Doctors warn that 60 million Americans may be at risk of a fatal stroke due to the “silent killer” vascular disease.
By Cassidy Morrison, chief health correspondent for Dailymail.Com
21:54 02 February 2024, updated 21:59 02 February 2024
- The unknown type of cholesterol runs in families and nearly doubles the risk of stroke
- The type of cholesterol like LDL and HDL cannot be changed with diet and exercise
- Read more: Scientists could treat heart disease with drugs that alter DNA
Experts have warned that up to 65 million Americans may be at risk of a fatal stroke or heart attack in middle age, due to the little-known “silent killer” cholesterol disease.
Fatty deposits called high cholesterol — specifically the type called LDL — are known to be a major risk factor for heart disease and stroke, because they damage blood vessels, increasing your risk of deadly blood clots.
However, doctors are now warning of the harmful effects of a specific type of this substance called lipoprotein A.
It is known to be more harmful than other types of LDL, because it is made of “sticky” proteins that enable it to quickly form a clump, interfering with healthy blood flow.
Also known as Lp(a), levels of this type of cholesterol are determined almost entirely by genetics and there are currently no approved treatments to lower it.
Studies show that people living with high levels of lipoprotein have a two to three times higher risk of having a heart attack and approximately two times greater risk of stroke than those with normal levels.
People with high levels often have heart attacks or strokes at a relatively young age, such as in their 40s and 50s.
Even if someone’s low-density lipoprotein (LDL) cholesterol level is low, their Lp(a) may be high, meaning regular tests for high cholesterol will not be able to detect it.
Now, a growing group of doctors is calling for more comprehensive cholesterol testing that can detect high levels of Lp(a) to help patients reduce their risk of heart disease and stroke.
“The challenge was, if you test for something and you don’t have a treatment for it, do you offer the patient any treatment?” Dr. Sahil Parikh, director of vascular services at Columbia University Irving Medical Center in New York, told NBC News. Deeds?
“I used to not test things I couldn’t treat. But now I do, because I know that on the horizon, we will have good treatments. It gives patients hope.”
An estimated 65 million Americans, or nearly one in five, have high levels of Lp(a).
Because the amount of lipoprotein in a person’s blood is determined almost entirely by the lipoprotein(a) gene, many patients and providers feel helpless.
Testing is available at some specialist centers around the country – usually at a high cost.
But many doctors choose not to measure it. This means that millions of Americans live their lives without knowing that their life expectancy may be much lower than the national average of 77 years.
“A patient’s Lp(a) levels are one of the strongest indicators of their genetic risk for cardiovascular disease,” said Dr. Enkhma Byamba, a cardiovascular disease researcher at the University of California, Davis.
“Despite the association between Lp(a) and cardiovascular disease, it flies under the radar. It is not as well understood as other risk factors and current tests are not well standardized.
There are no treatments on the market for high Lp(a), although several are in the works.
However, doctors say it’s still worth testing patients — as there are steps they can take to reduce their risk of high LDL cholesterol, which often combines with high Lp(a) to produce the most serious health problems.
Lori Welsh, 51, of Dublin, Ohio, said revealing her family history of high lipoprotein A has proven invaluable to her health as well as her mother’s.
“If you go back five generations in my mother’s family, everyone died of a heart attack or a stroke. No one was over 54,” Ms. Welsh told NBC News.
She was 47 years old when she had a heart attack. Doctors later told her she had a 90% blockage in her anterior descending artery, meaning almost no blood was getting to her heart.
Her mother had the first of three heart attacks in her late 40s. When doctors finally tested my Lp(a) levels, I was able to manage other risk factors better through a healthy diet and regular exercise.
She eventually lived into her 70s, decades longer than her predecessors.
“The only difference between her and all those five generations is knowing she has lipoprotein A,” Ms. Welch said. This is what made the difference.
“One of the arguments I’ve made before is that enabling patients to understand risk is big,” said Dr. Gregory Katz, a cardiologist and professor at New York University’s Grossman School of Medicine. But knowing Lp(a) doesn’t just empower the patient – it changes the way I treat someone, whether in terms of diagnostic tests or treatment.
‘If Lp(a) is high, I’m a little more aggressive in addressing other risk factors – I’m more likely to recommend antihypertensives and lipid-lowering medications, and I’m definitely a little more aggressive in checking the calcium score for personal risk prediction.’
Lp(a) consists of particularly sticky clusters of protein and lipid molecules.
A person with high levels of Lp(a) molecules in their blood is more likely to see a buildup of generally “bad” LDL cholesterol, which can build up in blood vessels over time.
It sticks to the walls of the arteries to form plaques, making them more narrow and reducing blood flow.
Some of the plaques that build up in the arteries may rupture.
The body views the rupture of the plaque as an injury and immediately goes to work to stop excess bleeding by forming a clot.
This grows continuously, obstructing healthy blood flow and leading to a serious heart attack or stroke.
Major pharmaceutical companies currently have several treatments for high Lp(a) in development.
Eli Lilly’s drug candidate lepodisiran was shown in a trial to reduce Lp(a) protein levels by more than 94 percent after a single treatment, and levels of the protein remained low for about a year.
Amgen is working on its own drug called olpassiran that was shown in a trial to reduce Lp(a) levels by more than 95 percent, while Novartis’ pelacarsen reduced Lp(a) by 72 to 80 percent depending on the dose.
Lori Welsh is currently enrolled in a trial of belacarcin at Ohio University Wexner Medical Center, although she doesn’t know whether she is receiving the candidate drug or a placebo dose.
The goal for most cardiologists who treat people with high Lp(a) is to keep them alive until one of several drug candidates comes on the market.
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