For decades, the prevailing understanding in cardiology has been that damaged heart muscle is irreparable. However, new research suggests the human heart possesses a limited capacity to regenerate muscle cells following injury. This discovery offers a potentially new avenue for improving recovery after a heart attack and managing heart disease.
Heart attack remains a leading cause of death in Germany, and survivors often experience lasting heart damage. Medical professionals long believed that once heart muscle cells died, they could not be replaced. While treatments focused on restoring blood flow and minimizing complications, complete healing of the damaged heart muscle seemed unattainable.
A recent study challenges this long-held belief, demonstrating that the human heart can, to some extent, form new muscle cells after a heart attack. This finding shifts the understanding of the heart’s regenerative capabilities and opens possibilities for therapies aimed at enhancing this natural repair process.
First Evidence in Humans – Not Just Mouse Models
A blockage in a coronary artery cuts off oxygen supply to the heart muscle, triggering a heart attack. A team led by Dr. Robert D. Hume analyzed human heart tissue following an acute heart attack. The research, conducted by the University of Sydney, the Baird Institute, and the Royal Prince Alfred Hospital, is significant because its results are based on human tissue, unlike many previous studies that relied on animal models.
The analysis focused on a specific case: a 48-year-old man who experienced a complete blockage of his left coronary artery. Five days later, his heart was removed for research purposes during an organ donation. To ensure precise analysis, researchers preserved the tissue within 15 minutes. The left ventricle, the heart’s main pumping chamber, was the primary focus of the investigation.
Scientists found significantly elevated levels of mitosis markers – a process where the cell nucleus divides in preparation for cell division. The next step, cytokinesis, involves the complete division of the cell, resulting in two new heart muscle cells.
“We were able to show that adult human heart muscle cells undergo increased mitosis and cytokinesis in response to oxygen deprivation,” explained Hume. The damaged tissue showed considerably more evidence of active cell division than healthy tissue.
Natural Regeneration Remains Limited
Despite these encouraging findings, the body’s ability to heal itself remains limited. A severe heart attack can destroy up to one-third of the approximately three billion heart muscle cells. The observed cell division is not sufficient to fully compensate for this loss.
“This intrinsic ability to undergo mitosis is not enough to completely replace the heart muscle cells lost after an infarction,” explained Lal. Scar tissue continues to be a challenge. However, the discovery is medically significant: it demonstrates that, after severe damage, the heart does not exclusively form scar tissue, but also initiates a repair process – albeit to a limited extent.
Why This Study Matters for Patients
Many patients develop heart failure after a heart attack. The heart’s pumping ability declines, exercise tolerance decreases, and hospitalizations become more frequent. Current treatments primarily focus on slowing the progression of the disease.
The new findings highlight:
- The adult heart possesses its own repair potential
- Oxygen deprivation can activate these processes
- Specific molecules play a crucial role
While complete healing after a severe heart attack is not yet possible, the previous view of a completely irreparable heart is being challenged. For the first time, there is clear evidence that human heart muscle cells can regenerate, at least partially, after a heart attack. Future therapies could aim to enhance this natural repair mechanism.
In Brief:
- Adult human heart muscle cells can divide after a heart attack in response to oxygen deprivation – this has now been directly demonstrated in human tissue for the first time.
- Natural regeneration, however, is not sufficient to fully compensate for the large cell loss; scar tissue remains.
- The study provides an important foundation for new therapies that could specifically strengthen the body’s own repair potential and thus better treat heart failure after a heart attack.
By Sina Trepte
