Role of advanced cardiovascular imaging in chemotherapy-induced cardiotoxicity

Cannizzaro, Maria Teresa; Inserra, Maria Cristina; Passaniti, Giulia; Celona, A.; D’Angelo, Tommaso; Romeo, Placido; Basile, Antonio

doi:10.1016/j.heliyon.2023.e15226

Cited by 7 publications

(9 citation statements)

References 86 publications

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“…A recent review by Cannizzaro and coworkers, described current cardiac imaging methods for cardiotoxicity. The authors recognized that cardiac metabolic dysfunction, e.g., myocardial perfusion and mitochondrial function, might be found in these patients [119]. Citing Cadour, Thuny, and Sourdon [118] they dismissed the clinical utility of these imaging methods.…”

Section: Nuclear Medicine Diagnostic Imaging Of Cardiotoxicity Using ...mentioning

confidence: 99%

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Moncayo,

Moncayo

2024

Preprint

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Cardiotoxicity is an unwanted side-effect arising from different medications. The term describes a diminution of heart function, affecting especially left ventricular ejection fraction, which can progress to heart failure. Pediatric oncology patients treated with drugs of the anthracycline group, e.g., doxorubicin, can evolve to heart failure patients in adult age. Nuclear Medicine imaging of fatty acid oxidation and glycolysis accurately describes normal and altered heart metabolism. The most common finding is a state of cardiac glycolysis, which is reflected by increased uptake of 18F-desoxyglucose (18F-FDG) at a time when fatty acid oxidation is decreased. Glycolysis has recently been recognized as being the result of coenzyme Q10 deficiency as part of adaptation to hypoxia. Low LEVF correlates with impaired fatty acid oxidation. This deficiency can arise from chemotherapy and radiation and can be corrected by supplementation. Drugs like enalapril can improve fatty acid utilization. We will review relevant Nuclear Medicine imaging studies as well as fundamental biochemical data that demonstrate this pathogenetic path.

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Section: Nuclear Medicine Diagnostic Imaging Of Cardiotoxicity Using ...mentioning

confidence: 99%

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Moncayo,

Moncayo

2024

Preprint

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“…Also, 2-[18F]FDG PET is useful in detecting altered metabolism of the myocardium or in detecting cardiac inflammatory effects. Finally, cardiac perfusion PET may be applied for the effective detection of myocardial ischemia in patients who are candidates for potentially cardiotoxic cancer treatments or as a late sequelae after therapy, to monitor myocardial blood flow (MBF) or myocardial flow reserve (MFR) and cardiotoxic therapy or to explore mechanisms of cardiotoxicity [11,[13][14][15][16].…”

Section: Cardiac Imaging Modalities and Cardiac Biomarkers In Patient...mentioning

confidence: 99%

Applied Cardio-Oncology in Hematological Malignancies: A Narrative Review

Mandala,

Lafara,

Kokkinovasilis

et al. 2024

Life

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Applied cardio-oncology in hematological malignancies refers to the integration of cardiovascular care and management for patients with blood cancer, particularly leukemia, lymphoma, and multiple myeloma. Hematological cancer therapy-related cardiotoxicity deals with the most common cardiovascular complications of conventional chemotherapy, targeted therapy, immunotherapy, chimeric antigen receptor T (CAR-T) cell and tumor-infiltrating lymphocyte therapies, bispecific antibodies, and hematopoietic stem cell transplantation. This narrative review focuses on hematological cancer-therapy-related cardiotoxicity’s definition, risk stratification, multimodality imaging, and use of cardiac biomarkers to detect clinical and/or subclinical myocardial dysfunction and electrical instability. Moreover, the most common cardiotoxic profiles of the main drugs and/or therapeutic interventions in patients with hematological malignancies are described thoroughly.

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“…Previous research has shown that CMR-ECV can predict the occurrence of myocarditis caused by cardiotoxic chemotherapeutic drugs such as doxorubicin early and effectively ( 16 ). Another study also showed that the elevated myocardial ECV closely correlates with diastolic dysfunction, which can be displayed by CMR ( 17 ). However, CMR has many disadvantages, such as long scan time, high heart rate requirements, and unsuitability for patients with claustrophobia; CMR imaging has not been widely utilized in clinical practice in medical institutions.…”

Section: Introductionmentioning

confidence: 98%

Myocardial extracellular volume derived from contrast-enhanced chest computed tomography in longitudinal evaluation of cardiac toxicity in patients treated with immune checkpoint inhibitors

Wang,

Ouyang,

Tang

et al. 2024

Quant Imaging Med Surg

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Background The immune-related adverse effects after immune checkpoint inhibitors (ICIs) treatment have always been a hot topic. Although the incidence of myocarditis is not high among the related adverse effects, the mortality rate is extremely high once it occurs. In the past, the risk of cancer therapy-related cardiac dysfunction (CTRCD) after drug treatment was evaluated based on imaging examinations, but this evaluation still had certain limitations. Currently, the extracellular volume (ECV) score measurement calculated using cardiac magnetic resonance T1 mapping has become a reliable method for evaluating myocardial toxicity and computed tomography (CT) examination may become an alternative. This study aimed to longitudinally evaluate the cardiac toxicity of patients treated with ICIs using myocardial ECV derived from contrast-enhanced chest CT. Methods A total of 500 patients with III–IV lung cancer and esophageal cancer treated with ICIs were evaluated. Participants underwent baseline examination and at least 1 follow-up examination after treatment. Contrast-enhanced chest CT-ECV, left ventricular ejection fraction (LVEF), and measurement of cardiac troponin T (cTnT) were conducted before the first treatment, 3–6 months after the first treatment, and about 12 months after the first treatment, respectively. The ECV value of the middle part of the left ventricular septum was evaluated on CT venography and plain scan, the LVEF value was evaluated by color Doppler ultrasound, and the quantity of cTnT was detected by chemiluminescence. Cancer therapy-related cardiac dysfunction was recorded. Results The mean baseline LVEF value was 68.51%±4.81% (N 0 =500), and those of LVEF 1 , LVEF 2 , and LVEF 3 were 68.77%±4.30%, 68.16%±3.59%, and 66.23%±4.20%, respectively (N 1 =500, N 2 =467, and N 3 =361, respectively). There was no significant difference between LVEF 1 , LVEF 2 , and LVEF 0 (P 1 =0.095, P 2 =0.062), whereas LVEF 3 was significantly lower than LVEF 0 (P<0.001). The average baseline cTnT 0 value was 7.42±3.95 (N 0 =500). The values of cTnT 1 , cTnT 2 , and cTnT 3 were 10.05±11.40, 12.24±13.59, and 14.54±14.49, respectively (N 1 =500, N 2 =467, N 3 =361). The values of cTnT 1 , cTnT 2 , and cTnT 3 were significantly higher than cTnT 0 (P ...

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Role of advanced cardiovascular imaging in chemotherapy-induced cardiotoxicity

Cited by 7 publications

References 86 publications

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Applied Cardio-Oncology in Hematological Malignancies: A Narrative Review

Myocardial extracellular volume derived from contrast-enhanced chest computed tomography in longitudinal evaluation of cardiac toxicity in patients treated with immune checkpoint inhibitors

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