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A 75–year–old overweight man, affected by hypertension, diabetes mellitus and atrial fibrillation since 2020. After 3 unsuccessful attempts of electrical cardioversion it was opted for a strategy of rate control with beta blocker and anticoagulant therapy with Rivaroxaban 20 mg. Following episodes of rectal bleeding; adenocarcinoma of the colon was diagnosed. The patient underwent hemicolectomy and started therapy with Pembrolizumab. The anticoagulant was replaced with Edoxaban 60 mg. In August 2022, he was admitted to the emergency department for severe signs and symptoms of heart failure. On ECG, atrial fibrillation with a heart rate of 90 bpm and non–specific changes in ventricular repolarization. The echocardiogram showed a severe reduction of the ejection fraction (FE 30%), which was not present at previous controls. On blood tests, troponins were negative and BNP increased. The patient underwent coronarography which was negative for significant lesions, and heart failure therapy was prescribed. Three months later the patient came to our cardio–oncology outpatient clinic; we repeated the echocardiogram which showed a recovery of the ejection fraction to 45% and planned a cardiac MRI. Cardiac MRI (CMR) showed global left ventricular hypokinesia (FE 42%) and late subepicardial gadoline enhancement in the basal segment of the inferior wall and transmural in the basal segment of the lateral wall without signs of oedema. Report described as compatible with myocarditis. The case was discussed collegially with radiologists and oncologists, and it was decided to discontinue immunotherapy (ICI). Myocarditis is the most common cardiovascular adverse events of ICI therapy, although it has a very low incidence. Generally, myocarditis related to ICI therapy has a high mortality rate and requires discontinuation of ICI. In addition, CMR may have a lower sensitivity in this setting. There is also a possibility of developing left ventricular dysfunction without associated myocarditis in the absence of increase in cardiac troponin and active myocardial inflammation at CMR. Although our case has been defined as myocarditis, it presents some unclear aspects due in part to the early non–diagnosis as a complication of ICI therapy. Although cancer patients taking ICI has expanded considerably in recent years, the evidence on cardiovascular complications is scarce and unknown to the clinical cardiologist.

Case description: a previously healthy 26–year–old man presented with dyspnea on exertion and dry cough. CT scan revealed a large mediastinal mass with displacement of great vessels and trachea and pericardial effusion. Cardiac MRI showed the huge mediastinal mass, literally leaning on the heart with signs of compression of the pulmonary artery (Figure 1) with the typical D–shape of inter ventricular septum. Pericardial effusion did not compress the RV due to high intraventricular pressure. At baseline echo the mass simulated pulmonary artery stenosis as a consequence of pulmonary artery “ab extrinseco” compression. Surgical biopsy showed Ewing sarcoma lately redefined into undifferentiated round cell sarcoma so the patient started chemotherapy with VAI (vincristine, adriblastine, and ifosfamide) x6 followed by maintenance etoposide and ifosfamide (no anthraciclines for risk of cardiac toxicity). After induction phase MRI showed a partial response to treatment; mediastinal mass further reduced at the end of maintenance (Figure 2). Pericardial effusion disappeared and peak velocity of pulmonary artery went back to normal level at echo. Our patient underwent surgery with en–block removal of mediastinal mass with pericardium and anonymous vein and partial pulmonary upper left lobe resection with R0 resection. Pathology report confirmed an undifferentiated round cell sarcoma (possible embryonal origin, FISH analysis for EWS/FUS genes and 12p negative). Adjuvant mediastinal radiotherapy was delivered. The patient is alive without disease recurrence at one–year follow–up.

A 78 years old woman presented in our cardio–oncology out–patient clinic to renew apixaban treatment plan. In her medical history she was a former smoker, with a chronic kidney disease in IIIb stadium according to KDIGOI guidelines with a creatinine of 1,54 mg/dl, GFR according CKD 32 ml/min/1.73m2 and according Cockcroft e Gault 28 ml/min/1.73m2. In 2010, she had a right lobe pulmonary cancer diagnosis treated in neo–adjuvant with gemcitabine. After chemotherapy, she underwent surgical lobectomy. During hospitalization she had a deep venous thrombosis complicated by pulmonary thromboembolism, heparin sc was given with resolution of the clinical picture. In 2012 she had a recurrence of pulmonary thromboembolism. Heparin and warfarin in a second time was given. In 2016 for cancer disease progression, she underwent various oncological treatments and she found a stability disease with osimertinib and stereotaxic radiotherapy. Warfarin was switched to apixaban low–doses for low weight and chronic kidney disease. In 2021 in osimertinib therapy, cancer was under control. She was continuing low–dose apixaban. One year later, a CT scan demonstrated a disease progression and inferior cava venous thrombosis. A cardiac evaluation in our unit was required: patients was asymptomatic. EKG and Echocardiogram were normal. Apixaban low dose was changed to edoxaban 30 mg. There was a complete vein recanalization. Unfortunately, patient died after 8 months for cancer. It is important, in the direct oral anticoagulation therapy in cancer patient, to consider not only the indication for dose reduction known by the registration studies but also cancer and therapy factors.