Reacción a "Results are presented from the unsuccessful first clinical trial that aimed to reduce cardiovascular risk by lowering lipoprotein(a) levels"

This is a well-conducted study. It involved over 8,000 patients who were followed for nearly five years, and the drug was compared against a placebo—which is exactly how such a study should be designed. The medication significantly reduces Lp(a) levels—by more than 70%. The issue, however, is that patients who received the drug experienced the same rates of heart attacks, strokes, and cardiovascular deaths as those who received the placebo: 12.3% versus 12.1%. There was no difference, even among those with the highest Lp(a) levels. The result is clear and negative. That said, for now, we only have the summary; the full article will need to be read.

Genetic studies had indicated that high Lp(a) levels increase the risk of heart attack, so these results have come as a surprise to us all. Yet, this is not the first time such a scenario has unfolded in medicine.

In my view, there is a fundamental difference between being born with high Lp(a) levels—and living with them throughout one’s life—versus lowering those levels with a drug at age 60, by which point atherosclerotic plaques have already formed and arterial damage has already occurred. Genetics is often more useful for identifying paths to avoid than for charting a clear course forward.

What, then, should we do? Measuring Lp(a) once in a lifetime remains useful, as it helps identify those at higher risk. For these individuals, the goal should be to lower their LDL cholesterol even further—an approach we know to be effective. As for targeted treatments, the outlook is less promising, at least for patients who have already experienced a heart attack or stroke. Other drugs are currently being studied, including trials involving healthy individuals who are not taking statins and have higher cholesterol levels; the outcomes there might differ. If they do, those treatments would need to be compared directly against statins.

The study has several limitations. The patients had already experienced a cardiovascular event and were receiving good treatment, so these findings cannot be applied to young or healthy individuals. Five years may be too short a period for something that has an effect over an entire lifetime. The events recorded include some that are less severe, such as urgent catheterizations. We also do not know how many patients stopped receiving the monthly injection. Furthermore, it is unclear whether the drug might be effective for aortic stenosis, another condition linked to Lp(a). On the positive side, the medication appears to be safe: there were actually slightly fewer serious adverse events than with the placebo.