Clinical Images

Metastatic Renal Cell Carcinoma Masquerading as ST-Segment Elevation Myocardial Infarction

Danai Kitkungvan, MD, *Sandeep Sharma, MD, *Luigi Pacifico, DO, *David H. Spodick, MD, DSc From the Department of Medicine, and the *Division of Cardiology, Saint Vincent Hospital, Worcester, Massachusetts. The authors report no conflicts of interest regarding the content herein. Manuscript submitted December 16, 2008, provisional acceptance given February 5, 2009, and final version accepted February 11, 2009. Address for correspondence: Danai Kitkungvan, MD, Department of Medicine, Saint Vincent Hospital, Worcester, MA 01608. E-mail: kitkungvan@hotmail.com
Danai Kitkungvan, MD, *Sandeep Sharma, MD, *Luigi Pacifico, DO, *David H. Spodick, MD, DSc From the Department of Medicine, and the *Division of Cardiology, Saint Vincent Hospital, Worcester, Massachusetts. The authors report no conflicts of interest regarding the content herein. Manuscript submitted December 16, 2008, provisional acceptance given February 5, 2009, and final version accepted February 11, 2009. Address for correspondence: Danai Kitkungvan, MD, Department of Medicine, Saint Vincent Hospital, Worcester, MA 01608. E-mail: kitkungvan@hotmail.com
Case Presentation. A 60-year-old male presented to the emergency department with exertional dyspnea. His past medical history was significant for hypertension and renal cell carcinoma (RCC), which had been diagnosed 2 years previously. He underwent a left nephrectomy followed by combination chemotherapy. However, the cancer was resistant to the chemotherapy and had progressed. His case had been followed by an oncologist from outside the hospital. Therefore, the full details of his medical record were not available to us upon his arrival. In the emergency department, his electrocardiogram (ECG) revealed new ST-segment elevation in leads V2–V6, which was different from his ECG 1 month previously (Figure 1). Emergent cardiac catheterization was performed and demonstrated no significant acute obstructive coronary artery disease. The patient’s serum creatine phosphokinase-myocardial band and troponin were checked upon admission and every 6 hours for 18 hours. All results were within normal limits. Transthoracic echocardiography revealed a large echodense lesion at the apical and lateral walls of the left ventricle, but without significant pericardial effusion and without any remarkable effects on ventricular function (Figure 2). Computed tomography (CT) of the chest showed a large lung mass invading the pericardium and the myocardium (Figure 3). Discussion. The common tumors that involve or metastasize to the heart are lung, stomach, breast and esophageal cancer, as well as those of malignant melanoma and lymphoma.1–3 While cardiac metastasis occurs in as many as 22–31% of lung cancer patients, the majority experience pericardial metastasis, and myocardial metastasis is described in 5.3–10.6% of patients.1,3,4 The symptoms of myocardial metastasis are nonspecific, therefore, most of the cases are diagnosed at autopsy.1,3 Changes in the ECG as a result of myocardial metastasis include heart rhythm disturbances, low voltage, ST-segment alterations and T-wave alterations.3,4 These findings are not specific for myocardial metastasis and can occur in patients with solely pericardial metastases or with other conditions.3,4 It is uncommon that an ECG corresponds to the pattern of acute myocardial infarction, including localized ST-segment elevation with or without the development of Q-S waves.4 The causes of ST-segment elevation in myocardial metastasis are not completely understood.3 Hartman et al postulated that the inflammatory reactions surrounding metastasis and potassium ion release from necrotic tissue and the adjacent myocardium are potential causes.2 Rosenbaum et al, however, suggested other possible explanations, including persistent myocardial injury caused by pressure, physicochemical action or by the interference of the blood supply as a result of malignant tissue invading the heart.5 ST-segment elevation in myocardial metastasis can be persistent, and several case reports demonstrate prolonged and even gradual progression of ST-segment elevation over time.2,3 A Q-S pattern due to myocardial metastasis is an unusual observation, and is probably caused by complete transmural invasion of the tumor into the myocardium.4 Similar to what is noted in the majority of the prior reports, our patient had prolonged ST-segment elevation in the absence of evolving changes, including Q waves, even after a follow-up visit at 3 months.1,4 Echocardiography and computed tomography of the chest are very useful tools that helped us to make a correct diagnosis in this patient. We believe the etiologies of his presentation are a combination of obstructive pneumonitis and the progression of his cancer. He showed some improvement after treatment with antibiotics and after receiving supportive care. As early as 1944, ST-segment elevation has been reported in cases of tumor invasion of the heart. The exact explanation of this phenomenon remains unclear. In a patient who presents with symptoms atypical of acute coronary syndrome, especially in a patient who has a history of cancer, the finding of persistent ST-segment elevation should raise suspicion of myocardial invasion.
References
1. Pan KL, Wu LS, Chung CM, et al. Misdiagnosis: Cardiac metastasis presented as a pseudo-infarction on electrocardiography. Int Heart J 2007:399–405.

2. Hartman RB, Clark PI, Schulman P. Pronounced and prolonged ST segment elevation: A pathognomonic sign of tumor invasion of the heart. Arch Intern Med 1982;142:1917–1919.

3. Matana A, Zaputovic L, Lucin K, Kastelan ZM. Persistent and progressive ST segment elevation caused by myocardial metastasis. Tumori 2006;92:452–454.

4. Abe S, Watanabe N, Ogura S, et al. Myocardial metastasis from primary lung cancer: Myocardial infarction-like ECG changes and pathologic findings. Jpn J Med 1991;30:213–218.

5. Rosenbaum FF, Johnston FD, Alzamora W. Persistent displacement of the ST segment in a case of metastatic tumor of the heart. Am Heart J 1944;27:667–675.