Drug-induced cardiac toxicity and adverse drug reactions, a narrative review

Destere, Alexandre; Merino, Diane; Lavrut, Thibaud; Rocher, Fanny; Viard, Delphine; Drici, Milou-Daniel; Gérard, Alexandre O.

doi:10.1016/j.therap.2023.10.008

Cited by 2 publications

(1 citation statement)

References 69 publications

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“…55 Several studies have suggested that sorafenib can lead to QT prolongation, which is a disturbance in the heart's electrical system that can potentially lead to serious arrhythmias and sudden cardiac death (Table 1). 48,56 However, the exact mechanism by which sorafenib causes QT prolongation is not fully understood. It may involve inhibition of ion channels involved in cardiac repolarization, such as the human ether-a-go-go-related gene (hERG) potassium channel 57 (Table 2).…”

Section: Sorafenib and Its Cardiovascular Toxicity Hypertension Eventsmentioning

confidence: 99%

Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications

Li,

Zhang,

et al. 2024

DDDT

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Tyrosine kinase inhibitors (TKIs) have been recognized as crucial agents for treating various tumors, and one of their key targets is the intracellular site of the vascular endothelial growth factor receptor (VEGFR). While TKIs have demonstrated their effectiveness in solid tumor patients and increased life expectancy, they can also lead to adverse cardiovascular effects including hypertension, thromboembolism, cardiac ischemia, and left ventricular dysfunction. Among the TKIs, sorafenib was the first approved agent and it exerts anti-tumor effects on hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC) by inhibiting angiogenesis and tumor cell proliferation through targeting VEGFR and RAF. Unfortunately, the adverse cardiovascular effects caused by sorafenib not only affect solid tumor patients but also limit its application in curing other diseases. This review explores the mechanisms underlying sorafenib-induced cardiovascular adverse effects, including endothelial dysfunction, mitochondrial dysfunction, endoplasmic reticulum stress, dysregulated autophagy, and ferroptosis. It also discusses potential treatment strategies, such as antioxidants and renin-angiotensin system inhibitors, and highlights the association between sorafenib-induced hypertension and treatment efficacy in cancer patients. Furthermore, emerging research suggests a link between sorafenibinduced glycolysis, drug resistance, and cardiovascular toxicity, necessitating further investigation. Overall, understanding these mechanisms is crucial for optimizing sorafenib therapy and minimizing cardiovascular risks in cancer patients.

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Section: Sorafenib and Its Cardiovascular Toxicity Hypertension Eventsmentioning

confidence: 99%

Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications

Li,

Zhang,

et al. 2024

DDDT

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Efficacy and Bioavailability of silymarin on Plasma S100B Level in Cardiotoxicity-induced Rats

Jalil,

Altaei

2024

Biomed. Pharmacol. J.

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Cardiotoxicity is a cause of death by drug overdose. Silymarin, a cytoprotective agent used in this research to protect against induced-cardiotoxic effects in Albino Wister rats; exhibited signs of heart damage, such as elevated levels of S100B, troponin I, and CK-MB. Seventy albino Wister rats of both genders were divided randomly with each group having 10 rats. Silymarin-treated, cardiotoxic-induced, and control groups were treated for ten days. The bioavailability of silymarin was assessed, and evaluation of the efficacy of silymarin on the biomarker S100B and cardiac biomarkers (Troponin I, and CK-MB), also the histopathological assessments of the heart, liver, and kidney, in addition to the coefficient correlation of the studied biomarkers were analyzed. Research’s outcome indicated that the sets subjected to silymarin presented substantial differences in rat weight and food consumption, compared to a decrease in cardiotoxic clusters. S100B plasma level was increased in cardiotoxic groups, reduced in those subjected to silymarin, and eliminated by pretreatment with silymarin. Troponin I & CK-MB expressively elevated significantly in cardiotoxic prompted rats, which declined with silymarin treatment and were prohibited in pretreatment by silymarin. The shielding characteristic of silymarin detected in end organs, like the liver, kidneys, and hearts when exposed to the cardiotoxic agent clozapine was extremely significant. The consequences of the histopathological examination of this study illustrated silymarin’s cardioprotective effects. A significant positive coefficient correlation of S100B with troponin I & CK-MB was recorded. In conclusion, silymarin reduces and prevents to a larger extent the cardiotoxicity brought about by clozapine and averts heart injury. The cardioprotective efficacy of silymarin is explained by its new mechanism of action as decreasing S100B, troponin I & CK-MB levels with a strong significant correlation to each other. The cardioprotective efficacy of silymarin gives promise for monitoring the cardiotoxicity adverse drug reaction induced by drugs.

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Drug-induced cardiac toxicity and adverse drug reactions, a narrative review

Cited by 2 publications

References 69 publications

Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications

Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications

Efficacy and Bioavailability of silymarin on Plasma S100B Level in Cardiotoxicity-induced Rats

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