Abstract
The cardiotoxicity of anti-cancer drugs presents as a challenge to both clinicians and patients. Significant advances in cancer treatments have improved patient survival rates, but have also led to the chronic effects of anti-cancer therapies becoming more prominent. Additionally, it is difficult to clinically predict the occurrence of cardiovascular toxicities given that they can be transient or irreversible, with large between-subject variabilities. Further, cardiotoxicities present a range of different symptoms and pathophysiological mechanisms. These notwithstanding, mechanistic pharmacokinetic (PK) and pharmacodynamic (PD) modeling offers an important approach to predict cardiotoxicities and offering precise cardio-oncological care. Efforts have been made to integrate the structures of physiological and pharmacological networks into PK-PD modeling to the end of predicting cardiotoxicities based on clinical evaluation as well as individual variabilities, such as protein expression, and physiological changes under different disease states. Thus, this review aims to report recent progress in the use of PK-PD modeling to predict cardiovascular toxicities, as well as its application in anti-cancer therapies.
Highlights
Advances in cancer treatment have dramatically improved patient survival rates
Cardiovascular complications have been identified as one of the leading causes of mortality in cancer survivors, regardless of the cancer type [1, 2]. This has led to the development of a novel field, cardio-oncology, which focuses on reducing or managing the cardiotoxicity of anti-cancer agents, while maximizing therapeutic effects and managing patients with cancer having cardiovascular comorbidities
Cardio-oncology is increasingly becoming part of the standardized care for patients with cancer [3], and cardiovascular complications associated with cancer therapies, including
Summary
The issue of preventing and managing treatment-associated chronic adverse events has become increasingly important. Cardiovascular complications have been identified as one of the leading causes of mortality in cancer survivors, regardless of the cancer type [1, 2]. This has led to the development of a novel field, cardio-oncology, which focuses on reducing or managing the cardiotoxicity of anti-cancer agents, while maximizing therapeutic effects and managing patients with cancer having cardiovascular comorbidities. Cardio-oncology is increasingly becoming part of the standardized care for patients with cancer [3], and cardiovascular complications associated with cancer therapies, including. The mechanisms behind these clinical symptoms can be categorized into: [1] drug-induced electrocardiograph changes; [2] drug-induced hemodynamic changes; and [3] drug-induced changes in molecular signaling pathways [4]
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