As many as one in five people – about 64 million in the United States – the levels of a compact particle were increased in the blood. It can significantly boost the risk of heart attacks and strokes.
But few know about it and hardly test doctors because there was not much to do. The diet does not support. He doesn’t exercise. There were no drugs.
But in the near future this may change.
On Sunday, cardiologists announced that the experimental drug of Eli Lilly, Lepodisiran, can reduce particles, LP (A), by 94 percent with one injection. The effects lasted six months and there were no significant side effects.
But it has not yet been confirmed that the reduction of LP (A) levels also reduces the risk of heart attacks and strokes. This is waiting for enormous clinical trials, which are currently underway.
Lilly’s research was presented on Sunday at the annual American College of Cardiology meeting and at the same time published At the Fresh England Journal of Medicine. At least four other companies also test novel drugs that block LP (A) production in the body, a mixture of lipids and protein.
Dr. David Maron, a cardiologist from preventing Stanford, who was not involved in Lilly’s research, said that evidence of a deep and long -term reduction in the level of lipoproteins with Lepodisiran was “invigorating”.
Dr. Martha Gulati, a preventive cardiologist at Cedars-Sinai Medical Center, also not involved in the study, said that the study was “really elegant”.
Eli Lilly is now conducting a enormous clinical examination asking whether his drug can prevent heart attacks, strokes or cardiovascular deaths. The clinical trials of other drugs focused on LP (A) will end in 2029. The first of these will be the Novartis drug, injected every month, from the results expected in 2026.
However, cardiologists warn that there is no guarantee that medicines will protect people. They remember the lesson too well from assuming that changing the risk factor can change the risk. Cardiologists were once enthusiastic about drugs that raised the level of HDL, known as “good cholesterol”. People with a naturally high HDL level had a lower heart disease indicator. These HDL raising drugs did not support.
LP (A) “is a huge fresh border in cardiovascular medicine,” said Dr. Daniel Rader, a preventive cardiologist from Pennsylvania Perelman School of Medicine. Dr. Rader is a member of the Scientific Novartis Advisory Council and wrote an editorial article accompanying a fresh job.
Treatments focused on LP (A) have passed for a long time.
Lipoprotein was identified in 1974 as A Risk factor for heart disease It is controlled by genes, not a lifestyle or environment.
People with LP (A) levels, which are slightly higher than usual, have about 25 percent of an increased risk of heart attack or stroke. And very high levels – as you can see in 10 percent of the population – they can double the risk.
Cardiologists say that often in patients without obviously a heart attack or stroke – whose cholesterol and blood pressure are normal and who do not smoke – find out that patients have a high level of LP (A). It usually turns out that they also have family stories of unexplained heart disease.
The same applies to heart attacks at a adolescent age, said Dr. Steven Nissen, a preventive cardiologist at Cleveland Clinic, who is an academic leader in Lilly Drug study and clinical trials of three other fresh drugs.
“If you enter the coronary ward and see someone who is 40 years aged with a acute heart attack, you must know their level of their LP (A),” he said, referring to myocardial infarction. He said that too often their levels are 250 nanomole per liter or even higher. The upper limit of the norm is 75.
Dr. Maron said that his clinic was full of people who had no idea why they developed heart disease until they learned that they had a high level of LP (A).
One of them is Monte Wooden, a 71-year-old retired fireman who lives in Redding, California. Its LDL cholesterol was moderately increased. His blood pressure was normal. He didn’t smoke. However, he had his first heart attack in 2006, taking a reduced cholesterol statin.
It seemed that almost everyone in the family of Mr. Wooden died of heart disease.
His father’s grandmother had her first heart attack when she was 40 years aged. She died of a heart attack at the age of 63. His father and brother of his father died of heart disease. Mr. Wooden’s brother died of a heart attack.
When Dr. Maron tested the level of LP (a) Mr. Wooden, he was greater than 400.
Dr. Maron and other preventive cardiologists, such as Dr. Gulati, Dr. Nissen and Dr. Rader, claim that they routinely test all levels of LP (a) their patients. Because LP (A) levels are controlled by genes, they add, patients must be tested only once.
Dr. Nissen is blunt against his patients with LP (A).
“We say: you have a disorder with sedate implications. I want to take every risk factor you have from the table,” he said.
However, Dr. Gulati said that one study was fair 0.3 percent The US population was carried out by the LP (A) test – paid by insurance – and only 3 percent of people with heart disease were tested.
She and other preventive cardiologists say that all adults should have an LP (A) test. If the levels are high, doctors should aggressively treat any other risk factor.
For Mr. Wooden, this meant taking a powerful drug that reduces cholesterol, a repatha, which reduced LDL cholesterol to 30.
However, the case of Mr. Woodens is not over. Dr. Maron introduced him to a clinical examination, which tested one of the fresh drugs that reduce LP (A) levels.
During the study, Mr. Wooden did not have symptoms of heart disease – without pain in the chest, lack of narrow. When the study ended, his symptoms returned, which leads to a four -time circumvent surgery.
“It’s anecdotal,” said Dr. Maron, “but he says that these drugs prevent heart attacks.”