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+In January 2009, a 57-year-old woman emergently presented with acute shortness of breath.
+She had a 1-month history of progressive shortness of breath and a gradual decrease in exercise capacity secondary to mild dyspnea.
+She reported no additional symptoms.
+At age 40, she had been diagnosed with a stage IIA, T1bN1, left-sided breast cancer.
+Initial treatment had included a lumpectomy and axillary node dissection.
+She subsequently underwent 4 cycles of DOX therapy (75 mg/m2), followed by 8 cycles of cyclophosphamide, methotrexate, and 5-fluorouracil.
+Multigated acquisition scans before and after chemotherapy showed normal cardiac function.
+After chemotherapy, she underwent left whole-breast radiation with an axillary boost.
+Because the tumor had been estrogen receptor-positive, her subsequent medical regimen consisted only of anti-estrogen therapy.
+She took tamoxifen for 5 years, and, ever since, the aromatase inhibitor letrozole.
+In the 17 years after chemotherapy, she had been active and in relatively good health.
+In addition to her other symptoms, she now presented with tachycardia, tachypnea, and hypertension.
+She had marked jugular venous distention, an S3, pulmonary rales, and trace peripheral edema.
+Initial laboratory values were within normal limits except for an elevated level of N-terminal pro-brain natriuretic peptide (>2,000 pg/mL).
+Results of investigation into the new-onset cardiomyopathy included normal cardiac enzyme levels, an electrocardiogram (ECG) that revealed no ischemic changes, and a coronary angiogram of normal appearance.
+The ECG showed sinus tachycardia with frequent premature ventricular complexes, left-axis deviation, left atrial enlargement, and low-voltage QRS complexes with nonspecific ST changes (Fig.1).
+A 2-dimensional echocardiogram revealed a left ventricular ejection fraction (LVEF) of 0.20, severe diffuse left ventricular (LV) hypokinesis, and a mildly dilated left atrium.
+To better define the cause of the LV systolic dysfunction, cardiovascular magnetic resonance (CMR) was performed.
+It confirmed the LVEF of 0.20.
+The T2-weighted sequence showed slow flow secondary to LV dysfunction, and no myocardial edema (Fig.2A).
+Late gadolinium enhancement disclosed diffuse myocardial thinning and no scarring (Fig.2B).
+The patient was treated medically.
+Her symptoms progressively improved during therapy, which consisted of a β-blocker, an angiotensin-converting enzyme inhibitor, digoxin, and a diuretic.
+The therapy was slowly tapered, and her LVEF increased from 0.20 to 0.55 during an 8-month period.
+All medications except for low-dose metoprolol were discontinued after 1 year, and she remained asymptomatic.