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.