‘Heart Attack on a Chip’ Sheds Light on Personalized Drugs Trials

Researchers from the University of Southern California have developed a microscale model that can replicate important aspects of myocardial infarction. This novel ‘heart attack on a chip’ model might one day serve as a testbed for new personalized heart drugs.   

The development appeared in the journal Science Advances recently.

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Demystifying the Leading Cause of Death Worldwide

Coronary heart disease is the most commonly-diagnosed heart disease worldwide. An estimated 200 million people are living with coronary heart disease. Severe coronary heart disease can cause a heart attack, which occurs when fat, cholesterol, and other substances in the coronary arteries severely reduce the flow of oxygen-rich blood to a particular part of the heart. 

Patients who survive a heart attack can become increasingly fatigued, enervated, and sick over time, while some even die due to heart failure. That is because heart cells do not regenerate like other muscle cells. Instead, immune cells appear at the site of injury and lead to scarring, which weakens the heart and limits the amount of blood it can pump.  

However, the complete mechanism of this process remains a mystery. How heart cells in the healthy and injured parts of the heart communicate with each other and how and why they change after a heart attack has become the main focus of scientists.

A Micro-Scale Model to Mimic Heart Attacks

The whole system is built from the ground up. At the base is a 22-mm-by-22-mm square microfluidic device made from a rubber-like polymer called PDMS, with two channels on opposing sides through which gases flow.  

Above that sits a thin, oxygen-permeable layer of the same rubber material. A micro layer of protein is then patterned on the top of the chip to ensure that the heart cells align and form the same architecture in normal hearts. Finally, rodent heart cells are grown atop the protein.  

To mimic a heart attack, gas with oxygen and gas without oxygen is released through each channel of the microfluidic device to mimic oxygen gradient exposure that happens in real life. As the microfluidic device is small, clear, and easy to see on a microscope, it allows researchers to observe in real-time functional changes in the heart after a heart attack, including arrhythmia and contractile dysfunction.  

In the future, researchers hope to improve the model by adding immune cells or fibroblasts, which generate the scar after a heart attack. Researchers could not watch changes to heart tissue in real-time with animal models before introducing this model. Moreover, traditional cell culture models uniformly expose heart cells to specific levels of oxygen rather than in a gradient. This means they cannot mimic what happens to damaged heart cells in the so-called border zone after a heart attack.  

Author

Nai Ye Yeat