DEAR DR. ROACH: I am a woman in my late 60s with a family history that includes an older brother who had a heart attack at a young age. My total cholesterol has hovered around 200 mg/dL for many years, but my HDL and LDL numbers are good.

A few years ago, I had a highly elevated level of lipoprotein(a), about 164 nmol/L. My doctor prescribed 1,500 mg of niacin daily, which was split into three 500-mg doses at meals. This treatment did dramatically lower my Lp(a) into the optimal range but caused nausea, so she said to lower the dose to what I could tolerate, which has only been 500 mg over time.

Last year, my Lp(a) was 185 nmol/L, so I decided to try 1,500 mg of niacin again. I, again, experienced horrendous nausea and weakness. The symptoms subsided and haven’t returned, but I discontinued niacin completely for six months, after which a test showed that my Lp(a) was 197 nmol/L.

My doctor says I should keep taking the level of niacin that I can tolerate. My question is whether there is a significant enough difference between a level of 185 nmol/L with 500 mg of niacin and a level of 197 nmol/L without any niacin to justify continuing to take it? I understand there are trials being conducted for a pharmaceutical treatment for this condition. — L.B.

ANSWER: Lpa(a) is a special type of low-density lipoprotein (LDL) that is a risk factor for heart disease, beyond the usual risk factors of an elevated total and LDL cholesterol and low levels of HDL cholesterol. The higher the Lp(a), the greater the risk, with levels less than 125 nmol/L showing a clinically relevant increase in risk.

You are right that there is much interest in the specific treatment for high Lp(a). However, the drugs we have tried so far that lower Lp(a) haven’t reduced the risk of heart attack by much. Most experts treat people who have high Lp(a) with therapies that are known to decrease the risk of heart disease. For most people, this means a high-dose statin (often ezetimibe). Neither of these treatments lowers Lp(a), but they do what we want them to do, which is to lower the risk of a heart attack and lower the risk of death in high-risk people.

Before statins, niacin was commonly used to lower the risk of heart disease, but it has side effects, including severe flushing and nausea. It is seldom used now. Niacin does lower Lp(a) levels by about 25% to 40%, but it is unproven whether niacin reduces the risk of heart attack and death in people with elevated Lp(a) levels.

A large study found that niacin didn’t provide an additional benefit when added to a statin. Many experts no longer use niacin in people with high Lp(a) levels. Given the side effects, the lack of proven effectiveness at what’s really important, and the modest improvement in your levels, I am hesitant to continue recommending it.

The drug class that has been shown to give additional benefits on top of a statin is the PCSK-9 inhibitor class, such as evolocumab (Repatha) and alirocumab (Praluent), both of which reduce the risk of heart attack and death when given along with a statin. These are expensive drugs and must be given by injection, but they have years of safety and effectiveness data.

Two new classes of drugs are being studied: antisense oligonucleotides (pelacarsen) and small interfering RNAs (olpasiran and lepodisiran), all of which are effective at reducing Lp(a) levels by 80% to 94%. But once again, their ability to prevent heart attacks is unknown, and none of them are approved by the Food and Drug Administration.