Case Reports

Atypical Acute Myocardial Infarction and Concomitant Acute Cerebral Infarct

A 61-year-old woman presented with symptoms suggestive of a stroke. On further evaluation, she described symptoms of an atypical acute myocardial infarction.


 

References

A 61-year-old woman without any known medical history presented with a chief complaint of right arm numbness and right-sided scalp numbness that had started 2 days earlier. She described a “pins and needles” sensation in her right upper extremity and right scalp, and said the numbness in her scalp was especially noticeable when she combed her hair. The patient denied any chest pain, shortness of breath, weakness in her arms or legs, headache, or blurred vision.

She said that 1 day prior to the onset of the paresthesias, she woke up fatigued and vomited once. Throughout that day, she had symptoms of nausea and fatigue, and sought treatment at an urgent care center that afternoon. At the urgent care center, she was diagnosed with a “stomach virus” and was given an antiemetic. The next day, her nausea improved, but the paresthesias began in her right hand and scalp. On the third day, the patient went to work, but the persistent paresthesias caused her to visit her primary care physician, who sent her to our ED for further work-up.

The patient said she had been in good health until 3 days ago. She reported no medical problems and was taking no medications. The patient denied smoking or using alcohol; her family history was significant only in that her father had a myocardial infarction (MI) while in his 50s.

On physical examination, the patient was alert, oriented, and in no apparent distress. Her body mass index was 28.3 kg/m2. Vital signs were: temperature, 99.2°F; blood pressure, 113/73 mm Hg; heart rate, 93 beats/minute; and respiratory rate, 18 breaths/minute. Oxygen saturation was 95% on room air.

Her head was normocephalic and atraumatic, and her eyes, ears, nose, and throat were normal. Her neck was supple and without jugular vein distension. The cardiac examination revealed normal heart sounds without murmurs, rubs, or gallops. Her lungs were clear without rales, wheezes, or rhonchi. Her abdomen was soft, without tenderness, guarding, or rebound, and she had normal bowel sounds.

Her musculoskeletal examination was normal, with +5/5 strength bilaterally in her upper and lower extremities. The patient’s skin examination also was normal. On neurological examination, her right upper extremity and right side of her face were noted to have decreased sensation via pinprick compared to the left side, but the examination was otherwise normal. The National Institutes of Health Stroke Scale score was 1.

The patient’s electrocardiogram (ECG) showed a normal sinus rhythm (rate, 90 beats/min), a lateral infarct of undetermined age, and a left atrial abnormality. Laboratory evaluation was significant only for a brain natriuretic peptide level of 334 pg/mL, a creatine phosphokinase (CPK) level of 782 IU/L, and a troponin I level of >50 ng/mL (Table). Serial cardiac enzyme levels were obtained and showed a decline of CPK from 782 IU/L to 331 IU/L over the following 36 hours. However, the troponin I levels remained >50 ng/mL for 5 days and then declined to 31.6 ng/mL.

A computed tomography (CT) scan of the brain without contrast revealed an acute to subacute infarct in the left occipital and left thalamic regions (Figure). A stat transthoracic echocardiogram (ECHO) performed in the ED revealed a dilated left ventricle with an ejection fraction of 20% to 25%, along with a hypokinetic anterolateral wall and an akinetic inferolateral wall. No atrial thrombus was visible on the ECHO. Doppler studies of the patient’s lower extremities were negative for deep vein thrombosis. Magnetic resonance imaging of her brain showed an infarct in the posterior circulation distribution involving the left occipital lobes and small areas in the left thalamic and right parietal-occipital regions. Hemorrhagic conversion of the left occipital infarct without mass effect was also noted. The patient was admitted to the neurological intensive care unit for frequent neurological examinations and close monitoring for worsening cerebral hemorrhage.

When the patient had still been in the ED, cardiology services were consulted; the cardiologist initiated a heparin drip with close monitoring of the coagulation studies. Cardiac catheterization was not done immediately because the ECG did not show acute ST elevations. The day after her presentation to the ED, the patient underwent a primary percutaneous coronary catheterization and was found to have a small rudimentary left anterior descending artery, with only small branches supplying the septal region. The right circumflex artery was very large and was supplying the lateral wall. No stents were placed during this procedure. A transesophageal ECHO (TEE) showed no evidence of a left atrial appendage thrombus.

The patient experienced an episode of coffee ground emesis while undergoing the TEE. Her hemoglobin declined from 11.9 g/dL to 7.9 g/dL, which led to a transfusion of 2 U of packed red blood cells and platelets. Heparin was discontinued and a proton pump inhibitor was started; however, no endoscopy was done at that time.

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