After months of chemotherapy, a double mastectomy and extensive radiation treatment for her breast cancer, Debra Grant hoped her time in hospitals was over.
But six years after her recovery a heart failure diagnosis dashed those dreams, and Grant muddled through a losing battle against her body for three years.
“It was to the point where I was not functioning,” said Grant, of Salt Lake City. “I could barely get off the sofa.”
After working with the University of Utah’s Division of Cardiology, she and a group of doctors developed a regiment of drugs that vastly improved her quality of life. Even so, Grant had to shift her energy from mountain biking and hiking to gardening and reading. Now, with atrial fibrillation and tachycardia added to her diagnoses, she has to pay out of pocket for expensive medications.
Heart disease is a global epidemic, affecting about 3% of the adult population. It’s frequent, pervasive, and deadly, with 50% of patients with heart failure expected to die within five years of diagnosis.
Though Grant has a number of treatments that can assist her, many heart failure treatments are experimental, based on individual needs, and only designed to delay an inevitable conclusion. However, a discovery by researchers at the University of Utah may change treatment altogether.
These researchers recently published a study on VDAC2, a protein that helps regulate calcium signaling within heart cells. Blockage of the signals causes severe impairment of heart cell contraction, making it harder for the organ to push blood through the body.
Taking away this protein made heart function sharply decline in laboratory mice, eventually leading to their death, while reintroduction of VDAC2 reversed many of the effects of heart failure. An experimental drug called efsevin was able to produce similar effects in other mice with heart failure.
“This is great,” said Stavros Drakos, director of cardiovascular research at the University of Utah. “There’s promising evidence emerging that this can emerge as a therapy so we can recover a patient’s heart. We’re committed to the next step.”
This research could be extremely vital for Utahns with heart failure. According to the Centers for Disease Control and Prevention, on average, 77 people died from heart disease every week in Utah in 2019. Once COVID-19 hit, the number of heart failure patients that died grew even higher.
COVID-19 is even more lethal in heart failure patients than in those with undamaged hearts. In any given hospital, 10% of the beds have patients with a medical history of heart failure, even if their heart isn’t the reason they’re in emergency care. Even out of the hospital, studies suggest that many COVID-19 survivors experience some type of heart damage. This leaves experts worried about an increase in heart failure as the delta variant brings case numbers up throughout the state.
“When you have better systems for heart failure, you’re preparing your hospital for dealing with diseases like COVID-19,” said Drakos. “You’re freeing up space and you’re able to use those beds to fight COVID-19 or other public health issues.”
Drakos and his team first noticed this protein by studying heart tissue from patients whose hearts had recovered from advanced heart failure. From this, they gained the clues of something distinctly different, but not the mechanism by which it was happening. Eventually, they found VDAC2 and saw the role it had in importing calcium to the mitochondria, the factory of energy in the heart.
One remarkable part of this study, says cardiologist Dr. Michael Cutler, is that therapies targeting this previously unknown mechanism can improve a failing heart’s ability to pump blood.
“Most drugs to date that have targeted improving contractile function have been unsuccessful,” Cutler said. “Much work is needed to translate the findings from this study into the management of heart failure patients, but it is certainly an important step in increasing our understanding of the pathophysiology of heart failure humans.”
Though Drakos says that tests with human patients could be a few years off, he is hopeful that this could drastically change the outcomes of patients with heart failure.
“The natural history of this disease is multiple hospital visits that drain resources from families and systems,” said Drakos. “You can’t walk, you can’t talk, you can’t breathe because of fluid in the lungs. Most of the time, a patient just consumes a lot of resources because they’re in constant need for years. With this, we hope to lessen the burden of everything.”
Grant keeps a positive outlook wherever she can. She’s grateful for the good days when she’s healthy and can take care of her garden. When she has a bad day, she plops on the couch and finds joy in reading a book (usually about gardening, actually).
“The thing with heart failure to me is that I try to live every day like I don’t have it,” said Grant. “I don’t try to focus on it. But it will hit you square in the face sometimes because you do too much, or you’ll do something and think ‘Oh, my heart doesn’t work.’”
Drakos was the first doctor she saw at the heart failure clinic, and one that she really attributes her recovery to. Drakos chose an “old-school drug” that no other doctors thought of that changed the course of her heart failure.
A possible new treatment brings Grant added hope.
“It would change my life,” said Grant. “That’s such an odd thing to say, because my life is so changed. It would change it again. It’s a really exciting thing to hear.”