Dr Eliot Peyster is the Head of Cardiovascular Research at Wesley Research Institute and an Adjunct Professor of Medicine at the University of Pennsylvania and the University of Queensland. He is a cardiologist and transplant physician whose research integrates spatial biology, advanced computational methods, and novel human tissue models to drive precision medicine breakthroughs in cardiovascular disease, heart failure, and organ transplantation.

Every year, thousands of patients with advanced heart failure wait for a life-saving heart transplant, but many will never receive one. At the same time, a surprising number of donated hearts are declined. These decisions are often made quickly, based on limited information, and understandably err on the side of caution. But this caution can come at a cost: potentially healthy hearts may go unused, while patients continue to wait.

Our research is focused on changing that. By combining advanced imaging of heart tissue with detailed molecular analysis, we are developing a new way to assess donor heart quality – one that goes far beyond the traditional “yes or no” judgement. Early results suggest that many hearts previously considered too risky may in fact be suitable for transplant. With further development, this approach could help doctors make more confident decisions, increase the number of usable donor hearts, and ultimately save more lives.

Despite major advances in treating coronary artery disease, many patients still go on to develop heart failure. One reason may be that we still do not fully understand the earliest damage coronary disease causes within the heart itself. Most previous studies have examined tissue from patients with end-stage heart failure, when the heart has already undergone extensive scarring and remodeling. That makes it difficult to identify the earlier biological changes that might be most important – and most treatable.

Our team is taking a different approach. Using human heart tissue from donors with varying degrees of coronary disease, we are studying how the heart changes before severe dysfunction appears. We have found evidence that even earlier-stage coronary disease is associated with important changes in the heart’s small blood vessels, supporting tissue, and energy-producing machinery. These findings suggest that coronary artery disease affects far more than the major arteries alone. By revealing these hidden early processes, our research may help open the door to new therapies aimed at protecting the heart before permanent damage and heart failure occur.

Heart failure affects millions of people worldwide, yet it is not a single disease. Many patients are told they have “heart failure” even though the underlying causes - and the best treatments - can differ dramatically. This is especially true for a common form known as HFpEF, where patients often experience severe symptoms but have limited treatment options.

Our work aims to change this by identifying distinct subtypes of heart failure based on how the heart actually functions. Using a combination of imaging, biomarkers, and advanced analysis of heart tissue, we are working to pinpoint which patients have problems with how the heart relaxes, rather than how it contracts. This distinction is critical, because it opens the door to entirely new types of treatments tailored to the specific problem. By better matching patients to therapies, we hope to improve outcomes and bring more effective, personalized care to people living with heart failure.

For patients who receive a heart transplant, the journey does not end with surgery. One of the greatest ongoing risks is rejection—when the body’s immune system begins to attack the new heart. Detecting rejection early is critical, but current methods rely on examining small tissue samples under a microscope, which can be subjective and may miss subtle warning signs.

Our research is developing new tools that use advanced image analysis and artificial intelligence to detect early patterns of injury in transplanted hearts—patterns that may not be visible to the human eye alone. By combining this with clinical data and molecular signals, we aim to create more accurate and timely ways to identify rejection before it becomes severe. This could allow doctors to intervene earlier, reduce complications, and help transplant patients live longer, healthier lives.

Some forms of heart disease are driven by inflammation—immune activity within the heart that can damage tissue and disrupt normal function. In conditions like cardiac sarcoidosis, this inflammation can be patchy and difficult to detect, sometimes leading to delayed diagnosis or incomplete treatment.

Using cutting-edge techniques that allow us to map proteins and cells within heart tissue at high resolution, our research is uncovering how inflammation spreads and affects different regions of the heart—even in areas that appear normal under a microscope. These insights are helping us identify new markers of disease and may lead to better diagnostic tools and targeted therapies. Ultimately, this work aims to make invisible disease visible—and more treatable.

Breakthroughs in cardiovascular care don’t happen in isolation — they rely on strong partnerships between clinicians, researchers and patients. The collaboration between Wesley Research Institute, UQ Institute for Molecular Bioscience and Critical Care Research Group, is strengthening pathways for clinicians and researchers to work together to translate science into improved patient outcomes.