Case 20

Published on 02/03/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

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Case 20

A 43-year-old woman is admitted to the hospital for evaluation of chest pain. She had a prior history of hypertension, peripheral vascular disease, coronary artery disease, congestive heart failure, and defibrillator implant for primary prevention. She underwent coronary artery bypass grafting and pericardial stripping 12 years earlier. The details of this surgery and the indication are not available. Six years earlier, she underwent multivessel angioplasty in another hospital. She also had end-stage renal disease and was on hemodialysis. During her current admission to the hospital with chest pain, acute myocardial infarction was ruled out, and she was sent for pharmacologic stress perfusion imaging. She was on diltiazem, carvedilol, and pantoprazole. She underwent 2-day rest/stress perfusion imaging using 25 mCi of 99mTc-sestamibi on both days.

Pharmacologic stress was carried out using 5-minute adenosine infusion protocol. Her heart rate remained unchanged at 86 beats/min, and blood pressure changed from 144/64 to 122/63 mm Hg. There was no chest pain with adenosine infusion.

Her baseline electrocardiogram showed normal sinus rhythm. There was poor R-wave progression from V1 to V3, suspicious of an old anteroseptal myocardial infarction, and there were Q-waves in leads I and aVL, indicative of old lateral wall infarction. Electrocardiogram did not show changes from baseline with adenosine infusion.

Her stress images show a large area of perfusion abnormality involving the anterior wall and apex, which does not change on rest images. There is another moderate-sized area of perfusion abnormality involving the inferolateral wall, which also does not change on rest images. On gated SPECT imaging, the anteroapical wall is akinetic, and the remaining left ventricle is hypokinetic. The left ventricular ejection fraction is depressed at 29%. There is significant tracer activity in the gut on stress images, that is close to the heart. Nevertheless, the inferolateral perfusion abnormality does not appear to be contributed by gut activity alone. The patient was unable to lift her left arm above her head, and the left arm does result in attenuation artifact.

In addition, there is a large photopenic area in the left side of her chest involving the lower two-thirds of the hemithorax, raising suspicion of a large loculated left pleural effusion, a large bullous lesion, or a very large mass in the left hemithorax. This lesion seems to be pushing the mediastinum to the right and compressing on the lateral wall of the heart. The right lung is clear.

The raw transmission images indicate this to be radiodense lesion, excluding the possibility of a large bullous lesion. This dense mass could have also resulted in an attenuation artifact involving the inferior and lateral defects. However, the attenuation-corrected stress and rest images are not different from images not attenuation corrected. Therefore, it appears that despite the presence of a large thoracic mass and her left arm on her side, both anterior and inferolateral fixed perfusion abnormalities are real.

This study raises a question about the nature of her left thoracic mass. Her chest x-rays show a very large calcified mass in the left lower hemithorax extending into the upper abdomen. The patient suffered from massive left hemothorax in the past following pericardial stripping surgery, which resolved slowly over a long period and resulted in a large calcified mass in her left lung.

Computed tomography scan of the patient’s chest shows a large, peripherally calcified hematoma measuring 14 × 14 × 10 cm. Echocardiography showed global hypokinesia, with left ventricular ejection fraction 25%. There is a reverberation echo artifact, noted on the lateral wall of the left ventricle from the calcified mass.

This patient was treated medically for heart failure. She subsequently succumbed to gangrene of her legs due to peripheral vascular disease followed by amputations. She died 2 years later of fulminant sepsis from nonhealing stump ulcers.