Acute myocardial infarction in early pregnancy: definition of myocardium at risk with noncontrast T2-weighted cardiac magnetic resonance
We report a case of a 34-year-old woman who had a left anterior wall myocardial infarction develop in the first trimester of pregnancy. Despite urgent and successful revascularization, she demonstrated persistent segmental wall motion abnormalities by transthoracic echocardiography. To manage this patient safely through pregnancy with a better definition of myocardium at risk, a cardiac magnetic resonance examination was performed. This identified a large territory of acutely edematous myocardium in addition to providing accurate volumetric measurements of left ventricular size and function. Because of her gravid state, gadolinium was not administered nor was it required to delineate the region of myocardium at risk.
A 34-year-old multiparous woman experienced sudden chest pain during the 10th week of her pregnancy. She underwent urgent coronary angiography that demonstrated complete occlusion of the proximal left anterior descending (LAD) artery without evidence of coronary dissection. She underwent successful percutaneous intervention (PCI) with balloon angioplasty and delivery of a drug eluting stent. Postintervention, she remained free of chest pain and the remainder of her hospital course was unremarkable. Her recovery was uneventful with no further episodes of chest pain. She was discharged to home on a maintenance dose of clopidogrel, aspirin, and prenatal vitamins. Because of increasing symptoms of dyspnea on exertion at 13 weeks’ fetal gestational age, she was referred for further evaluation.
On further history she reported preeclampsia with prior pregnancies, a 15 pack-year smoking history and a remote history of oral contraceptive use. Review of systems revealed easy fatigability and difficulty providing care for her children that she had not experienced during her previous pregnancies. She denied lower extremity edema or paroxysmal nocturnal dyspnea.
On physical examination, the upper extremity blood pressure was 98/60 and heart rate was 64 beats per minute. She had a dyskinetic cardiac impulse. The first and second heart sounds were normal. A soft grade II/VI systolic ejection murmur at the left upper sternal border and a second soft grade II/VI holosystolic murmur were appreciated at the left lower sternal border that radiated to the apex. There were no gallops present. Abdominal examination showed no hepatomegaly. There was no lower extremity edema.
Diagnostic evaluation included electrocardiography (ECG), transthoracic echocardiography (TTE), and cardiovascular magnetic resonance (CMR) imaging. The ECG showed normal sinus rhythm, normal axis, and deep Q-waves in the anteroseptal leads with poor R-wave progression. The TTE revealed moderate segmental wall motion abnormality of the left ventricle. There was mild left atrial enlargement and mild mitral regurgitation.
Clarification of the extent of the edema was obtained from the T2-weighted images from the CMR study and offered additional information beyond that of the echocardiogram. On the basis of her cardiovascular symptoms and the information obtained from the CMR study (moderately diminished segmental ejection fraction, moderate mitral regurgitation, and extensive myocardial edema), she was counseled about the inherent risks of carrying this pregnancy to term. Despite the reported risks, she decided to continue with the pregnancy at this time and was initiated on beta-blockade therapy. Lastly, hypokinesis of the apical segment of the left ventricle identified by CMR imaging prompted initiation of prophylactic low-molecular weight heparin to prevent apical thrombus formation in the setting of hypercoagulable state associated with pregnancy.
She then returned at approximately 17 weeks’ fetal gestational age with increasing shortness of breath and easy fatigability with routine household chores. Her examination at this point was significant for increased jugular venous distension. During this evaluation, a submaximal Exercise stress test was performed. She exercised 5 minutes of a standard Bruce protocol experiencing dyspnea with exercise. There were no new ECG changes, arrhythmias, or wall motion abnormalities with exercise. On the basis of this additional information, she was further counseled regarding the inherent risks of carrying this pregnancy to term. The increased risk of ventricular arrhythmias and sudden cardiac death in the presence of her underlying ventricular dysfunction after her recent myocardial infarction were reviewed. The intravascular volume changes of pregnancy that often result in stretching of the cardiac chambers accompanied by an increase in catecholamines and hormonal changes may increase the risk of ventricular arrhythmias and sudden cardiac death and therefore it was strongly recommended that she consider implantation of an implantable cardioverter-defibrillator (ICD) to manage her safely through the remainder of this pregnancy. The risks and benefits of this procedure were described as well as the ease of performing this procedure during pregnancy without deleterious effects to the mother or the fetus was also described.
Despite our attempts to lower the risk of ventricular arrhythmias and sudden cardiac death and improve survival to term with the option to undergo implantation of an ICD, she ultimately decided to terminate the pregnancy. Therefore, at approximately 18 weeks’ fetal gestational age, she safely underwent dilatation and evacuation without complication. Before discharge she was initiated on an appropriate medical regimen including beta-blockers, angiotensin-converting enzyme inhibitors, clopidogrel bisulfate, and aspirin therapy.
One month later she was evaluated in the outpatient setting and reported frustration with ongoing symptoms of easy fatigability and dyspnea on exertion despite compliance with medical therapy. She now reported smoking 1-2 cigarettes daily. A repeat CMR examination was performed during this visit that continued to demonstrate left ventricular enlargement and moderately severe left ventricular systolic dysfunction with an ejection fraction of 34%. Still, there was mild-to-moderate mitral insufficiency and mild left atrial enlargement. Delayed myocardial enhancement was performed, demonstrating areas of hyperenhancement suggestive of extensive myocardial fibrosis in the territory of the previous left anterior descending myocardial infarction. Interestingly, T2-weighted images continued to demonstrate an area of high-signal intensity suggesting residual edema. Her medical therapy was titrated accordingly and because she continued to demonstrate significant left ventricular dysfunction, she ultimately underwent ICD implantation.
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Ali N. Zaidi, MD, Subha V. Raman, MD, Stephen C. Cook, MD
Reprints: Stephen C. Cook, MD, 473 W 12th Ave, DHLRI Suite 200, Columbus, OH 43210.