Cancer Chemotherapy-Induced Sinus Bradycardia: A Narrative Review of a Forgotten Adverse Effect of Cardiotoxicity

Tamargo, Juan; Caballero, Ricardo; Delpón, Eva

doi:10.1007/s40264-021-01132-5

Cited by 7 publications

(2 citation statements)

References 169 publications

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“… 14 They can be caused by anti-cancer-induced fibrosis and radiation therapy, directly affecting the heart conduction system. 17 Concerning bradycardia, paclitaxel is considered as the main causative agent among chemotherapeutic drugs via its direct effect on Purkinje fibers or extracardiac autonomic control. 18 QT prolongation causative mechanisms remain unknown and are still quite rare, especially related to small molecule tyrosine kinase inhibitors.…”

Section: Cardiotoxicity Manifestations and Mechanismsmentioning

confidence: 99%

Multimodality imaging in cardio-oncology: the added value of CMR and CCTA

Lisi

Catapano

Rondi

et al. 2023

The British Journal of Radiology

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During the last 30 years, we have assisted to a great implementation in anticancer treatment with a subsequent increase of cancer survivors and decreased mortality. This has led to an ongoing interest about the possible therapy-related side-effects and their management to better guide patients therapy and surveillance in the chronic and long-term setting. As a consequence cardio-oncology was born, involving several different specialties, among which radiology plays a relevant role. Till the end of August 2022, when European Society of Cardiology (ESC) developed the first guidelines on cardio-oncology, no general indications existed to guide diagnosis and treatment of cancer therapy-related cardiovascular toxicity (CTR-CVT). They defined multimodality imaging role in primary and secondary prevention strategies, cancer treatment surveillance and early CTR-CVT identification and management. Cardiac computed tomography angiography (CCTA) has acquired a central role in coronary assessment, as far as coronary artery disease (CAD) exclusion is concerned; but on the side of this well-known application, it also started to be considered in left ventricular function evaluation, interstitial fibrosis quantification and cardiac perfusion studies. Cardiac magnetic resonance (CMR), instead, has been acknowledged as the gold standard alternative to trans-thoracic echocardiography (TTE) poor acoustic window in quantification of heart function and strain modifications, as well as pre- and post-contrast tissue characterization by means of T1-T2 mapping, early Gadolinium enhancement (EGE), late Gadolinium enhancement (LGE) and extracellular volume (ECV) evaluation. Our review is intended to provide a focus on the actual role of CMR and CCTA in the setting of a better understanding of cardiotoxicity and to draw some possible future directions of cardiac imaging in this field, starting from the recently published ESC guidelines.

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Section: Cardiotoxicity Manifestations and Mechanismsmentioning

confidence: 99%

Multimodality imaging in cardio-oncology: the added value of CMR and CCTA

Lisi

Catapano

Rondi

et al. 2023

The British Journal of Radiology

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“…This damage leads to a weakened heart, diminishing its ability to pump blood effectively. Radiation therapy, chemotherapy agents like anthracycline, anorexia nervosa issues, heavy metal exposure, chronic cocaine usage, or incorrectly administered drugs like doxorubicin (DOX) can all cause cardiotoxicity as a side effect [ 1 ]. Manifestations of cardiotoxicity vary widely, from minor blood pressure fluctuations to severe outcomes like arrhythmias and cardiomyopathy, potentially leading to death or chronic heart failure [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Azilsartan improves doxorubicin-induced cardiotoxicity via inhibiting oxidative stress, proinflammatory pathway, and apoptosis

Janabi,

Al-Chlaihawi

2023

JMedLife

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Azilsartan, a known angiotensin receptor blocker, has shown potential in reducing 24-hour blood pressure and may have protective effects against cardiac complications. Increased oxidative stress in cardiac tissue is directly related to the cardiac complications of doxorubicin. This study investigated whether azilsartan could mitigate doxorubicin-induced cardiotoxicity. We divided 28 male rats into four groups: the control group receiving a standard diet and water, the vehicle group given DMSO orally for two weeks, doxorubicin group receiving 2.5 mg/kg of doxorubicin three times a week for two weeks, and azilsartan group treated with 5 mg/kg/day of azilsartan orally and doxorubicin. Doxorubicin-induced cardiotoxicity was evidenced by a significant increase in TNF-α, IL-1β, MDA, and caspase-3 levels and significantly decreased TAC and Bcl-2 levels in the cardiac tissues of treated rats compared to the DMSO and control groups. Azilsartan significantly decreased doxorubicin-induced cardiotoxicity, as evidenced by a decline in serum levels of both TNF-α and IL-1β. Additionally, MDA significantly decreased in the cardiac tissue, although TAC was significantly increased when comparing the azilsartan group to the group receiving doxorubicin-only. These results suggest that azilsartan effectively reduced doxorubicin-induced cardiotoxicity, likely by mitigating apoptosis, inflammation, and oxidative stress in cardiac tissues.

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