A single dose of an experimental drug has considerably reduced the levels of a deadly form of cholesterol, often considered as unexploited, up to a year.
Lipoprotein (A) is a type of cholesterol that is hidden in the body, not detected by routine tests and not discouraged by the existing drugs, food or exercise.
The results, say cardiologists, are a critical step towards the treatment of millions of Americans genetically predisposed to abnormally high levels of lipoprotein (A) or LP (A).
“This is remarkable,” said Dr. Eric Brandt, director of preventive cardiology at the cardiovascular center at the University of Michigan Frankel in Ann Arbor, who was not involved in the new research. “These drugs have the potential to eliminate this lipoprotein almost.”
People with high levels of LP (A) – Some 64 million adults in the United States – are at an extremely high risk of cholesterol accumulation in their arteries. This accumulation raises their chances of heart attack, stroke and early death of cardiovascular problems.
The results of a previous test of the drug Eli Lilly, called Lepodisiran, showed that the drug was sure.
The latest study, a phase 2 clinical trial funded by Lilly, included 320 people. An injection, according to the researchers, reduced the levels of LP (A) by 93.9% after six months. After a year, the effects decreased, but only slightly, with levels measured at 88.5% less than the basic line. People in the trial who obtained a second dose at six months suffered a reduction of 94.8% at the bar of one year.
“This is a major source of cardiovascular morbidity and mortality,” said Dr. Steven Nissen, university director of the Cleveland vascular and thoracic institute and the Lepodisiran trial. “We have never been able to treat lipoproteins (A) so far,” he said.
Lepodisiran works by targeting mRNA, or Messenger RNA, which tells the body to make LP (A). Message RNA carries instructions to body proteins to produce certain substances, in this case, LP (A). The medication works by pulling mainly on the messenger.
Nissen’s conclusions were presented on Sunday at the annual meeting of the American College of Cardiology in Chicago and published in the New England Journal of Medicine.
A triple threat
Lipoprotein (A) is dangerous in three ways: it sticks to LDL (the “bad” cholesterol), which makes it more likely to plug the arteries; This is particularly good to cause inflammation; And this tends to lead to blood clots.
Routine blood cholesterol tests could look for LP (A) but not – largely because there has never been an effective treatment for this.
A high LP diagnosis (A) was a shock for Donald Kosec, 61, from Stow, Ohio. Kosec said that he had never had any of the risk factors typical of heart disease: he worked regularly, has kept healthy weight and that the doctor has shown normal cholesterol and blood pressure levels.
Eight years ago, when he was 53 years old, Kosec went to see his doctor after feeling a little out of breath. It was not until that time that he learned that all the major arteries pumping blood towards and from his heart were blocked. The high LP (A) was the culprit.
Within three weeks, he underwent a pontage of quintuple.
“Going not to have care in the world all of a sudden in front of your own death, your own mortality,” said Kosec. “It took me off guard, a lot of time.”
He entered a clinical trial for a treatment similar to Lepodisiran, of the AMGEN medication manufacturer. The first results showed that the drug, called OLPASIRAN, fell LP (A) at least 95% in nine months.
It turns out, however, that Kosec obtained the placebo in the trial – not the real deal. He does not know if his LP (A) remains high. Without additional treatment, this is probably the case.
All he can do now is waiting for one of these promising LP (A) therapies to be available.
“Right now, I’m looking at my weight, I’m doing the exercise and I’m doing it all, and so far, everything is fine,” said Kosec. “I will be much happier when I can take a medication that improves this.”
