Up to one in five people – about 64 million in the United States – have elevated levels of tiny particle in their blood. It can significantly increase the risk of heart attacks and strokes.
But few know about it, and almost no doctor is trying for it, because it didn’t have to be much. Nutrition does not help. Not even the exercise. There were no drugs.
But in the near future, this may change.
On Sunday, cardiologists announced that an experimental drug made by Eli Lilly, Lepodisiran, could reduce particle levels, LP (A), by 94 % with a single infusion. The results lasted six months and there were no significant side effects.
But it has not yet been confirmed that the decrease in LP (A) levels also reduces the risk of heart attacks and strokes. This awaits large ongoing clinical trials.
The Lilly research was presented on Sunday at the annual meeting of the American Cardiology College and at the same time published in the New England Journal of Medicine. At least four other companies also test innovative drugs that prevent the production of LP (A) of the body, a mixture of lipids and protein.
Dr. David Maron, a preventive cardiologist in Stanford not involved in Lilly research, said the evidence for deep and long -term reduction in Lipoprotein levels with Lepodisiran were “exciting”.
Dr. Martha Gulati, a preventive cardiologist at the Cedars-Sinai Medical Center, who also did not participate in trial, said the study was “really elegant”.
Eli Lilly is now conducting a large clinical trial asking if his medicine can prevent heart attacks or strokes or cardiovascular deaths. It will be completed in 2029. The clinical trials of other drugs aimed at LP (A) will be completed earlier. The first will be a study of a monthly Novartis drug, with the results expected in 2026.
However, cardiologists warn that there is no guarantee that medicines will protect people. They remember very well a lesson from assuming that changing a risk factor can change the risk. Cardiologists were once enthusiastic about drugs that raised HDL levels, known as “good cholesterol”. People with natural HDL levels had lower rates of heart disease. These-raising HDL medicines did not help.
LP (A)-which results in “is a huge new border in cardiovascular medicine,” said Dr. Daniel Rader, a preventive cardiologist at Perelman Medicine, Perelman, Pennsylvania. Dr. Rader is a member of Novartis’s scientific advisory council and wrote a constitution to accompany the new paper.
Treatments aimed at LP (A) come a long time.
Lipoprotein was identified in 1974 as a risk factor for heart disease controlled by genes and not by lifestyle or environment.
People with LP (A) who are slightly higher than normal have about 25 % increased risk of heart attack or stroke. And very high levels – as shown in 10 % of the population – can double the risk.
Cardiologists say that often in patients for no apparent reason for heart attack or stroke – whose cholesterol levels and blood pressure are normal and who do not smoke – they learn that patients have high levels of LP (A). It usually turns out that they also have family stories of unexplained heart disease.
The same is true for people with heart attacks at an early age, said Dr. Steven Nissen, a preventive cardiologist at the Cleveland Clinic, who is the academic leader of the Lilly Drug test and for clinical trials of three other new drugs.
“If you go to the coronary care unit and see someone who is 40 years old with acute myocardial infarction, you should know the level of LP (A),” he said, referring to a heart attack. Very often, he said, their levels are 250 nanomoles per liter or even higher. The upper limit of normal is 75.
Dr. Maron said his clinic was full of people who had no idea because they developed heart disease until they discovered that they had high levels of LP (A).
One is Monte Wooden, a 71 -year -old retired firefighter living in Redding, California. Its cholesterol LDL levels were moderately increased. Its blood pressure was normal. Does not smoke. However, he had his first heart attack in 2006, and he got a cholesterol reduction statin.
It seemed like almost everyone died in Mr. Wooden’s family of heart disease.
His father’s grandmother had her first heart attack when she was 40. He died of a heart attack at the age of 63. His father and his father’s brother died of heart disease. Mr. Wooden’s brother died of a heart attack.
When Dr. Maron examined Mr Wooden’s LP (A) level, it was greater than 400.
Dr. Maron and other preventive cardiologists, such as Dr. Gulati, Dr. Nissen and Dr. Rader, they say that they usually test all LP (A) levels of their patients. Because LP (A) levels are controlled by genes, they add, patients should only be tested once.
Dr. Nissen is blunt with LP (A) patients.
“We say: You have a disorder with serious consequences. I want to take on every risk factor you have from the table,” he said.
However, Dr. Gulati said a study found that only 0.3 % of the US population had been tested LP (A) – which is paid by insurance – and only 3 % of people with heart disease have been tested.
She and other preventive cardiologists say that all adults must have a LP (A) test. If the levels are high, doctors should be aggressively facing any other risk factor.
For Mr Wooden, this meant taking a strong cholesterol reduction drug, Repatha, which took the level of LDL cholesterol at 30.
Mr Wooden’s case, however, was not over there. Dr. Maron took him in a clinical trial test one of the new drugs that reduce LP (A) levels.
During the trial, Mr Wooden had no symptoms of heart disease – no breast pain, without breathing. When the test was over, its symptoms returned, leading to a quadruple bypass mode.
“It’s anecdotal,” said Dr. Maron, “but he talks about the possibility that these drugs prevent heart attacks.”
