This report presents a case of a patient with AMI caused by coronary tumor embolism. Tumor emboli originated from an UTUC invading the left renal vein. Paradoxical coronary embolism through the PFO was thought to be the mechanism of AMI. Aspiration of the tumor embolus without stenting restored coronary blood flow.
Coronary embolism is the underlying cause of 2.9% of AMI . Embolus in coronary artery is commonly thromboembolus. Coronary tumor emboli, especially malignant tumor emboli, are very rare. Of the 147 patients with coronary embolism, two patients (1.4%) had malignancy as the etiology for coronary embolism . In patients with malignant coronary tumor embolism, lung carcinoma was the most common source of tumor embolus because lung carcinoma can directly invade the pulmonary vein and left atrium . Lung metastasis could cause coronary tumor embolism via the same mechanism. To the best of our knowledge, this is the first case report of coronary embolism caused by an UTUC. Contrast-enhanced CT showed no evidence of lung metastasis into the pulmonary vein in the patient. Clinicians should thus pay attention to the possibility of coronary tumor embolism in patients with malignancies other than lung tumors.
PFO is the most common congenital heart abnormality. A previous autopsy-based study reported that the prevalence of PFO was about 27% . About half of patients with cryptogenic stroke, which accounts for approximately 40% of ischemic strokes, have a PFO . Paradoxical embolism via PFO is a likely mechanism for stroke in this population. On the other hand, paradoxical embolism is a rare cause of AMI. Previous study reported that there were 33 (0.51%) presumed paradoxical coronary embolisms among 6502 patients with AMI . The mechanism of the low incidence of AMI is not well understood; however, blood flow distribution could contribute to the low incidence of AMI. In our case, transesophageal echocardiography revealed a PFO. In addition, contrast-enhanced CT showed tumor invasion of the left renal vein but no lung metastasis. Taken together, we believe that paradoxical embolism caused AMI in our patient.
PFO closure should be considered for secondary prevention of paradoxical embolism. Several studies showed that percutaneous PFO closure significantly reduced the risk of recurrent stroke [7,8,9]. However, patients aged > 60 years were excluded from these studies. In addition, the efficacy and the safety of PFO closure in patients with advanced cancer remain unclear. For these reasons, we did not perform PFO closure in this patient.
If there is angiographic evidence of coronary embolism, embolus aspiration should be considered. Although routine thrombus aspiration for AMI does not appear to improve clinical outcomes , embolus aspiration could restore coronary blood flow and may assist in the determination of the origin of the embolus by pathological examination . In our case, coronary blood flow was restored by aspiration without stenting because CAG and intravascular ultrasound revealed no evidence of atherosclerotic plaques. Histopathological examination revealed that the aspirated material was a tumor embolus originating from UTUC.
Cisplatin-based chemotherapy is associated with an increased risk of thromboembolic events . In our case, tumor embolus was the exact cause of AMI, which was revealed by the histopathological examination. On the other hand, the origin of the pulmonary emboli was unknown because the autopsy of this patient was not carried out. Although the size and echotexture of the mass attached to the tricuspid valve indicated that pulmonary emboli were tumor emboli, thromboemboli might partially contribute to pulmonary embolism.
In conclusion, malignant tumor embolus can induce AMI in a patient with upper UTUC without lung metastasis. Although it is a rare cause of AMI, we must be aware of it.