A 57-year-old man presented to an outside ED complaining of chest and upper abdominal pain that had started a few hours ago.
The patient reported shortness of breath, weakness, weight loss, lightheadedness, voice hoarseness, and dry heaves of a few weeks' duration. He denied hemoptysis or fever. He had no reported episodes of syncope or sputum production. His past medical history was significant for stage IV squamous cell lung carcinoma of the left upper lobe, diagnosed about 6 months ago, with metastases to the left adrenal gland and liver. He stated he was undergoing chemotherapy and radiation therapy, with his last chemotherapy treatment 4 months ago. Other relevant medical history included chronic obstructive pulmonary disease, hypertension, and distal neuropathy secondary to chemotherapy. The patient had an 18-pack-year history of smoking. He denied use of alcohol, but admitted to recreational marijuana use.
The patient's vital signs were BP, 119/81 mm Hg; pulse, 101 beats/minute; respirations, 18; oral temperature, 97.6° F (36.4° C), and SpO2, 100% on room air. Cardiopulmonary auscultation revealed distant heart sounds, but no murmurs, gallops, or rubs. Diminished breath sounds on the right side also were noted.
Abnormal laboratory values included leukocyte level of 20,500 cells/mcL (normal range, 4,000 to 11,000 cells/mcL), hematocrit of 23.7% (normal range, 41% to 53%), calcium of 11.6 mg/dL (normal range, 8.6 to 10.2 mg/dL), troponin I of 1.26 ng/mL (normal range, 0.4 ng/mL or less), brain natriuretic peptide of 3,110 pg/mL (normal range, 300 pg/mL or less), procalcitonin of 2.38 ng/mL (normal range, 0.1 ng/mL or less), and lactate of 1.2 mmol/L (normal range, less than 1.3 mmol/L). An ECG revealed persistent inferior ST-segment elevation myocardial infarction (STEMI) (Figure 1).
- Pulmonary embolism
- Primary cardiac tumor
- Metastatic cardiac tumor
- Infiltrative disease of the heart
The patient was initially treated with fibrinolytic therapy for the STEMI, but had no sign of reperfusion, as evidenced by persistence of chest pain and ST-segment elevation. He was transferred to our facility for rescue coronary angiogram, which revealed no coronary artery disease, thus ruling out a spontaneous MI due to plaque rupture. However, the unusual displaced appearance of the posterolateral ventricular branch and posterior descending artery of the right coronary artery suggested possible extrinsic compression (Figure 2). The patient underwent a CT scan of the chest to further evaluate the extrinsic compression. The imaging revealed a large low-density mass (8.2x7.1x8.8 cm) along the inferior aspect of the heart in the pericardium. The mass invaded the right ventricle, almost completely obliterating the cavity and extended into the interventricular septum and to a lesser extent the left ventricle. The scan also revealed a partially necrotic central left upper lobe mass that extended to the left hilum and measured 3.8x4.1x2.7 cm.
An echocardiogram revealed moderate hypokinesis of the inferior wall of the left ventricle. Furthermore, mobile vegetation-like, fluctuant echodensities were seen in both ventricles attached to the septum (Figure 3). The tumor infiltrated the right ventricle, interventricular septum, and to a lesser extent the left ventricle. The patient's ejection fraction was 55% and he had mild tricuspid regurgitation. Right ventricular systolic pressure was elevated at 30-40 mm Hg. He had no pericardial effusion.
In this patient, CT and echocardiogram findings led to a diagnosis of metastatic cardiac tumor, predominantly in the right ventricle and interventricular septum with mobile tumor clots. The most likely explanation of the STEMI in this patient was the extrinsic compression or infiltration of the posterior descending artery or the posterolateral ventricular branch of the right coronary artery by the tumor, rather than an embolus from tumor clots. Embolism was extremely unlikely because it was not evident at the cardiac catheterization and tumor clots are not likely to dissolve spontaneously with fibrinolytic therapy before cardiac catheterization.
After the diagnosis of metastatic cardiac tumor was established, the patient's condition deteriorated and he sought palliative care.
Primary cardiac tumors are extremely rare, occurring in less than 0.1% of postmortem analyses, and the prevalence of secondary metastatic tumors is underreported.1 Cardiac metastases can be found in up to 25% of patients who have died of malignancies.2 In one examination series, squamous cell carcinomas of the lung spread to the heart in 23.4% of patients.3 The most common site for cardiac metastases is the pericardium, occurring 64% to 69% of the time in reported case series.1
Primary cardiac tumors such as cardiac myxoma are predominantly benign.4 Only 25% of primary cardiac tumors are malignant.5 Cardiac sarcomas, the most common type, tend to occur in young patients with a mean age of 44 years and affect both sexes equally.6
Secondary cardiac tumors, on the other hand, are by definition malignant. The most common cause of cardiac metastases is malignant melanomas, due to their susceptibility to spread hematogenously.1
Malignancies can travel to the heart by one of four pathways: lymphatic, hematogenous, direct extension, and transvenous extension via the venae cavae.7 The pathway taken often influences the location where the metastasis takes hold. For example, pericardial metastases often arise from lymphatic spread; myocardial metastases often arise from hematogenous spread.2 The most common site for cardiac metastases is the pericardium, occurring 64% to 69% of the time in reported case series. Other sites, in decreasing order of prevalence, are the epicardium, myocardium, and endocardium.2 The most likely mechanism by which the squamous cell carcinoma spread to the heart in this patient was via the lymphatic route.
Patient presentation is chiefly determined by the size of the cardiac metastasis. If the tumor is small, the clinical picture is often silent. Clinical features that accompany a cardiac metastasis include tachycardia due to pericardial effusion, heart failure, and atrial or ventricular dysrhythmias.
Certain clinical features may present depending on the location of the metastases. A pericardial metastasis may cause pericarditis, serosanguineous or hemorrhagic pericardial effusion, and, in severe cases, cardiac tamponade. Although more likely to occur in myxomas, left-sided cardiac metastasis can lead to systemic emboli. In addition, angina pectoris, myocardial ischemia, and MI may be caused by a coronary embolism or compression of a coronary artery, as was seen in this patient.1
Overall, the incidence of MI presentation of cardiac tumors has not been well established due to their rarity. However, ECG findings of ST-segment elevation without symptoms of ischemia have a high specificity for cardiac metastases.8 However, other patients may present with features of acute coronary syndrome with an ECG mimicking a STEMI. In one literature review, 18 patients with metastatic cardiac tumor had STEMI-like ECG changes. Most had ST-segment elevation in the precordial or lateral leads, with only one patient having elevations in the inferior leads, as was seen in our patient.9
In terms of formal diagnosis, advanced radiographic techniques tend to be the test of choice. Echocardiography, CT, and MRI may all be employed to visualize cardiac and mediastinal structures to a great degree of specificity. These imaging techniques can be used for a definitive diagnosis and to narrow the differential, which may include vegetation, thrombus, and foreign body.2
Once confirmed, most patients who present with advanced cardiac metastases are often at a late stage of disease. Palliative treatment often is the best choice of action except in limited cases where surgical resection may be beneficial to the patient, such as decompressing a symptomatic pericardial effusion.10 Of note, invasions of the right atrium transvenously have been successfully resected in a number of cases.11
This case highlights an uncommon presentation of acute MI secondary to metastatic cardiac tumor in a patient without coronary artery disease. Clinicians should be aware of such an atypical cause of acute coronary syndrome and how symptomology of such an unusual case is based on size of the metastasis as well as its location.
1. Goldberg AD, Blankstein R, Padera RF. Tumors metastatic to the heart. Circulation
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4. Colin GC, Gerber BL, Amzulescu M, Bogaert J. Cardiac myxoma: a contemporary multimodality imaging review. Int J Cardiovasc Imaging
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6. Ramlawi B, Leja MJ, Abu Saleh WK, et al. Surgical treatment of primary cardiac sarcomas: review of a single-institution experience. Ann Thorac Surg
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8. Cates CU, Virmani R, Vaughn WK, Robertson RM. Electrocardiographic markers of cardiac metastasis. Am Heart J
9. Suga T, Akuzawa N, Hatori T, et al. ST segment elevation in secondary cardiac cancer: a case report and review of the literature. Int J Clin Exp Med
10. Poole GV Jr, Meredith JW, Breyer RH, Mills SA. Surgical implications in malignant cardiac disease. Ann Thorac Surg
11. Timmis AD, Smallpeice C, Davies AC, et al. Intracardiac spread of intravenous leiomyomatosis with successful surgical excision. N Engl J Med