Newly discovered clues to how some common cancer drugs cause heart failure may open the way to treatments that let patients keep taking the drugs while preventing the damage, researchers said.
Millions of cancer patients take a class of chemotherapy medicines known as anthracyclines, but a third of them develop some degree of irreversible cardiac injury. In more than 5%, that injury leads to chronic heart failure, the researchers explained in a report published on Tuesday in JACC CardioOncology.
How these drugs induce their damage has been a mystery, until now. It turns out that injury to heart cells’ mitochondria – their “energy factories” – is the main driver of the damage, the researchers discovered.
“The heart beats without interruption throughout life and has one of the most intense energy requirements of any organ in the body,” study coauthor Dr. Borja Ibanez of the Centro Nacional de Investigaciones Cardiovasculares (CNIC) in Madrid said in a statement.
“Any failure in the energy production chain has major consequences,” he said.
The researchers found that these anthracyclines alter cardiac metabolism, causing a change in the supply of these fuels and an irreversible dysfunction in energy production by mitochondria.
The metabolic changes begin soon after the start of anthracycline treatment, long before the heart begins to lose its pumping strength, the researchers also found.
“As a consequence of these metabolic alterations, the heart begins to atrophy (its cells lose volume) in one of the first signs of irreversible damage,” said coauthor Anabel Diaz-Guerra, also of the CNIC.
One possible intervention involves a specific dietary adjustment. The team is conducting a study in animals to test the ability of a protein-enriched diet to prevent muscle atrophy, including cardiac muscle atrophy, induced by anthracycline chemotherapy.
“If the encouraging preliminary results are confirmed this will be pursued in a clinical trial,” said Dr. Ibanez.
This newsletter was edited by Bill Berkrot. Additional reporting by Shawana Alleyne-Morris.
