Up to one of five people – estimated 64 million in the United States – have an increased mirror of a tiny particle in the blood. It can significantly increase the risk of heart attacks and strokes.
But only a few know about it, and almost no doctors test it because there was not much to do. Diet does not help. Also not exercised. There were no drugs.
But that can change in the near future.
On Sunday, cardiologists announced that an experimental medication from Eli Lilly, Lepodisisiran, could reduce 94 percent with a single injection. The effects lasted six months and there were no significant side effects.
However, it has not yet been confirmed that the reduction of the LP (a) level also reduces the risk of heart attacks and strokes. This is waiting for large clinical studies that are now in progress.
The Lilly Research was presented on Sunday at the annual conference of the American College of Cardiology and was also released in the New England Journal of Medicine. At least four other companies also test innovative medication that block the production of LP (A) through the body, a mixture of lipids and a protein.
Dr. David Maron, a preventive cardiologist at Stanford, who is not involved in Lilly research, said the evidence of a profound and long-lasting reduction in the lipoprote level with lepodisiran are “exciting”.
Dr. Martha Gulati, a preventive cardiologist at the Cedars-Sinai Medical Center, also not involved in the exam, said the study was “really elegant”.
Eli Lilly is now carrying out a large clinical study in which he is asked whether his medication can prevent heart attacks or strokes or cardiovascular deaths. It will be completed in 2029. Clinical studies with other drugs aimed at LP (A) will close earlier. The first will be a study of a monthly Novartis medication, the results of which are expected in 2026.
However, cardiologists warn that there is no guarantee that the medication will protect people. They remember a lesson that has been learned from the assumption that a change in a risk factor can change the risk. Cardiologists were once enthusiastic about drugs, the HDL values increased, known as “good cholesterol”. People with naturally high HDL mirrors had a lower rate of heart disease. These HDL-Reich medication did not help.
LP (A) -Lower “is a huge new border in cardiovascular medicine,” said Dr. Daniel Rader, a preventive cardiologist at the Perelman School of Medicine at the University of Pennsylvania. Dr. Rader is a member of the Scientific Advisory Board for Novartis and wrote an editorial to accompany the new paper.
Treatments aimed at LP (a) have come for a long time.
The lipoprotein was identified in 1974 as a risk factor for heart disease, which is controlled by genes rather than lifestyle or environment.
People with LP (A) levels that are slightly higher than normal have a 25 percent increased risk of a heart attack or a stroke. And very high values - as in 10 percent of the population – can double the risk.
Cardiologists say that often in patients for no obvious reason for a heart attack or a stroke – whose cholesterol and blood pressure is normal and do not smoke – that patients have a high level of LP (A). Usually it turns out that they also have family stories of unexplained heart disease.
The same applies to people who have heart attacks at a young age, said Dr. Steven Nissen, a preventive cardiologist in the Cleveland Clinic, who is the academic director of the Lilly drug study and clinical studies with three other new drugs.
“When you go to the Koronar -Care unit and see someone who is 40 years old, with an acute myocardial infarction, you have to know the level of your LP (a),” he said, referring to a heart attack. Too often, he said, their values are 250 nanomole per liter or even higher. The upper limit of the normal is 75.
Dr. Maron said his clinic was full of people who had no idea why they developed heart disease until they found that they had a high level of LP (A).
One is Monte Wooden, a 71-year-old retired firefighter who lives in Redding, California. His LDL cholesterol was moderately increased. His blood pressure was normal. He didn’t smoke. Nevertheless, he had his first heart attack in 2006 when he took a cholesterol -reflective statin.
It seemed as if almost everyone in Mr. Wooden’s family died of heart disease.
His grandmother had her first heart attack when she was in the forties. She died of a heart attack at the age of 63. His father and his father’s brother died of heart diseases. Mr. Wooden’s brother died of a heart attack.
As Dr. Maron Mr. Woodens LP (A) -LaGel tested, it was larger than 400.
Dr. Maron and other preventive cardiologists like Dr. Gulati, Dr. Nissen and Dr. Rader say you routinely test all LP (A) levels of your patients. Since the LP (a) level of genes are controlled, the patients only have to be tested once.
Dr. Nissen is dull with his LP (A) patients.
“We say: You have a serious impact. I want to take every risk factor you have off the table,” he said.
According to Dr. Gulati found that only 0.3 percent of the US population of an LP (a) test – which is paid by insurance – and only 3 percent of those with heart disease were tested.
You and other preventive cardiologists say that all adults should have an LP (a) test. When the values are high, doctors should treat any other risk factor aggressively.
For Mr. Wooden, this meant that Repatha was able to take a mighty cholesterol-reflecting drug that lowered his LDL cholesterol level to 30.
However, Mr. Wooden’s case did not end there. Dr. Maron brought him to a clinical study in which he tested one of the new drugs that lower the LP (a) level.
During the experiment, Mr. Wooden had no symptoms of heart disease – no chest pain, no shortness of breath. When the attempt ended, his symptoms came back, which led to a four -time -bypass surgery.
“It’s anecdotic,” said Dr. Maron, “but it speaks for the likelihood that these medication will prevent heart attacks.”
(Tagstotranslate) Heart
