# Extensive myocardial calcification following cytokine release syndrome and sepsis: a novel case report with advanced echocardiographic assessment

**Authors:** Lucía Canales-Muñoz, Clara Ugueto-Rodrigo, Carlos Rodríguez-Carneiro, Alejandro Lara-García, Leonel Diaz-González, Raúl Moreno

PMC · DOI: 10.1093/ehjcr/ytag071 · 2026-02-18

## TL;DR

A patient with leukemia developed rare heart calcification after a severe immune reaction and sepsis, detected using advanced imaging techniques.

## Contribution

First reported case of rapid myocardial calcification linked to cytokine release syndrome and sepsis, using advanced echocardiographic methods.

## Key findings

- Computed tomography revealed extensive left ventricular myocardial calcification in a patient with acute myeloid leukemia.
- Advanced echocardiography showed progressive systolic dysfunction and impaired contractility despite preserved global work efficiency.

## Abstract

Myocardial calcification is a rare complication, typically associated with chronic myocardial injury or severe metabolic disturbances. Rapid development in the setting of cytokine release syndrome (CRS) and sepsis is exceptional and, to our knowledge, has not been previously reported.

We describe a 44-year-old man with acute myeloid leukaemia who developed CRS and subsequent septic shock, requiring high-dose vasopressor support and continuous renal replacement therapy. On day 70 of hospitalization, a computed tomography scan revealed extensive intramyocardial calcification of the left ventricle. Serial transthoracic echocardiography demonstrated progressive systolic dysfunction, with global longitudinal strain deteriorating from −22% to −9%, and a markedly reduced global work index (GWI 780 mmHg%), indicating impaired intrinsic contractility. Global work efficiency (GWE 96%) remained preserved.

This is the first reported case of rapidly progressive myocardial calcification associated with CRS, documented using advanced non-invasive imaging modalities such as GLS and myocardial work. These techniques enabled early detection and objective assessment of functional decline in a critically ill patient, in whom conventional diagnostic options were limited.

## Linked entities

- **Diseases:** acute myeloid leukaemia (MONDO:0015667), cytokine release syndrome (MONDO:0600008)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IDH2 (isocitrate dehydrogenase (NADP(+)) 2) [NCBI Gene 3418] {aka D2HGA2, ICD-M, IDH, IDH-2, IDHM, IDP}, NPM1 (nucleophosmin 1) [NCBI Gene 4869] {aka B23, NPM}, CD33 (CD33 molecule) [NCBI Gene 945] {aka CD33rSiglec, SIGLEC-3, SIGLEC3, p67}, CALCA (calcitonin related polypeptide alpha) [NCBI Gene 796] {aka CALC1, CGRP, CGRP-I, CGRP-alpha, CGRP1, CT}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}
- **Diseases:** vascular leak (MESH:D019559), phosphate (MESH:D007015), acute myeloid leukaemia (MESH:D054218), myocardial infarction (MESH:D009203), infection (MESH:D007239), end-stage renal disease (MESH:D007676), thrombocytopenia (MESH:D013921), sarcoidosis (MESH:D012507), neutropenia (MESH:D009503), contrast retention (MESH:D016055), ascites (MESH:D001201), microvascular dysfunction (MESH:D017566), systolic impairment (MESH:D000092244), sepsis (MESH:D018805), infectious (MESH:D003141), septic shock (MESH:D012772), hyperphosphatemia (MESH:D054559), necrosis (MESH:D009336), systemic (MESH:D015619), cardiac involvement (MESH:D006331), CRS (MESH:D000080424), amyloidosis (MESH:D000686), disturbances in calcium (MESH:D002128), ventricular dysfunction (MESH:D018754), multiorgan failure (MESH:D051437), Haematological pancytopenia (MESH:D010198), Myocardial calcification (MESH:D002114), haematologic malignancies (MESH:D009369), hyperparathyroidism (MESH:D006961), calcific deposition (MESH:D000079822), syndrome (MESH:D013577), lower limb oedema (MESH:D038061), inflammation (MESH:D007249), renal and hepatic dysfunction (MESH:D008107), volume overload (MESH:D019190), metabolic disturbances (MESH:D024821), critical illness (MESH:D016638), hypoxia (MESH:D000860), dystrophic (MESH:D020388), AML (MESH:D015470), cardiotoxicity (MESH:D066126), hypotension (MESH:D007022), ventricular ectopic beats (MESH:D018879), ARDS (MESH:D012128), arrhythmic (OMIM:212500), fever (MESH:D005334), cardiomyopathies (MESH:D009202), acute kidney injury (MESH:D058186), myocarditis (MESH:D009205), respiratory (MESH:D012131), left ventricular calcification (MESH:D018487), multiorgan dysfunction (MESH:D009102), arrhythmia (MESH:D001145), alveolar infiltrates (MESH:D017254), febrile (MESH:D000071072), alveolar haemorrhage (MESH:D006470)
- **Chemicals:** linezolid (MESH:D000069349), catecholamine (MESH:D002395), dexamethasone (MESH:D003907), amphotericin B. (MESH:D000666), urea (MESH:D014508), creatinine (MESH:D003404), calcium (MESH:D002118), hs- (MESH:D006859), ampicillin (MESH:D000667), cytarabine (MESH:D003561), cefiderocol (MESH:C000612166), idarubicin (MESH:D015255), phosphate (MESH:D010710), oxygen (MESH:D010100), tocilizumab (MESH:C502936), ceftolozane/tazobactam (MESH:C000594038), T (MESH:D014316), norepinephrine (MESH:D009638), gemtuzumab (MESH:D000079982), meropenem (MESH:D000077731), methylprednisolone (MESH:D008775)
- **Species:** Homo sapiens (human, species) [taxon 9606], Pseudomonas aeruginosa (species) [taxon 287], Enterococcus faecalis (species) [taxon 1351]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12966006/full.md

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Source: https://tomesphere.com/paper/PMC12966006