Protected Heart: A visual representation of safeguarding cardiac health during cancer treatment.

Drug-Induced Cardiotoxicity: How to Protect Your Heart

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Reese Marlowe in Health & Wellness May 2025 • 4 min read.

"Protecting the Heart: New Strategies for Predicting and Preventing Cardiotoxic Side Effects of Chemotherapy"


Cancer treatments, while life-saving, can sometimes have unintended consequences for the heart. Cardiotoxicity, or heart damage caused by drugs, is a significant concern in cancer therapy. Many chemotherapeutic agents can lead to a range of cardiovascular issues, from mild arrhythmias to severe heart failure. Understanding and mitigating these risks is crucial for improving patient outcomes and quality of life.

Researchers are actively investigating new methods to predict and prevent cardiotoxic side effects before they manifest in patients. These efforts include using advanced cell models and sophisticated computer simulations to assess the potential impact of drugs on the heart. By identifying risks early, doctors can make informed decisions about treatment plans, potentially adjusting dosages or selecting alternative therapies that are less harmful to the cardiovascular system.

This article delves into the latest research and strategies for protecting the heart during cancer treatment. We'll explore how scientists are using innovative approaches to identify cardiotoxic risks early, offering hope for safer and more effective cancer therapies.

Predicting Cardiotoxicity with hiPSC-Derived Cardiomyocytes

Protected Heart: A visual representation of safeguarding cardiac health during cancer treatment.

One promising approach involves the use of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). These cells, created from human stem cells, mimic the behavior of actual heart cells and can be used to study the effects of drugs in a controlled laboratory setting. Researchers can expose these cells to various chemotherapeutic agents and monitor their functional and structural responses to assess potential cardiotoxicity.

A recent study highlighted the potential of hiPSC-CMs to capture clinically relevant cardiotoxic effects of chemotherapeutics. The researchers treated hiPSC-CMs with drugs like lapatinib and sunitinib, which are known to have cardiotoxic potential. They then measured both functional toxicity (changes in cell activity) and structural toxicity (damage to cell structure) using sophisticated techniques like microelectrode array (MEA) impedance technology and cardiac Troponin I (cTnI) level measurements.

Here’s what the study revealed:
  • Functional Toxicity: Lapatinib altered the excitation-contraction coupling in cardiomyocytes, while sunitinib caused arrhythmic beating.
  • Structural Toxicity: Sunitinib induced a dose-dependent release of cTnI, a marker of heart damage, while lapatinib did not significantly affect cTnI levels.
  • Cell Viability: Sunitinib reduced cell viability, correlating with the increased release of cTnI.
These findings demonstrate that hiPSC-CMs can effectively model the diverse cardiotoxic effects of different drugs. By investigating both functional and structural toxicity, researchers gain a more comprehensive understanding of the potential risks associated with chemotherapeutic agents. This approach could lead to better risk assessment and more informed treatment decisions in the future.

Future Directions: Towards Safer Cancer Therapies

The development and application of advanced techniques like hiPSC-CMs and PBPK modeling represent significant strides in predicting and preventing drug-induced cardiotoxicity. As research progresses, these tools will likely become integral to the drug development process, helping to ensure that new cancer therapies are both effective and safe for the heart. By prioritizing cardiac safety, we can improve the overall well-being and long-term health of cancer patients.

Everything You Need To Know

1

What exactly is cardiotoxicity and why should I be concerned about it during cancer treatment?

Cardiotoxicity refers to heart damage caused by drugs, particularly cancer treatments like chemotherapy. It's significant because many chemotherapeutic agents can lead to cardiovascular issues, ranging from arrhythmias to heart failure, impacting patient outcomes and quality of life. Understanding and mitigating cardiotoxicity is crucial for safer cancer therapies.

2

What are hiPSC-derived cardiomyocytes, and how are they used in the context of cancer treatment?

HiPSC-derived cardiomyocytes (hiPSC-CMs) are human heart cells created from stem cells in a lab. They're important because they mimic real heart cells and allow researchers to study the effects of drugs in a controlled setting. This helps predict potential cardiotoxic side effects of chemotherapy by assessing how drugs impact the cells' function and structure.

3

How do researchers actually use hiPSC-CMs to predict if a chemotherapy drug will damage my heart?

Researchers use hiPSC-CMs by exposing them to chemotherapeutic agents and monitoring their responses. They measure functional toxicity (changes in cell activity) and structural toxicity (damage to cell structure). For example, they can measure cardiac Troponin I (cTnI) levels, a marker of heart damage, or use microelectrode array (MEA) impedance technology to assess changes in cell activity.

4

What's the difference between functional toxicity and structural toxicity when talking about heart damage from drugs?

Functional toxicity refers to changes in the activity of heart cells, while structural toxicity refers to physical damage to the heart cells. Functional toxicity can manifest as altered excitation-contraction coupling or arrhythmic beating, while structural toxicity involves the release of markers like cardiac Troponin I (cTnI), indicating heart damage. Assessing both provides a comprehensive understanding of potential risks.

5

Why is it so important to predict cardiotoxicity early on during cancer treatment?

Predicting cardiotoxicity early allows doctors to make informed decisions about cancer treatment plans. They might adjust dosages or select alternative therapies that are less harmful to the cardiovascular system. Techniques like using hiPSC-CMs to investigate functional and structural toxicity are useful for early risk detection.

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