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Background Cardiac tumours are typically secondary in nature, and the most common malignancies metastasizing to the heart are cancers of the lung, breast, oesophagus, melanoma, and lymphoma. We present a unique case of squamous cell carcinoma of the tongue, metastasizing to the heart and manifesting with ST elevation in the inferior-leads on electrocardiogram (ECG). Case summary A 25-year-old woman was initially diagnosed with squamous cell carcinoma of the tongue at the age of 23 and treated with hemi-glossectomy with clear-margins. Sixteen months later, the tumour recurred in the oropharynx and the left upper lobe of the lung. She was treated with chemotherapy; however, the tumour progressed. Thus, she was initiated on immunotherapy and radiation therapy. One month later, she presented with chest pain. Electrocardiogram revealed ST elevation in the inferior-leads. Troponin-I was elevated. Transthoracic echocardiogram revealed focal areas of thickening within the left and right ventricular myocardium with associated hypokinesis. These findings suggested ECG changes were likely secondary to infiltrative metastases and not acute-coronary-syndrome. Cardiac magnetic resonance imaging showed infiltrative masses with increased T2-signal and heterogeneous enhancement on perfusion and delayed enhancement sequences. Imaging also demonstrated numerous extra-cardiac metastases. She was treated with analgesics and discharged to home hospice. Discussion Head and neck cancers are a rare cause of cardiac metastasis. ST elevation and troponin release are thought to be due to tumour extension into the myocardium. Cardiac metastases usually present in patients with advanced widespread malignancy. In a cancer patient with cardiac symptoms or ECG changes, it is important to consider a broad differential diagnosis and entertain the possibility of cardiac metastasis.

Background While technological advances have made it possible to profile the immune system at high resolution, translating high-throughput data into knowledge of immune mechanisms has been challenged by the complexity of the interactions underlying immune processes. Tools to explore the immune network are critical for better understanding the multi-layered processes that underlie immune function and dysfunction, but require a standardized network map of immune interactions. To facilitate this we have developed ImmunoGlobe, a manually curated intercellular immune interaction network extracted from Janeway’s Immunobiology textbook. Results ImmunoGlobe is the first graphical representation of the immune interactome, and is comprised of 253 immune system components and 1112 unique immune interactions with detailed functional and characteristic annotations. Analysis of this network shows that it recapitulates known features of the human immune system and can be used uncover novel multi-step immune pathways, examine species-specific differences in immune processes, and predict the response of immune cells to stimuli. ImmunoGlobe is publicly available through a user-friendly interface at www.immunoglobe.org and can be downloaded as a computable graph and network table. Conclusion While the fields of proteomics and genomics have long benefited from network analysis tools, no such tool yet exists for immunology. ImmunoGlobe provides a ground truth immune interaction network upon which such tools can be built. These tools will allow us to predict the outcome of complex immune interactions, providing mechanistic insight that allows us to precisely modulate immune responses in health and disease.

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Adult-onset Still’s disease (AOSD) has a vast array of clinical presentations. Myopericarditis is one of the rarest cardiopulmonary manifestations of the disease and due to its rarity, the literature on the association of myocarditis with AOSD is sparse. Herein, we describe an interesting case of a 44-year-old male who presented with chest pain following exertion. He was febrile at the time of presentation and exam revealed inflammation in various joints. Electrocardiogram showed diffuse ST segment elevations in the precordial leads. Laboratory results revealed elevated troponin of 3.17 (<0.05 ng/mL) and CK-MB of 6 ng/mL along with elevated ferritin of 6225 (16-336 ng/mL). Cardiac MRI showed early and late gadolinium enhancement consistent with myocarditis. The patient was started on steroids and non-steroidal anti-inflammatory drugs (NSAID) resulting in clinical improvement. This case highlights the critical importance of diagnosis of pericarditis and myocarditis in patients with AOSD, as a missed diagnosis can lead to significant morbidity and mortality.

Cardiac involvement is rare in inflammatory bowel disease (IBD) but can occur as a complication of either the disease itself or drug therapy. We describe an interesting clinical scenario of acute myopericarditis during Crohn’s flare-up.
 A 37-year-old patient with severe Crohn's disease started having multiple bloody bowel movements associated with abdominal pain. These symptoms were attributed to Crohn's disease flare-up, prompting the addition of steroids and an increase in the dose of mesalamine without any significant relief. Two weeks later, he presented to the emergency department with pleuritic chest pain. Electrocardiogram (EKG) revealed ST segments elevation in leads I and aVL. Laboratory work revealed elevated troponin I of 1.82 ng/mL, with increased erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) of 121 mm and 180.1 mg/L, respectively. Cardiac magnetic resonance imaging (MRI) revealed early gadolinium enhancement consistent with myocarditis. The patient was started on colchicine with an increase in the dose of steroids, resulting in clinical improvement. The patient reported having similar chest pain during a previous episode of Crohn's disease flare-up, suggesting underlying IBD as the likely etiology.

Introduction Coronary artery aneurysms (CAA) are not commonly seen in the general population, with an incidence of approximately 0.37% to 2.53%. Patients are typically asymptomatic but symptomatic presentation varies from dyspnea and angina to myocardial infarction or even sudden cardiac death. Methods We conducted a retrospective analysis using the National Inpatient Sample Healthcare Cost and Utilization Project (NIS-HCUP) database to query individuals with the diagnosis of CAA with the International Classification of Disease (ICD) code 414.11 in all discharge diagnoses for the years 2006-2014. History of Kawasaki disease was determined by ICD code 446.1. Results From 2006 to 2014, there were 23,033 patients identified with CAA, correlating to approximately one case per 10,000 patients or an incidence of close to 0.01%. Of this, 1,405 or approximately 6.1% of these patients had Kawasaki disease. The mortality rate of CAA was 1.79%. In terms of demographics, Caucasians were the most likely to develop CAA, with 73.8% of cases. The mean age was 61.2 years, with a mean length of stay of 5.1 days. The average cost of admission was $70892. The presence of perivascular disease (15.5% vs 4.5% p<0.05), hypertension (66.1% vs 39.1% p<0.05), chronic lung disease (20.2% vs 15.1% p<0.05), diabetes (21.7% vs 15% p<0.05), renal failure (11% vs 8.8% p<0.05), coagulopathy (6.2% vs 3.4% p<0.05), and obesity (13.1% vs 8.2% p<0.05) were all risk factors for CAA as compared to those without. It was noted that weight loss (3.28% vs 1.91% p<0.05), electrolyte abnormalities (18.2% vs 15.5% p<0.05), and blood loss (2.1% vs 0.9% p<0.05) were protective of CAA. Conclusion CAA risk factors appear to be similar to those of coronary artery disease risk factors, with hypertension, diabetes, perivascular disease, and renal failure. Additionally, obesity was noted to be a risk factor but weight loss appeared to be protective. Interestingly, Kawasaki disease was seen at almost similar rates as these cardiac risk factors. The incidence of CAA we found, of almost 0.01%, is much less than in the quoted literature, however, previous studies did not have as many cases as our study.

Serum troponin is a marker of cardiac myocyte damage that is typically used to assess for myocardial infarction in the setting of acute coronary syndrome. However, many conditions, including cardiomyopathy, pulmonary embolism, or myocarditis, can cause an elevation in serum troponin. The most common use of this tool is to determine whether acute coronary syndrome (ACS) is occurring, but other differentials include cardiomyopathy, pulmonary embolism, and even acute heart failure. We present the case of a patient who presented with symptoms consistent with viral myocarditis but ultimately was found to have severe coronary artery disease (CAD). A 33-year-old Caucasian male with no cardiac risk factors other than a five-pack year smoking history, presented with progressively worsening upper respiratory symptoms, including sore throat and a non-productive cough that began a few weeks ago. These symptoms were associated with fevers, and 24 hours prior to admission, he developed intermittent chest pain at rest, radiating to the back, worsening in the supine position. In the emergency room (ER), the patient was found to have an elevated serum troponin of 15.61 ng/L (normal <0.05 ng/L). The electrocardiogram (EKG) showed T-wave inversions in the lateral leads. Based on his presentation and age, there was a high suspicion of viral myocarditis. However, non-ST elevation myocardial infarction (NSTEMI) had not yet been ruled out and the patient was started on started on a heparin infusion per the ACS protocol. A transthoracic echocardiogram showed wall motion abnormalities with low-normal left ventricular ejection fraction. A coronary angiogram showed severe CAD and he underwent staged a percutaneous coronary intervention with the resolution of symptoms. CAD and viral myocarditis, at times, can share common presenting symptoms, EKG changes, and laboratory findings. Out of all possible diagnoses, an elevation in serum troponin correlates to an MI up to 60% of the time. Myocarditis is the second leading cause of troponin elevation and accounts for 25% of cases. We highlight this case to discuss the importance of maintaining a broad differential and pursuing complete work-up when treating younger patients with chest pain and elevated serum troponin who lack typical risk factors for CAD.