A 44-year-old G4, P3 patient who is 36-weeks pregnant and has a past medical history of hypertension and type-II diabetes is brought in by ambulance for respiratory distress. Initial O2 saturation was 60% and continuous positive airway pressure was started in the field, with an improvement in her O2 saturation to 82%. Upon arrival to the emergency room, she was intubated for respiratory distress and transferred to the intensive care unit.
On arrival, her temperature was 98.9°F, heart rate was 140, blood pressure was 180/90 mm Hg, and intubated O2 saturation was 100% on an FiO2 of 100%. Her exam was notable for an elevated jugular venous pressure to 18 cm H20, a prominent S3 gallop, bilateral pulmonary crackles, and 2+ lower extremity edema. Electocardiogram revealed sinus tachycardia at a rate of 140 with nonspecific ST and T wave abnormalities but no evidence of acute ischemia. Her creatinine was 0.84mg/dL, glucose was 254 mg/dL, lactate was 1.2 mmol/L, liver function tests were normal and her N-terminal B-type natriuretic peptide (NT-BNP) was elevated at 3000 pg/mL. Her initial troponin T was <0.01 pg/mL but rose over the next 24 hours to a peak of 0.29pg/mL. Thyroid stimulating hormone (TSH) was normal at 2.95 uU/mL. Complete blood count and coagulation tests were normal. D-Dimer was elevated at 2871ng/mL. Urinalysis was notable for the absence of protein. Chest X-ray revealed diffuse, bilateral, hazy opacities consistent with pulmonary edema. A bedside echocardiogram revealed a dilated left ventricle with an ejection fraction of 23% and right ventricular dyfunction. Two months prior to presentation, the patient had undergone an echocardiogram at another institution for progressive shortness of breath that documented an ejection fraction of 55%. Notably, the patient's pregnancy had been normal to date. She did not have a history of IVF assistance or pre-eclampsia.
She received 10 mg of IV labetolol for her elevated heart rate and blood pressure, and her blood pressure fell precipitously to the 80s/doppler. Fetal bradycardia was appreciated, and an emergent c-section was performed. The patient was supported with epinephrine, neosynephrine, and phenylephrine during the surgery.
After surgery, she was weaned from pressors and extubated. She was aggressively diuresed, her creatinine rose to 1.44mg/dL, but her urine output remained excellent, and her creatinine subsequently normalized. She was started on a beta-blocker and angiotensin-converting enzyme inhibitor (ACEI). A repeat transthoracic echocardiogram was obtained one week later, showing an ejection fraction of 28%, no left ventricular thrombus, and normalization of her right ventricular function. Her blood pressure remained difficult to control, so hydralazine and nitrates were added to her regimen. She was never started on and aldosterone antagonist. She was discharged home with a plan for a cardiac MRI in two weeks.
The correct answer is: C. Peripartum cardiomyopathy.
Answer Option A: The diagnosis of pre-eclampsia requires: new onset of hypertension (systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg), and either proteinuria (≥0.3 grams in a 24-hour urine specimen or protein:creatinine ratio ≥0.3) or end-organ dysfunction (platelet count <100,000/microliter, serum creatinine >1.1 mg/dL or doubling of the serum creatinine, elevated serum transaminases to twice normal concentration) after 20 weeks of gestation.1 This patient only had hypertension. Pre-eclampsia does not affect the myocardium directly, and the ejection fraction usually remains normal.2
Answer Option B: The diagnosis of HELLP syndrome requires: hemolysis with a microangiopathic blood smear, elevated liver enzymes, and low platelet count.3 Hemolysis is defined as the presence of helmet cells, an elevated indirect bilirubin or low serum haptoglobin. Liver function enzyme elevation is defined as a serum AST >70 IU/L and total bilirubin >1.2 mg/dL. Throbobytopenia is defined as a platelet count <100,000.3 The patient did not have any evidence of this. The relationship between HELLP and systolic heart failure is not well studied.
Answer Option C: Peripartum cardiomyopathy is defined as: the development of heart failure toward the end of pregnancy, left ventricular function almost always <45% (without or without ventricular dilitation) and the absence of another identifiable cause of heart failure. She had other classic signs (elevated JVP, +S3 and pulmonary crackles and lower extremity edema) of peripartum cardiomyopathy. She also had many objective findings consistent with peripartum cardiomyopathy including: electrocardiogram (ECG) with sinus tachycardia and nonspecific ST/T wave changes, chest X-ray with pulmonary edema, elevated N-terminal B-type natriuretic peptide, and echocardiogram with a dilated left ventricule with severely depressed ejection fraction. Most importantly, she had no other likely cause of her cardiomyopathy.4
Answer Option D: Pregnancy-associated myocardial infarction is diagnosed by the same principles as myocardial infarction in non-pregnant populations: ischemic symptoms, ECG abnormalities, and elevations in cardiac biomarkers.5 The management is also the same as non-pregnant populations including medical therapy and urgent revascularization including percutaneous coronary intervention and coronary artery bypass graft if indicated.6 Low-dose 81 mg of aspirin is safe in pregnancy, and heparin does not cross the placenta. Beta-blockers are safe, but ACEIs are contraindicated due to the risk of fetal renal damage. Statins are contraindicated due to a lack of information about them in acute myocardial infarction in pregnancy. Nitrates are safe in pregnancy. Radiation to the fetus should be taken into account, and creative shielding is often required in the catheterization lab. In one large series, heart failure and/or cardiogenic shock occurred in 38% of acute myocardial infarctions during pregnancy and left ventricular ejection fraction ≤40 percent occured in 64% of patients, ≤30% in 24% of patients and ≤20% in only 9% of patients.7
References
- American College of Obstetricians and Gynecologists; Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy. Obstet Gynecol 2013;122:1122-31.
- Rafik Hamad R, Larsson A, Pernow J, Bremme K, Eriksson MJ. Assessment of left ventricular structure and function in preeclampsia by echocardiography and cardiovascular biomarkers. J Hypertens 2009;27:2257-64.
- Sibai BM, Ramadan MK, Usta I, Salama M, Mercer BM, Friedman SA. Maternal morbidity and mortality in 442 pregnancies with hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome). Am J Obstet Gynecol 1993;169:1000-6.
- European Society of Gynecology (ESG), Association for European Paediatric Cardiology (AEPC), German Society for Gender Medicine (DGesGM), et al. ESC Guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). Eur Heart J 2011;32:3147-97.
- Nallamothu BK, Saint M, Saint S, Mukherjee D. Clinical problem-solving. Double jeopardy. N Engl J Med 2005;353:75-80.
- James AH, Jamison MG, Biswas MS, Brancazio LR, Swamy GK, Myers ER. Acute myocardial infarction in pregnancy: a United States population-based study. Circulation 2006;113:1564-71.
- Elkayam U, Jalnapurkar S, Barakkat MN, et al. Pregnancy-associated acute myocardial infarction: a review of contemporary experience in 150 cases between 2006 and 2011. Circulation 2014;129:1695-702.
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