her family’s report, the patient had several days of worsening lower extremity edema, headaches, and general malaise followed by a generalized tonic-clonic seizure. She seized a second time during transport by emergency medical services to her local emergency department. Initial evaluation in the emergency department revealed an arterial blood pressure of 171/105 mm Hg. She seized a third time shortly after arrival, with subsequent obtundation and hypoxemia (SpO2 78%). Endotracheal intubation was performed, a magnesium sulfate infusion was started for presumed eclampsia, and she was transferred emergently to our institution.
Bedside ultrasound on arrival suggested an approximate fetal gestational age of 29 3/7 weeks. Urinalysis predicated 24-hour proteinuria of 12 g. Laboratory studies were otherwise significant for a mild leukocytosis and minimal elevations in hepatic aspartate aminotransferase. Troponin I was elevated at 0.25 ng/mL, and troponin T was mildly elevated at 0.06 ng/mL, with no significant 6-hour change. An electrocardiogram demonstrated sinus tachycardia without evidence of ischemia. Cranial computed tomography findings were suggestive of posterior reversible encephalopathy syndrome without evidence of hemorrhage, thrombus, or mass effect. Chest radiograph showed opacifications consistent with pulmonary edema with significant hypoxemia (PaO2 93 mm Hg on 100% FIO2), which improved with pulmonary recruitment and increase in positive end-expiratory pressure. Transthoracic echocardiogram (TTE) demonstrated normal LV size (LV end-diastolic dimension index [LVEDDI] 23.6 mm/m2), normal cardiac valves, LV ejection fraction (LVEF) 35%, and with regional wall motion abnormalities consistent with reverse apical ballooning (reverse takotsubo), that is, the LV basal and midventricular segments were hypokinetic while the apex was hypercontractile (Fig. 1; Supplemental Digital Content 1, Video 1, http://links.lww.com/AACR/A34).
We administered 2 doses of IV labetalol (10 mg each) for hypertension. The overall fetal status was reassuring as assessed by continuous fetal heart rate monitoring. However, because of recurrent eclamptic seizures with impaired cardiac function, the decision was made to proceed with urgent cesarean delivery.
The patient was brought to the operating room. We placed a right internal jugular multilumen introducer with pulmonary artery catheter. In addition, a radial arterial line was placed for hemodynamic monitoring. General anesthesia was maintained with a propofol infusion (20–60 μg/kg/min) and isoflurane (end-tidal concentration 0.4%–0.5%). Her oxygen saturation was initially 88% but improved to >95% on 15 cm H2O of positive-end expiratory pressure (PaO2 96 mm Hg on 50% FIO2). Her systolic blood pressure was maintained between 94 and 128 mm Hg, diastolic blood pressure between 59 and 87 mm Hg, and heart rate between 92 and 109 beats/min. Intraoperative transesophageal echocardiography demonstrated findings similar to the preoperative TTE findings (Supplemental Digital Content 2, Video 2, http://links.lww.com/AACR/A35). Pulmonary artery systolic pressures remained between 24 and 33 mm Hg. Cardiac index measured using thermodilution was 3.9 L/min/m2 without vasopressor or inotropic support. A viable female infant weighing 1280 g was delivered via uncomplicated primary lower transverse cesarean delivery with Apgar scores of 1, 4, and 6 at 1, 5, and 10 minutes, respectively. Neonatal resuscitation and intubation were performed, and the infant was transported to the neonatal ICU for further care.
During the initial 24 hours postpartum, the patient remained hemodynamically stable without requiring inotropic or vasopressor support but required administration of IV labetalol on 2 more occasions for control of systolic hypertension. Her trachea was extubated on postoperative day 2. A standard heart failure regimen of carvedilol 12.5 mg twice a day and lisinopril 5 mg daily was commenced for presumptive diagnosis of peripartum cardiomyopathy. We also started levetiracetam 500 mg twice a day because of antepartum diagnosis of posterior reversible encephalopathy syndrome. At the time of discharge on postoperative day 5, she was counseled that a subsequent pregnancy presented greatly increased risk based on her clinical presentation and diagnosis of peripartum cardiomyopathy.3 After a 1-month hospitalization, the patient’s daughter was discharged to home without significant sequelae of prematurity.
TTE obtained 1 month later showed normalization of LVEF (56%) with no regional wall motion abnormalities (Fig. 2; Supplemental Digital Content 3, Video 3, http://links.lww.com/AACR/A36). Based on the patient’s rapid clinical recovery and normalization of her LVEF, she was subsequently diagnosed with eclampsia-related “stress-induced cardiomyopathy.” With this diagnosis, the previous recommendation to avoid further pregnancy was revised, and she was advised that subsequent pregnancy was not contraindicated provided she sought appropriate prenatal care.
We present a case of eclampsia-related cardiomyopathy with rapid recovery of cardiac function. Because of this patient’s clinical and echocardiographic recovery in <4 weeks, this case is a separate clinical entity from classic peripartum cardiomyopathy with different outcomes and risk of recurrence in a subsequent pregnancy.
Stress-induced cardiomyopathy, including apical ballooning (takotsubo) and reverse apical ballooning (reverse takotsubo) cardiomyopathies, has been reported during the peripartum period.4–6 Several cases have been reported around the time of cesarean delivery.6–11 Unlike our case, these were not associated with eclampsia. In 1 case series, 13 women who had elective cesarean delivery developed symptoms intraoperatively or within 24 hours postdelivery.2 LV apical ballooning (takotsubo pattern) was noted in 8 patients and reverse apical ballooning (reverse takotsubo pattern) was observed in 5 patients. Similar to our patient, recovery of LV function was rapid in these patients, ranging from 4 to 28 days. All patients (where follow-up data were available) had full recovery of LV function.
TTE is crucial in the diagnosis and management of cardiomyopathy related to pregnancy.12–14 Classic peripartum cardiomyopathy, pre-eclampsia, and our patient’s eclampsia-related stress-induced cardiomyopathy demonstrate different echocardiographic findings. In classic peripartum cardiomyopathy, the LV is generally dilated and global LV dysfunction usually predominates. In contrast, with reverse apical ballooning syndrome, the LV size is normal and LV dysfunction is segmental in a nonvascular distribution.1 There are established echocardiographic criteria for peripartum cardiomyopathy, including LVEF <45%, fractional shortening <30%, and an LVEDDI of >27 mm/m2.15 Although our patient demonstrated an LVEF of <45%, her LVEDDI was normal (23.6 mm/m2). Our patient’s echocardiogram findings also differed from cardiomyopathy of pre-eclampsia, in which diastolic dysfunction with preserved LVEF predominates.12
Prognosis for recovery is also different between the 2 entities. In classic peripartum cardiomyopathy, LV recovery occurs in approximately 50% of patients, generally within 6 months after diagnosis.16 Some peripartum cardiomyopathy patients do not experience improvement in cardiac function after delivery and may require mechanical support (i.e., ventricular assist devices) or cardiac transplantation. In the largest series of patients with apical (takotsubo pattern) and reverse apical (reverse takotsubo pattern) stress-induced ballooning patterns, similar to our patient, full recovery occurred in all reported patients within 1 month.2,11
The acute management of both entities involves a similar strategy. Our patient demonstrated acceptable hemodynamic variables. Oxygenation was improved with mechanical ventilation. The obstetric anesthesia team ably managed her during cesarean delivery by using multiple modalities of invasive monitoring. β-Blockers (labetalol) were administered before and after delivery. Other cases involving heart failure during the peripartum interval may require additional medical therapy with diuretics or inotropic infusions. After delivery, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be used for afterload reduction, with anticoagulation contingent on degree of LVEF impairment. In severe cases, an intra-aortic balloon pump, extracorporeal membrane oxygenation, or ventricular assist devices may be used.17
Subsequent pregnancy is not discouraged in the setting of reverse apical ballooning (reverse takotsubo) cardiomyopathy although patients should be carefully followed. Although stress-induced pattern of cardiomyopathy can recur, even outside the context of subsequent pregnancy, rapid recovery continues to be the norm without known long-term sequelae.2
In summary, we present a case of eclampsia-related, stress-induced cardiomyopathy with full recovery of LV function within 4 weeks. Using echocardiography, the diagnosis of pregnancy-related cardiomyopathy should be differentiated for appropriate management and counseling for the patient and entire peripartum medical team.
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