Friday January 24, 2020

Deaths Rising in U.S. Due To Heart Failure, Especially in Younger Adults

Between 1999 and 2012, annual heart failure death rates dropped from 78.7 per 100,000 people to 53.7 per 100,000, the researchers found. But then mortality rates started to climb, reaching 59.3 fatalities for every 100,000 people by the end of the study period.

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obesity
Two women converse in New York, June 26, 2012. The nation's obesity epidemic continues to grow, led by an alarming increase among women. Obesity is one of the risk factors of heart failure. VOA

More U.S. adults are dying from heart failure today than a decade ago, and the sharpest rise in mortality is happening among middle-aged and younger adults, a new study suggests.

Researchers examined data from the U.S. Centers for Disease Control and Prevention (CDC) on deaths from heart failure between 1999 and 2017 among adults 35 to 84 years old.

Between 1999 and 2012, annual heart failure death rates dropped from 78.7 per 100,000 people to 53.7 per 100,000, the researchers found. But then mortality rates started to climb, reaching 59.3 fatalities for every 100,000 people by the end of the study period.

“Up until 2012, we saw decline in cardiovascular deaths in patients with heart failure and this was likely due to advances in medical and surgical treatments for heart failure,” said senior study author Dr. Sadiya Khan of Northwestern University Feinberg School of Medicine in Chicago.

“However, this study demonstrates for the first time that the cardiovascular death rate is now increasing in patients with heart failure and this increase is especially concerning for premature death in people under 65,” Khan said by email.

A person receives a test for diabetes during Care Harbor L.A. free medical clinic in Los Angeles, Sept. 11, 2014.
A person receives a test for diabetes during Care Harbor L.A. free medical clinic in Los Angeles, Sept. 11, 2014.

Heart failure by the numbers

About 5.7 million American adults have heart failure, according to the CDC, and about half of the people who develop this condition die within five years of diagnosis. Heart failure happens when the heart can’t pump enough blood and oxygen to supply vital organs.

In the study, African Americans were more likely to die of heart failure than whites, and this disparity was especially pronounced among younger adults, researchers report in the Journal of the American College of Cardiology.

Compared to white men, black men had a 1.16-fold higher risk of death from heart failure in 1999 but a 1.43-fold higher mortality risk by 2017, the study found.

And, compared to white women, black women started out with a 1.35-fold higher risk of death from heart failure and had a 1.54-fold greater risk by the end of the study period.

When researchers looked just at adults 35 to 64 years old, the racial disparity was even starker: by 2017 black men had a 2.60-fold higher risk of death from heart failure and black women had a 2.97 fold higher risk of death.

heart
“Heart failure is preventable and treatable,” Fonarow said. “There is an urgent need … to eliminate the healthcare policy that has been associated with the increase in heart failure deaths. Pixabay

“More than 50 percent of black adults have hypertension and have high rates of obesity and diabetes, and this may explain a portion of the disparities in heart failure mortality,” Khan said.

Risk factors, access to care

“Beyond differences in risk factor prevalence, disparities in access to care unfortunately contribute to both inadequate prevention and diagnosis,” Khan added. “We need to do better in terms of access to care for all Americans.”

The study used data from the CDC that includes the underlying and contributing cause of death from all death certificates in the U.S. between 1999 to 2017, for a total of more than 47.7 million people.

The study wasn’t designed to determine what might be causing the rise in heart failure deaths.

“Some have speculated this mortality increase has to do with increased prevalence of heart failure risk factors of diabetes and obesity,” said Dr. Gregg Fonarow, a cardiologist and researcher at the University of California, Los Angeles, who wasn’t involved in the study.

However, it’s also possible that a recent shift in Medicare payment rules designed to curb repeat hospitalizations may have “also contributed to the increases in mortality by restricting necessary care, particularly in the most vulnerable heart failure patients,” Fonarow said by email.

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While black men are more likely to develop heart failure at younger ages, and less likely to receive recommended treatments, they’re also more likely to be treated at hospitals that are disproportionately impacted by Medicare efforts to curb repeat hospitalizations, or readmissions, Fonarow said.

“Heart failure is preventable and treatable,” Fonarow said. “There is an urgent need … to eliminate the healthcare policy that has been associated with the increase in heart failure deaths.” (VOA)

Next Story

Drugs That Treat Arthritis in Dogs Can Kill Cancer Cells: Study

Drug for arthritis in dogs can fight cancer in people

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Cancer Cells
Drugs for diabetes, inflammation, alcoholism and even for treating arthritis in dogs can also kill cancer cells. Pixabay

Drugs for diabetes, inflammation, alcoholism — and even for treating arthritis in dogs — can also kill cancer cells in the lab, according to a new health news and study.

The researchers systematically analysed thousands of already developed drug compounds and found nearly 50 that have previously unrecognised anti-cancer activity.

The findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.

“We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said study researcher Todd Golub from Harvard University in the US.

Cancer Cells
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. (Representational Image). Pixabay

The study, published in the journal Nature Cancer, yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs).

Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin’s cardiovascular benefits.

“We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way,” said study first author Steven Corsello, from Dana-Farber Cancer Institute and founder of the Drug Repurposing Hub.

The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad’s Cancer Cell Line Encyclopedia (CCLE).

Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment.

The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.

They found nearly 50 non-cancer drugs — including those initially developed to lower cholesterol or reduce inflammation — that killed some cancer cells while leaving others alone.

Some of the compounds killed cancer cells in unexpected ways.

“Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello.

Cancer Cells
The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cells lines from the Broad’s Cancer Cell Line Encyclopedia. (Representational Image). Pixabay

Some of the four-dozen drugs researchers identified appear to act not by inhibiting a protein but by activating a protein or stabilising a protein-protein interaction.

For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilising the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs.

These unexpected drug mechanisms were easier to find using the study’s cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.

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Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target.

For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. (IANS)