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A 60-year-old female without coronary risk factors was admitted to the hospital with ST-elevation acute coronary syndrome (ACS). She had previously suffered breast cancer and received radical mastectomy followed by chemotherapy and radiation. Emergent coronary angiography showed an occlusion of the proximal left anterior descending coronary artery (LAD) and coronary angioplasty was performed. Coronary computed tomography (CT) angiography (CTA) disclosed a tumor invading the left ventricular anterior wall and surrounding the coronary artery. Myocardial single-photon-emission CT (SPECT) using 123I-BMIPP showed a defect in the same portion. A fusion image of the CTA and the SPECT delineated a tumor surrounding the coronary artery. She finally died two months later from a terminal condition.
Autopsy demonstrated a tumor involving the left ventricular anterior wall and surrounding the LAD. Pathology of the affected LAD showed only fibrous plaque without vulnerable plaque, thrombus, or tumor invasion to the coronary wall. Thus, compression of the coronary artery by the metastatic tumor was the most likely mechanism of ACS.
]. We report a rare case of ACS, in which coronary obstruction was not due to plaque rupture but to compression of the coronary artery by a metastatic cardiac tumor. A fusion image of coronary computed tomography (CT) angiography (CTA) and myocardial single-photon-emission CT (SPECT) was very useful to delineate the relationship between the tumor and the affected coronary artery.
A 60-year-old female was admitted to our hospital because of strong chest pain from the morning. She had received radical mastectomy for breast cancer 16 years earlier and subsequent chemotherapy. Seven years later she underwent operation and chemotherapy for the tumor metastasis to the lumbar vertebra. Because of relapses of the metastatic lesion, she repeatedly received operation, chemotherapy, and radiation therapy, and was subjected to terminal home care.
On admission, her blood pressure was 110/60 mmHg and heart rate was 130 bpm with regular sinus tachycardia. An electrocardiogram showed pronounced ST-segment elevation in the precordial leads, indicating ST-elevation ACS (Fig. 1A ). Echocardiography showed hypokinesis of the left ventricular anterior wall, however it did not identify any abnormal mass. Emergent coronary angiography (CAG) showed an occlusion of the proximal left anterior descending coronary artery (LAD) and an intracoronary injection of nitrate did not relieve the occlusion. Thus, coronary angioplasty was performed.
At coronary angioplasty, we selected plain balloon angioplasty instead of stent deployment, because antiplatelet therapy after the stent deployment seemed unfavorable for both her terminal condition and persistent bloody urine as radiation cystitis. A guide-wire was easily crossed through the coronary lesion, however, an adequately size balloon slipped at the lesion on its inflation over 2 atm pressures. The lesion was finally dilated by a deep engaging technique with a guide-catheter. Final CAG showed relatively smooth coronary artery wall and no intracoronary thrombi. Chest pain and the ST-segment elevation disappeared after the angioplasty (Fig. 1B). During hospitalization, she did not have any arrhythmia or heart failure and a serum level of creatine kinase was within normal range.
Coronary CTA (Brilliance 64, Philips, Eindhoven, the Netherlands) performed one week later identified a mild stenosis in the proximal LAD (Fig. 2A ) and a tumor invading the anterior myocardium and involving the coronary artery (Fig. 2B). The mild stenosis suggested recoil of once dilated coronary artery. Myocardial SPECT with 123I-BMIPP showed a defect in the mid antero-septal and anterior wall (Fig. 3A ), whereas a fusion image (MultiDataFusion, Ziosoft, Inc., Tokyo, Japan) of the coronary CTA and the myocardial SPECT delineated the tumor overlying the LAD as well as the low radioisotope uptake in the anterior wall. The tumor was not involved in fatty acid metabolism (Fig. 3B).
She died two months later and autopsy defined a tumor overlying the left ventricular anterior wall and the LAD (Fig. 4A ). The transverse section of the left ventricle showed metastatic cardiac tumors invading the anterior wall and the ventricular septum (Fig. 4B). No continuity between these tumors was observed. The tumors were histologically composed of sarcoma and spotty hemorrhage was shown in the tumor surrounding the coronary artery. Cross-sections of the LAD disclosed a focal eccentric and fibrous plaque without vulnerable plaque, plaque rupture, or thrombus (Fig. 4C). There was no tumor invasion into the coronary artery wall. Metastatic tumors to the lumbar vertebra and the lung also showed sarcoma in histology.
About 5% of acute myocardial infarctions are not based on coronary atherosclerosis and plaque rupture [
], and various causes are involved such as infectious disease, amyloidosis, embolism, neoplasm, radiation-associated fibrosis, and cocaine abuse. Metastatic cardiac tumors are frequently asymptomatic but, depending on the tumor location and extent, heart failure, pericardial effusion, arrhythmia, and sudden cardiac death can occur [
As a mechanism of myocardial infarction in this case, we first suspected coronary tumor embolism, because she had no coronary risk factors and was in a terminal stage of breast cancer and its metastatic tumor to lumbar vertebrae. However, CAG documented neither tumor embolism nor thrombus formation. Further, CAG after angioplasty showed a relatively smooth coronary artery wall and no slow flow, indicating that plaque rupture or thrombus was not associated with the coronary obstruction. Thus, we speculated that ACS was caused by coronary compression of the metastatic cardiac tumor.
The autopsy finding macroscopically coincided with the CTA/SPECT fusion image. The coronary lesion showed focal fibrous plaque without thrombus, plaque rupture, or tumor invasion into the coronary artery wall. The plaque had histologically two differential layers (Fig. 4C). In the inner layer, most of the intimal thickening appeared to be composed of immature extracellular matrix, that is thought to reflect neointimal proliferation after balloon angioplasty two months previously.
Since the tumors in the heart and the lung histologically showed sarcoma, we considered that the metastatic tumor in the lumbal vertebrae was transformed to sarcoma by repeated radiation to the vertebrae and thus the tumors in the heart and the lung originated from the vertebral tumor.
Conclusively, ACS in this case was due to a coronary artery compression by a metastatic cardiac tumor. A CTA/SPECT fusion image is very useful to clarify the relationship between the tumor and the affected coronary artery.