Shortly after finishing breakfast six years ago, Brian Farrington felt some discomfort and thought it was heartburn. He popped a few Tums but hours later began perspiring profusely and experiencing chest pain. The next morning, Farrington, who was 53 and seemingly healthy, headed to the hospital and was shocked to learn he had suffered a heart attack. He had several blockages in his right artery. Previously, Farrington had been told his cholesterol was “borderline high” but did not require medication. As the resident of Columbus, Ohio, recovered, he considered a nagging question: Why was there so much premature heart disease in his family? His grandfather and three great-uncles had died of heart disease in their 40s, and his father had gotten a stent in his 60s. He decided to dig deeper. Farrington eventually discovered he had a heart threat that he — and many other people — had never even heard of: High levels of a fatty particle called Lipoprotein(a). The molecule is similar to LDL , the “bad” cholesterol that circulates in the blood and can promote coronary plaque, increasing the risk of heart attacks. But Lp(a) carries an extra protein that makes it an even bigger cardiac risk factor than LDL, studies have shown. Higher-than-normal levels encourage the development of blood clots as well as plaque, sharply raising the risk of stroke, heart attack and other severe problems — even among younger people with normal levels of LDL, doctors say. The condition “can cause an acceleration of vascular disease,” said Kristin Thomas, an internist in Washington. People with higher-than-normal Lp(a) might develop plaque in their arteries “in their 40s and 50s, rather than in their 60s and 70s.” For decades, Lp(a), first detected more than 60 years ago, has flown under the medical radar. Most patients are not familiar with it. Even many doctors don’t know much about it and don’t realize it’s a major risk factor, experts say. Testing has been uncommon, in large part because it has not been clear how to treat elevated Lp(a). Unlike with LDL, the levels of Lp(a) are set almost entirely by genetics and not affected by diet and exercise, or by statins or other cholesterol drugs on the market. The picture, however, is starting to change. In clinical trials, several experimental drugs have been shown to slash Lp(a) levels by as much as 94 percent by deactivating the gene responsible for the molecule. Now scientists are testing whether the drugs reduce heart attacks and strokes. If so, the treatments will be submitted to the Food and Drug Administration for approval. It’s possible the first drug for Lp(a) will be available within two years, scientists say. In the meantime, patients should take steps to improve their heart health — chiefly by reducing other risk factors, especially LDL cholesterol, doctors say. The importance of getting an effective Lp(a) treatment “cannot be overestimated,” said Steven Nissen, a cardiologist at Cleveland Clinic and academic leader of several trials involving the experimental drugs. At least 20 percent of the population — 65 million people in the United States and more than 1.5 billion worldwide — have elevated Lp(a), according to estimates. Lp(a) levels are detected by blood tests that measure the number of particles in the blood, or nanomoles per liter. A level below 75 is normal, while a reading between 75 and 125 indicates a moderately increased risk. A level above 125 suggests a high risk, according to the Florida-based National Lipid Association , whose members specialize in lipid disorders. The test for Lp(a) is not included in the conventional cholesterol test and must be ordered separately. Lp(a) was identified in 1963 by the renowned Norwegian medical geneticist Kare Berg and linked to heart disease in the early 1970s. Over the years, scientists have learned that elevated Lp(a) disproportionately affects certain demographic groups, including Black people of African descent. But the genetic condition cuts a wide swath across racial and ethnic groups. Because of that, many specialists say that everyone’s Lp(a) levels should be tested. In Europe and Canada, guidelines call for such universal testing. The National Lipid Association in Florida agrees. But the official U.S. guidelines for cholesterol, developed primarily by the American Heart Association and the American College of Cardiology, are more conservative , recommending testing only for certain patients, including those with a family or personal history of heart disease. Those guidelines are set to be updated in the first quarter of next year. A spokeswoman for the American Heart Association said the group did not have details about any possible revisions. Michelle O’Donoghue, a cardiologist at Brigham and Women’s Hospital in Boston and academic leader of a trial testing an Amgen Lp(a) drug, said there are several reasons people should be tested. For one thing, she said, parents and children of individuals with elevated Lp(a) should be tested to see if they have the condition, too. And people who are affected might decide to take part in a clinical trial. Some researchers say that patients with high Lp(a) levels should try to reduce their heart risks by lowering their LDL cholesterol to below 55 through lifestyle changes and perhaps medication. Some patients are eligible for apheresis, a procedure similar to dialysis, in which a machine removes Lp(a) and LDL cholesterol from the blood. But the method is expensive and not used much. For C. Michael Gibson, heart health has always been a priority, in part because his grandfather had a heart attack in his 40s. For years, Gibson, a cardiologist at Beth Israel Deaconess Medical Center in Boston, took a statin and another cholesterol medication to keep his LDL at about 70, generally considered a healthy level. So he was surprised when a heart scan a few years ago showed a potentially damaging buildup of plaque in his arteries. A subsequent blood test showed he has a high level of Lp(a), which he has concluded is the culprit. Since then, Gibson has moved aggressively to lower his cardiac risks, he says. He has lost 30 pounds and added a third cholesterol drug, driving down his LDL to 27. But his Lp(a) remains high, and he is eager to try one of the treatments in development. “I have taken control as best I can,” Gibson said. “But what is always in the back of my mind is: What else can I do?” Most of the drugs in development for Lp(a) are injections that go just under the skin, like insulin shots. A pill is also in the works. Scientists say the therapy that is furthest along is pelacarsen. A trial showed the drug reduced Lp(a) levels by up to 80 percent. Researchers are now testing whether a monthly shot reduces adverse cardiovascular events in people who have heart disease. Results are expected early next year. Another drug, called lepodisiran, made news in March when a study found that a single injection lowered Lp(a) levels by nearly 94 percent for six months. Results aren’t expected until 2029, though, on whether the therapy reduces the risk of strokes and heart attacks. Seven years ago, Don Kosec, now 61, thought he was in great shape — until he experienced shortness of breath while traveling. Three weeks later, the Stow, Ohio, resident underwent quintuple bypass surgery for blocked arteries. He found out later that he has elevated Lp(a) levels, a disorder he had never heard of. “I was dumbfounded,” Kosec said. “At some point, I would have had a heart attack, and who knows whether I would have survived.” He takes a statin and a baby aspirin but his Lp(a) remains high. Katherine Wilemon, who has two genetic cholesterol conditions, including elevated Lp(a), had a heart attack at 39. She later founded a nonprofit, the Family Heart Foundation , to draw attention to the disorders and encourage screening. She is encouraged about the potential for effective Lp(a) therapies but worries that it could take a long time to change medical practice. Thomas, the internist in Washington, agrees: “We are behind on this and it is time to catch up.”