A curious case of acute myocardial calcificationsA curious case of acute myocardial calcifications
Faculty of Medicine and Health Sciences
Antwerp Surgical Training, Anatomy and Research Centre (ASTARC)
2016Philadelphia :Lippincott williams & wilkins, 2016
Circulation / American Heart Association. - New York, N.Y.
133(2016):10, p. E426-E427
University of Antwerp
A 56-year-old woman was admitted to a regional hospital for increasing chest and abdominal pain after falling from the stairs. Initial screening showed a pulmonary contusion of the left lower lobe and signs of a myocardial contusion characterized by elevated troponins without ST-T abnormalities. She had acute renal failure without rhabdomyolysis and a highly elevated C-reactive protein (800 mg/L). As a result of increasing respiratory insufficiency, she was transferred to the intensive care unit for further treatment. Three days after hospital admission, she developed diffuse ST-segment elevations on ECG and elevated cardiac enzymes. Given the suspicion of coronary artery disease, she was transferred to our institution for an urgent coronary intervention. On arrival in our institution, laboratory findings revealed an elevated white blood cell count (15.3×109/L), a highly elevated C-reactive protein (578 mg/L), severe renal failure with a glomerular filtration rate of 6 mL·min-1·1.73 m-2, hypocalcemia (1.55 mmol/L), elevated troponins (troponin I, 86.5 µg/L), elevated creatine kinase (5429 U/L), and elevated creatine kinase-MB (97.9 µg/L). Despite the elevated cardiac enzymes, coronary angiography showed no coronary abnormalities. At this time, a tentative diagnosis was established of severe sepsis with concomitant septic cardiomyopathy. An initial contrast-enhanced computed tomography (CT) scan at hospital admission showed no morphological cardiac abnormalities, notably with a normal appearance of the left ventricular myocardium (Figure 1A). However, a follow-up CT scan 13 days after hospital admission revealed an ill-defined increased density of the left ventricular wall with a predominantly epicardial distribution (Figure 1B). A follow-up CT scan 44 days after hospital admission showed extensive myocardial calcifications in the left ventricle (apex, septum, and anterolateral and inferior wall; Figures 1C and 2A2C). Initial transesophageal echocardiography at hospital admission showed an estimated ejection fraction of 40% (Movie I in the online-only Data Supplement). Follow-up transthoracic echocardiography (5 months after hospital admission) showed a diffuse hypokinetic left ventricle with an estimated ejection fraction of only 20% (Movie II in the online-only Data Supplement). The right ventricular function, on the other hand, remained normal. This was illustrated by a normal tricuspid annular plane systolic excursion. No significant valvular disease was noted at baseline or at follow-up. On the basis of the combination of clinical, laboratory, and imaging findings, a final diagnosis of septic cardiomyopathy characterized by elevated cardiac enzymes without coronary abnormalities was established. This was further substantiated by the rapid appearance of myocardial calcifications, the concomitantly deteriorating cardiac function, and the absence of abnormal serum levels of calcium and phosphorus or any other relevant metabolic condition during hospital admission.