Experts have warned that as many as 65 million middle-aged Americans could be at risk of a fatal stroke or heart attack due to a little-known ‘silent killer’ cholesterol disease.
Fat deposits called high cholesterol – particularly a type called LDL – are known to be a major risk factor for heart disease and stroke because they damage blood vessels, increasing the risk of potentially fatal blood clots.
However, doctors are now warning about the harm 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 can cause it to quickly form a clot, disrupting 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 them.
Lipoprotein (a) has specific properties that make it particularly ‘sticky’. Once inside the blood vessel, the particles accumulate and adhere to the artery walls, restricting crucial blood flow
Studies show that people with high lipoprotein levels have a two to three times higher risk of a heart attack and a almost twice as high risk of stroke compared to people with normal levels.
Those with high levels often have a heart attack or stroke at a relatively young age, such as in their 40s or 50s.
Even if a person’s LDL cholesterol level is low, their Lp(a) may be high, meaning regular tests for high cholesterol may not detect it.
Now a growing chorus of doctors are calling for more comprehensive cholesterol tests that can detect high levels of Lp(a) to help patients reduce their risk of heart disease and stroke.
Dr. Sahil Parikh, director of endovascular services at Columbia University Irving Medical Center in New York, said NBC News: ‘The challenge was: if you test for something and there is no treatment for it, are you doing the patient a favor?
Lori Welsh (left) said she felt comforted knowing that her Lp(a) levels are high, something that runs in her family. With that knowledge, her mother was able to extend her own life decades longer than her ancestors, and use it to make better life choices that kept her risk of cardiovascular disease lower overall.
‘I used to not test for things I couldn’t treat. But now I do, because I know we’ll get good treatments on the horizon. It gives patients hope.’
An estimated 65 million Americans, nearly one in five, have high levels of Lp(a).
Because its levels in a person’s blood are almost entirely determined by the lipoprotein(a) gene, many patients and caregivers feel powerless.
Testing is available at a number of specialist centers across the country, usually at a high cost.
But many doctors choose not to measure it. That means millions of Americans live their lives without knowing that their life expectancy could be much lower than the national average of 77 years.
Dr. Enkhmaa Byambaa, a cardiovascular disease researcher at the University of California, Davis, said: ‘A patient’s Lp(a) levels are one of the strongest indicators of the genetic risk of cardiovascular disease.
‘Despite the association between Lp(a) and cardiovascular disease, it remains 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 elevated Lp(a), although several are in the pipeline.
However, doctors say it’s still worth testing patients because there are steps they can take to lower their risk of high LDL cholesterol, which often combines with high Lp(a) to be the most serious health problem. causes.
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Lori Welsh, 51, a native of Dublin, Ohio, said uncovering her family history of high Lp(a) has proven to be an immeasurable benefit to both her and her mother’s health.
Ms. Welsh told NBC News, “If you go back five generations in my mother’s family, everyone died of a heart attack or stroke. No one lived to be older than 54 years old.’
She was 47 when she had a heart attack. Doctors later told her she had a 90 percent blockage in her anterior descending artery, meaning almost no blood getting to her heart.
Her mother suffered the first of three heart attacks in her late forties. When doctors finally tested her Lp(a) levels, she was able to better manage her other risk factors through a healthy diet and regular exercise.
She eventually lived well into her seventies, decades longer than her ancestors.
Ms Welsh said: ‘The only difference between her and all five of those generations was knowing she had lipoprotein(a). That made the difference.’
Dr. Gregory Katz, cardiologist and professor at New York University’s Grossman School of Medicine, said: ‘One argument I have made before is that it is very important to enable patients to understand risks. But knowing Lp(a) not only empowers a patient; it also changes the way I treat someone, both in terms of diagnostic testing and treatment.
‘When Lp(a) is high, I am more aggressive in controlling other risk factors – I am more likely to recommend antihypertensives and lipid-lowering medications, and I am certainly a little more aggressive in monitoring a calcium score for personalized risk prediction.’
Lp(a) consists of particularly sticky combinations of protein and fat particles.
Someone with elevated levels of Lp(a) particles in their blood is more likely to have a build-up of the ‘bad’ LDL cholesterol, which can build up in the blood vessels over time.
It attaches to the walls of the arteries and forms plaques, narrowing them and reducing blood flow.
Some plaques that build up in the arteries can rupture.
The body views plaque rupture as an injury and immediately takes action to stop excessive bleeding by forming a clot.
This continually grows, blocking healthy blood flow and resulting in a potentially serious heart attack or stroke.
Major pharmaceutical companies currently have several treatments for high Lp(a) in development.
A study found that Eli Lilly’s lepodisiran candidate can reduce levels of Lp(a) protein by more than 94 percent after a single treatment, and levels of the protein remain low for almost a year.
Amgen is working on its own drug called olpasiran, which has been shown in a trial to lower Lp(a) levels by more than 95 percentwhile Novartis’ drug pelacarsen lowered Lp(a) by 72 to 80 percent depending on the dose.
Lori Welsh is currently participating in a trial of pelacarsen at Ohio University Wexner Medical Center, although she does not know whether she is receiving the drug candidate or a placebo dose.
The goal of most cardiologists who treat people with high Lp(a) is to keep them alive until one of the many drug candidates comes to market.