

My LDL came back at 60 and I finally understand why the new guideline draws the line at 55
Got my lipid panel back a couple weeks ago. LDL 60 mg/dL, calculated with Martin-Hopkins. That sits right on the threshold the new 2026 ACC/AHA dyslipidemia guideline drew for very-high-risk patients: <55 mg/dL. The guideline goes no lower than that.
I had to look into why. The trial evidence keeps going lower. In FOURIER-OLE, the long-term extension of the evolocumab outcomes trial, achieved LDL kept reducing cardiovascular events all the way down past 20 mg/dL. Lower kept being better. So if 30 is biologically better than 55, why didn’t the guideline say so?
The answer, in the editorial accompanying the guideline (Schwartz in JACC), is a cost ladder. From the PROVE-IT data: about 35% of high-risk patients reach LDL <55 on atorvastatin 80mg alone. Add ezetimibe and 55% reach goal. Two generic pills, combined cost of $20-40 a month at most US pharmacies.
To push below 55, about 45% of patients would need a third drug, typically a PCSK9 inhibitor. To push below 30, more than 90% would. Repatha’s cash price via GoodRx is around $2,900 a year right now (list price still around $6,000) — meaningfully cheaper than it was a few years ago but still a real step up from two generics.
The marginal benefit, per FOURIER-OLE, is about 1 percentage point of absolute reduction in cardiovascular death, MI, or stroke over 5 years when you go from LDL 55 down to 40. That’s the math the guideline writers balanced.
For me sitting at 60, this means I’m done. The third drug isn’t worth it for the marginal benefit. For someone with high Lp(a), bad family history, or established CVD with multiple events, the calculus tilts the other way and pushing lower is reasonable.
One thing worth noting: LDL on a routine panel includes the cholesterol carried inside Lp(a) particles. Statins and ezetimibe barely lower Lp(a). So if you’re comparing two people at LDL 80, the one with high Lp(a) has “less modifiable” LDL and a worse forecast. In FOURIER-OLE, patients who achieved LDL <20 had a median Lp(a) of 8 nmol/L; those who landed at 40-55 had a median of 41. Some of the apparent benefit of very-low achieved LDL may actually be the low-Lp(a) phenotype rather than the LDL number itself.
Has anyone here with established CVD or genetically high Lp(a) been pushed below 55 on PCSK9 inhibitor + statin + ezetimibe? Curious what your achieved LDL ended up being and whether the cost felt worth the additional reduction.