Abstract
A 72-year-old male with a history of chronic lymphocytic leukemia (CLL) was admitted to hospital with a productive cough and an episode of diarrhea and vomiting. He was initially treated for pneumonitis and sepsis. On the 12th day of his admission, he reported chest pain. Changes on his electrocardiogram were suggestive of myocardial ischemia and an elevated troponin rise was detected from his blood tests. A diagnosis of acute coronary syndrome was made but due to his frailty, he was medically managed. His echocardiogram revealed an external echogenic mass which invaded the anterolateral left ventricular wall. Further imaging with cardiac magnetic resonance imaging (MRI) and computed tomography (CT) thorax demonstrated external encasement of left circumflex coronary artery with mediastinal mass, leading into downstream myocardial ischemia and subsequent necrosis. He was considered suitable for aggressive radiotherapy/chemotherapy but passed away 7 days later. This case highlights the unusual case where an acute myocardial infarction can be attributed to direct infiltration and external compression of coronary artery by mediastinal tumor and the value of multi-modality imaging (echocardiogram, CT, and MRI) in identifying the cause of myocardial ischemia in patients with CLL in the end stages of the disease.
< Learning objective: It is unusual that acute coronary syndrome is caused by direct tumor infiltration and obstruction of a major epicardial vessel. This case highlights the interesting and unusual scenario where tumor growth results in complete occlusion of the obtuse marginal coronary artery in a patient with chronic lymphocytic leukemia. By using multi-modal imaging, we were able to characterize the lesion and the coronary involvement.>
Introduction
Chronic lymphocytic leukemia (CLL) is a malignancy of CD5 + B cells where there is an accumulation of mature-appearing neoplastic lymphocytes which can accumulate in the peripheral blood, bone marrow, and lymphoid tissues . The complications in CLL relate to the spread of malignant cells, which commonly involve spleen and liver. In advance stages of CLL, the neoplastic cells may invade other organs including prostate, pituitary, thyroid glands, and myocardium . There are rare case reports of acute myocardial infarction as the result of microvascular obstruction secondary to direct leukemic infiltration and vasoconstriction, with minor epicardial coronary artery luminal stenosis [ , ]. Here, we present a patient with known CLL who, during an admission with suspected recurrent pneumonitis, later developed an acute coronary syndrome caused by direct infiltration and obstruction of a major epicardial vessel.
Case report
A 72-year old Caucasian man presented to the accident and emergency department complaining of feeling generally unwell with a productive cough and an episode of diarrhea and vomiting. He was under surveillance for CLL and autoimmune hemolytic anemia. In addition, he had bronchiectasis and recurrent Klebsiella infections. His other comorbidities included previous transient ischemic attack and type 2 diabetes mellitus. He lived with his wife and was normally an independent, non-smoker and did not consume alcohol.
On examination he was found to be febrile (38.0 °C), tachycardic (123 beats/min), tachypneic (25 breaths/min), with reduced air entry to the left base of the lungs and widespread crepitations on auscultation of both lung fields. His blood pressure was 100/46 mmHg. He was hypoxic on arrival and his oxygen saturations became stable at 100% on 15 L of oxygen. The working diagnosis was recurrent pneumonitis.
His blood test showed hemoglobin 116 g/L, white cell count 9.2 × 10 9 /L, a low platelet count at 43 × 10 9 /L, profound neutropenia at 1 × 10 9 /L, raised C-reactive protein 109 mg/L, estimated glomerular filtration rate >90/min/1.73 m 2 , K 4.6 mM, Ur 8.7 mM, and the venous blood gas showed pH 7.39, pCO 2 4.58 kPa, lactate 2.7 mM, and HCO 3 − 21 nM.
His electrocardiogram was reported by the team reviewing as sinus tachycardia, rate: 150 bpm with no significant ST or T wave changes ( Fig. 1 A).
The chest X-ray demonstrated a left-sided chest wall opacity ( Fig. 1 B). He was started on intravenous hydrocortisone the next day with a provisional diagnosis of neutropenic sepsis, infection originating from chest. Blood cultures were obtained.
On day 12 of admission the patient fell in the bathroom, on questioning he reported having central chest discomfort, rate 5/10 in severity which caused him to fall. An electrocardiogram was performed which demonstrated 1 mm ST segment elevation and T wave inversion in leads I and aVL, as well as V4 to V6, compatible with high-lateral myocardial infarction, with repolarization abnormities ( Fig. 1 C). It was noted that the treating doctor highlighted the inferolateral T-wave inversion but there were typical changes consistent with an evolving high lateral ST-elevation myocardial infarction likely in the left circumflex territory. His troponin I was checked and was found to be significantly elevated at 1613 ng/mL; the patient was started on acute coronary syndrome regimen with dual antiplatelet, high-dose statin. As the patient’s symptoms had settled analgesia and nitrates were not commenced. An urgent echocardiogram was requested.
The echocardiogram showed an echogenic mass surrounding anterolateral left ventricular epicardial space, potentially infiltrating into the myocardium ( Fig. 2 ). There was a normal size left ventricular cavity with moderate left ventricular systolic impairment, due to antero-apical and lateral regional wall motion abnormality. Estimated left ventricular ejection fraction was calculated to be 40–44%. A computed tomography (CT) of the thorax, abdomen, and pelvis was arranged as well as a cardiac magnetic resonance imaging (MRI) scan.
