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'Mind Your Heart' Study To Enroll Patients Diagnosed With Heart Failure
Swollen legs, ankles and shortness of breath are just a few of the symptoms of congestive heart failure.
"My dad had heart failure. I learned a lot just to see him struggle with some of the challenges. For example, heart failure has a very complex treatment, so it's hard to remember to take all your meds," said Dr. Elena Salmoirago-Blotcher, a senior research scientist in the cardiology department at Rhode Island Hospital, and an associate professor at Brown University.
She talked about her late father, Dario. He's a major reason why she now focuses her research on how to get patients with heart failure better care for themselves.
Cognitive impairment, or forgetfulness, is a problem.
So is something called interoception, the ability to sense changes in the body, which leads to patients downplaying their symptoms until they land in the emergency department.
"Can a mindfulness training delivered over the phone so to make it reachable and easy for older folks improve the ability to pay attention, to increase your executive function and cognitive ability so that you're more able to take care of yourself," she said.
Mindfulness training is a type of meditative therapy that can help you focus and become more aware.
In an earlier pilot study funded by the NIH:
"We saw, we observed an improvement in several measures," said Salmoirago-Blotcher.
Now they're two years into a larger study, also funded by the NIH.
Half the participants receive heart failure educational pamphlets.
The others, a weekly half-hour phone call from a trained mindfulness coach for eight weeks.
"People don't really, they want the human contact," said Salmoirago-Blotcher.
After the eight weeks, it is hoped patients learn to do the mindfulness meditation on their own.
To make this more objective, they do lab tests before and after to actually see if it's making a difference.
So far, they've enrolled about 45 participants. They're looking for a total of 176 patients in Rhode Island with a diagnosis of heart failure to take part.
If you're interested in learning more call this number: 401-793-8233.
Decline In Heart Failure Deaths Has Been Undone, Led By People Under 45
Heart failure mortality rates are moving in the wrong direction, a new analysis reports, reversing a decline in deaths that means more people in the United States are dying of the condition today than 25 years ago. The concerning conclusion comes as newer medications are raising hopes for better outcomes in the years to come.
A research letter published Wednesday in JAMA Cardiology tracked U.S. Death certificate data from 1999 through 2021, revealing a steady drop in deaths until 2012, when rates plateaued, then began to rise steadily, and accelerated upward once the Covid-19 pandemic arrived. Disparities between men and women and among racial and ethnic groups moved up almost in lockstep, but there was one glaring exception: age.
The death rate for people under 45 spiked 906% between 1999 and 2021, compared to increases of 364% for people 45 to 64 years old and 84% for those 65 and older.
"If we are moving the obesity crisis, the liver crisis, and the diabetes crisis in the United States to younger ages, which is exactly what has been going on in the last decade, that is the result of what we are observing right now: shifting the heart failure incidence curve to a younger age group," said the paper's senior author, Marat Fudim. He is the medical director for the Heart Failure Research Unit and Heart Failure Remote Monitoring at Duke University Medical Center. "Many of the gains, and the acceleration, would actually be attributed to the young individuals with that age under 45."
Heart failure is a chronic, progressive condition in which the heart's ability to squeeze and then pump blood throughout the body weakens. Two main types are defined by a measure called ejection fraction. When the heart relaxes after squeezing normally, it's known as reduced ejection fraction; when it doesn't relax afterward, it's known as preserved ejection fraction. Symptoms can be the same for both groups, split roughly in half, but more medications are effective in treating symptoms for those with reduced than preserved ejection fraction.
The risk of hospitalization is higher for people with preserved ejection fraction and their quality of life is lower, often making it difficult for them to leave their homes to do basic activities like going grocery shopping or even going to the mailbox. Preserved ejection fraction tends to go along with cardiometabolic disease: obesity, high blood pressure, diabetes, inactivity, "all of those things that we recognize have gotten worse over the last few decades," said Sean Pinney, chief of cardiology at Mount Sinai Morningside. He was not involved in the JAMA Cardiology paper. "We're seeing premature coronary disease in patients who are in their 30s and 40s, which, you know, 20 years ago would have been unheard of."
Doctors are also seeing medications improve the prevention picture, said Clyde Yancy, chief of cardiology at Northwestern University, making it more urgent to use these and other measures early to control blood pressure, blood sugar, and other risk factors. He was not involved in the study but is deputy editor at the journal.
"We need to move way upstream and think about what we can do a priori to interrupt this process," he said about the data.
Yancy sees three explanations for higher death rates from heart failure: First, the persistence of risk factors and the necessity to intervene there. "That's actionable," he said. Second, the persistence of health inequities. "That is theoretically actionable, but it will require as much public policy as it will require medical therapeutics and lifestyle change." Third is the outsized influence of Covid-19, a phenomenon he said we have yet to understand.
Over the time period covered in the JAMA Cardiology paper, doctors have gotten better at recognizing heart failure, Fudim and the other experts told STAT. Better testing perhaps contributed to increased heart failure diagnoses, reflected in the dataset from the Centers for Disease Control and Prevention on which the analysis was based. More people are surviving heart attacks now, so more people are living long enough to develop heart failure, which could explain higher prevalence in recent years.
There are limitations to the study's methodology of mining death certificates, the paper's authors note. The cause of death may not be accurate: In the case of deaths from opioid overdoses, for example, heart failure may have been cited when cardiac arrest was the cause, Mount Sinai's Pinney said. The steeper climb in death rates coinciding with Covid could mean people sick enough to be hospitalized and later diagnosed with heart failure were suffering from infection-related inflammation as well as economic distress that limited their health and access to health care, study author Fudim said.
The data preceded wide uptake of the wildly popular new obesity drugs, developed to treat diabetes but also proven effective in improving heart health, among other conditions. These new medications appear to work for heart failure patients across the range of ejection fraction, Pinney said.
"We have to see whether or not these new medications can offset the recent worsening in cardiovascular mortality. But I think the paradox is that at a time that we're seeing these increases in mortality, we also have access to better medications," he said. "We need to do a better job focusing on our systems of care delivery, to get the medications to the patient. If you can get all four classes of heart failure medications into patients with heart failure with a reduced ejection fraction, you can cut mortality in half."
Northwestern's Yancy said he was neither surprised nor sobered by the research letter's findings.
"This really is quite the new day for those of us that have spent a career focused on heart failure," he said. "We've gone from having very little opportunity to offer hope to a scenario where we can not only offer hope but we can realistically talk about true improvement."
STAT's coverage of chronic health issues is supported by a grant from Bloomberg Philanthropies. Our financial supporters are not involved in any decisions about our journalism.
'Zombie Cells' In The Placenta May Cause Heart Failure In Pregnancy
"Zombie cells" lurking in the placenta may underpin a type of heart failure that strikes in late pregnancy or shortly after birth, a new study finds.
These undead cells point to potential ways to treat the poorly understood condition, known as postpartum cardiomyopathy (PPCM), which weakens the heart so it can't pump blood as efficiently. Symptoms of this type of heart failure range from mild to deadly, and it affects an estimated 1 in 1,000 live births in the U.S. And closer to 1 in 100 live births in Nigeria.
The new study, published Wednesday (April 17) in the journal Science Translational Medicine, may also shed light on biological aging — a process that appears to speed up during pregnancy, at least by some measures.
"We do believe that there may be a link here," first study author Dr. Jason Roh, an assistant professor of medicine at Harvard Medical School and a cardiologist at Massachusetts General Hospital, told Live Science in an email.
Studies of biological aging in pregnancy have looked mostly at epigenetics — chemical tags found on top of DNA — but the new study looked at proteins made by cells in the placenta. There isn't yet direct evidence linking these two processes, but that could potentially be revealed in later research.
Related: 'Mini placentas' may reveal roots of pregnancy disorders like preeclampsia
The exact cause of PPCM is a mystery, but the condition has been tied to preeclampsia, a condition involving persistent high blood pressure that emerges between midpregnancy and the postpartum period. It's well established that preeclampsia is a risk factor for this type of heart failure, but in recent years, emerging evidence has suggested that the two conditions may actually share underlying causes.
This overlap seems related to substances that increase in the blood during pregnancy.
The idea is that, in mothers with a genetic risk, these conditions are "unmasked by certain factors released into the blood during late pregnancy," said senior study author Dr. Anthony Rosenzweig, a professor of medicine at the University of Michigan and the director of the Stanley and Judith Frankel Institute for Heart and Brain Health. "These circulating factors are thought to have direct effects on the function of the mom's heart," Rosenzweig told Live Science in an email.
To identify what these factors might be, the team screened for more than 1,000 proteins in the blood of patients with PPCM or preeclampsia. They compared these patients to people with uncomplicated pregnancies; people with heart muscle problems unrelated to pregnancy; and people with gestational diabetes.
They found that, as shown in previous studies, people with PPCM or preeclampsia carried more proteins related to inflammation in their blood than the comparison groups did. But they also showed a distinct signature of biological aging, despite all of the study participants being in their 20s and 30s.
This signature has historically been tied to "senescence," a state that cells can enter following damage or stress. Senescent cells stop multiplying but start spewing molecules that alter the tissue around them, sparking inflammation, for example. The immune system then clears these cells away, but as the body ages, this cleanup becomes less efficient and the senescent cells accumulate. This buildup has been tied to age-related diseases such as cancer.
Because the placenta is a temporary organ that's not needed after pregnancy, it's known to show extensive signs of senescence toward the end of pregnancy. That part is normal. But the researchers speculated that maybe, in PPCM and preeclampsia, this aging process happens faster than usual.
"After picking up this signal in the blood, we knew we were on to something," Roh said. They found that 28 senescence-related proteins were boosted in the blood of people with the conditions, and the same proteins showed up in placental tissue from people with preeclampsia.
The most dramatically boosted protein was Activin-A, which has previously been tied to heart failure and cardiac complications of COVID-19 in older adults, Rosenzweig noted. To confirm the protein's relevance in this new context, the team looked at blood samples and medical records of two independent groups of women with preeclampsia or PPCM. In both, Activin-A levels were not only high but were also correlated with poor cardiac function and heart failure.
What's more, the team found that blocking Activin-A dramatically reduced the incidence of heart failure — at least in pregnant mice prone to PPCM. They tested two different methods of blocking the protein; one was tested in early pregnancy and one in late pregnancy.
"While these experiments [provide] exciting proof-of-concept validation for the role of these pathways," Rosenzweig said, "the safety and efficacy of this approach needs to be rigorously assessed in clinical studies." So while the mouse experiments hint at future treatments for people, much more work needs to be done.
"We still don't fully understand why placental senescence becomes so perturbed in these conditions," Roh said. "If we are to intervene on this process, it is absolutely critical that we first rigorously determine the best approaches to safely and effectively target it to optimize both the mom's and baby's health."
There's also a lingering question as to whether placental senescence could be partly responsible for the health effects of sped-up biological aging seen later in life, he added. In this particular study, though, the subjects weren't followed over time, so that's a question for future research.
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