About one in five people – about 64 million in the United States – have high levels of a small particle in the blood. It can significantly increase the risk of heart attacks and blows.
But few know it, and almost no doctor feels it, because there was not much to do. The diet does not help. Not even the exercise. There were no drugs.
But in the near future, this could change.
On Sunday, cardiologists have announced that an experimental drug made by Eli Lilly, Lepodisiran, could reduce the levels of particle, LP (A), of 94 percent with a single injection. The effects lasted for six months and there have been no significant side effects.
But it is not yet confirmed that the reduction of LP levels (A) also reduces the risk of heart attacks and shots. This awaits large clinical studies that are now underway.
Lilly’s research was presented on Sunday during the annual meeting of the American College of Cardiology and simultaneously published in the New England Journal of Medicine. At least four other companies are also testing innovative drugs that block the production of LP (a) by the body, a mix of lipids and a protein.
Dr. David Maron, Stanford’s preventive cardiologist not involved in Lilly’s research, said that the evidence of a profound and lasting reduction of lipoprotein levels with Lepodisiran was “electrifying”.
Even Dr. Martha Gualati, a preventive cardiologist at the Cedars-Sinai Medical Center is not involved in the process, said that the study was “really elegant”.
Eli Lilly is now conducting a large clinical study asking if her drug can prevent heart attacks or strokes or cardiovascular deaths. It will conclude in 2029. Clinical studies on other drugs aimed at LP (A) will end before. The first will be a study by a drug Novartis, injected monthly, with results expected in 2026.
Cardiologists warn, however, that there is no guarantee that drugs will protect people. They remember too well a lesson learned from the assumption that altering a risk factor can alter the risk. Cardiologists were once enthusiastic about drugs that collected HDL levels, known as “good cholesterol”. People with naturally high HDL levels had lower heart disease rates. Those HDL breeding drugs did not help.
LP (A) -Growerting “is a new huge frontier in cardiovascular medicine,” said dr. Daniel Rader, a preventive cardiologist at the Perelman School of Medicine of the University of Pennsylvania. Dr. Rader is a member of the scientific consultative committee for Novartis and wrote an editorial to accompany the new document.
The treatments intended for LP (A) have passed a long time.
Lipoprotein was identified in 1974 as a risk factor for heart disease controlled by genes rather than lifestyle or environment.
People with LP levels (A) who are slightly higher than normal have an increased risk of about 25 % heart attack or stroke. And very high levels – as seen in 10 percent of the population – can double the risk.
Cardiologists affirm that often in patients without any reason to have a heart attack or stroke – whose cholesterol levels and blood pressure are normal and that they do not smoke – learn that patients have high levels of LP (A). Usually it turns out that they also have familiar stories of inexplicable heart disease.
The same goes for people who have heart attacks at a young age, said dr. Steven Nissen, Cleveland Clinic’s preventive cardiologist who is the academic leader for Lilly Drug’s study and for the clinical studies of three other new drugs.
“If you go to the coronary care unit and see someone who is 40 years old with an acute myocardial infarction, you have to know the level of their LP (a),” he said, referring to a heart attack. Too often, he said, their levels are 250 nanomoli per liter or even higher. The upper limit of normal is 75.
Dr. Maron said that his clinic was full of people who had no idea why he had developed heart disease, until they discovered they have high levels of LP (A).
One is Monte Wooden, a 71 -year -old pensioner who lives in Redding, California. His LDL cholesterol levels were moderately high. Its blood pressure was normal. It wasn’t smoking. Yet he had his first heart attack in 2006 while taking a statin to lower cholesterol.
It seemed that almost everyone in Mr. Wooden’s family died from heart disease.
Her paternal grandmother had her first heart attack when she was 40. He 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 LP (A) level of Mr. Wooden, he was greater than 400.
Dr. Maron and other preventive cardiologists, such as Dr. Gualati, Dr. Nissen and Dr. Rader, claim to regularly testify to all levels of LP (a) of their patients. Since LP levels (A) are controlled by genes, they add, patients should be tested only once.
Dr. Nissen is frank with his LP patients (A).
“Let’s say: you have a disorder with serious implications. I want to take any risk factor you have out of the table,” he said.
However, said dr. Gualati, a study discovered that only 0.3 percent of the US population had an LP test (A) – which was paid by the insurance – and only 3 % of those with heart disease has been tested.
She and other preventive cardiologists say that all adults should have an LP test (A). If the levels are high, doctors should treat any other risk factor aggressively.
For Mr. Wooden, this meant taking a powerful drug that lowers cholesterol, repatha, which obtained its level of LDL cholesterol up to 30.
The case of Mr. Wooden, however, did not end here. Dr. Maron led him to a clinical experimentation by testing one of the new drugs that lower LP levels (A).
During the process, Mr. Wooden had no symptoms of heart disease: no chest pain, breathless. When the process is finished, its symptoms are back, leading to a quadruple bypass operation.
“It’s anecdotal,” said dr. Maron, “but speaks of the probability that these drugs prevent heart attacks.”