Speaking of inflammation, Caristo Diagnsotics recently received FDA approval. They are a spun off of Oxford and operatimng Cari Heart Care centers through out UK. Anyone from UK had it done??
Their Fat Attenuation Index (FAI) definitely is superior to flawed coronary angiogram and perhaps Calcium Scoing as you can see below.
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N = 1 from a general surgeon.
https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/647525
" I am a 53-year-old woman with a significantly elevated level of Lp(a) (27 mg/dL), but I found that I had to stop taking niacin primarily because of headaches. Thus, after a thorough review of the literature, I began to follow the advice of Linus Pauling. For individuals who have an Lp(a) level higher than 25 mg/dL and a family history of heart disease, the recommendation is to take 3 g/d of both ascorbic acid and L-lysine monohydrochloride.5 After 6 months of this regimen, with no adverse effects, my Lp(a) level decreased to 14 mg/dL, a reduction of 48%. The Lp(a) testing was done by the highly reliable Lawrence Berkeley National Laboratory/Berkeley HeartLab Department Technology Transfer program. The theory is that lysine is an Lp(a)-binding inhibitor and thus blocks the Lp(a) attachment to the arterial blood vessel wall and that ascorbic acid helps to repair the collagen injury to the blood vessel and acts as an antioxidant."
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Re: inflammation - if the issue is specific to vascular inflammation that compromises the endothelium kicking off the CVD cascade, and this inflammation being highly localized can therefore be missed by nonspecific inflammatory biomarkers like IL-6 and hsCRP, then we can make more sense of the hypothesis that the protective mechanism by which statins work is lowering inflammation (in addition to lowering ApoB/LDL) - the idea being that what is lowered is specifically the pathological vascular inflammation (thus protecting the endothelium). It is because of this specificity of statins’ impact on vascular inflammation that they are effective whereas more general anti-inflammatories that simply impact global inflammation are not effective against CVD. That’s all and good, but it does pose a bit of a puzzle. Because on the one hand we say that IL-6 and hsCRP don’t capture this specific vascular inflammation, and you can have low IL-6 and hsCRP and still have vascular inflammation and subsequent CVD, as well as general anti-inflammatories lowering IL-6 and hsCRP numbers and yet not being protective. In this scenario these inflammatory numbers are not at all informative vs CVD in general. On the other hand, we know well and good that in general statins do seem to lower inflammatory markers such as hsCRP. And some LLT agents too can have this effect - bempedoic acid lowers hsCRP. But then again, not all of them do: PCSK9i and ezetimibe don’t reliably lower these markers.
Bottom line, there is still a lot more to be learned about the nexus of LLT-inflammation-CVD.
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The study that Ethan Weiss (UCSF Cardiologist) just pointed to as perhaps foreshadowing this new negative result:
Lipoprotein(a) and recurrent atherosclerotic cardiovascular events: the US Family Heart Database
A study of 273,770 US adults who already had cardiovascular disease found that the higher their lipoprotein(a), the higher their chance of a second heart attack, stroke, or artery-opening procedure, with no upper limit where the risk stopped climbing. People in the top 5 percent of lipoprotein(a) values carried roughly 39 to 45 percent more risk than people in the bottom third, and that relationship held equally in women and men and in Black, Hispanic, and White participants. Lipoprotein(a) levels themselves differed sharply between these groups, but the risk carried per unit did not. A secondary and much weaker finding suggested that aggressive LDL cholesterol lowering may blunt some of that excess risk, though the study design cannot separate this from prescribing patterns.
Lipoprotein(a) has been a recognized cardiovascular risk factor for decades and has been largely ignored in clinical practice because nothing could be done about it. That is changing. Several drugs that cut lipoprotein(a) by 80 to 98 percent are in late-stage trials, and those trials need to know who stands to benefit. An analysis of US medical claims covering 340 million people offers the largest answer so far.
Researchers at the Family Heart Foundation, working with colleagues at Copenhagen University Hospital and Stanford, pulled 273,770 adults who already had atherosclerotic cardiovascular disease and who had a lipoprotein(a) test on file. They tracked them for a median of 5.4 years. In that time 41,687 of them, about 15 percent, had another cardiovascular event: a heart attack, an acute coronary syndrome, an ischemic stroke, or a procedure to reopen or bypass a blocked artery.
The pattern was clean. Risk rose with lipoprotein(a), and it kept rising. People above 300 nmol/L, the top 5 percent of the distribution, had 39 to 45 percent higher risk of a repeat event than people below 15 nmol/L, depending on how heavily the model adjusted. There was no ceiling. The curve continued climbing past 1000 nmol/L, where risk was roughly two and a half times baseline. This matters because an earlier and much smaller cohort had suggested the risk leveled off around 150 to 200 nmol/L in people with established disease. In a cohort sixteen times larger, it does not.
Two other findings stand out. Lipoprotein(a) levels differed markedly by group, running higher in women than men and higher in Black participants than in Hispanic or White participants. But the risk per unit of lipoprotein(a) was statistically indistinguishable across all of them. So the disparity in outcomes appears to come from carrying more of the particle, not from the particle behaving differently in different bodies. That argues against applying separate risk thresholds by sex or ancestry.
The second finding is the one that will get quoted, and it is the shakiest. Among people on aggressive LDL cholesterol lowering, the lipoprotein(a) signal shrank. In people taking no lipid drug, the top lipoprotein(a) category carried 57 percent excess risk. In people on high-intensity statins plus ezetimibe, that excess fell to 15 percent. In the small group on PCSK9 inhibitors it vanished, though only 397 events occurred in that entire subgroup and the confidence interval runs from a 30 percent benefit to a 46 percent harm.
The authors are candid that this is not a controlled comparison. Physicians prescribe the strongest drugs to the sickest patients, and it shows: absolute event rates were highest, not lowest, in the aggressively treated group. Whether lowering LDL genuinely blunts lipoprotein(a) risk, or whether the statistics are being pushed around by who gets which prescription, cannot be settled with claims data.
What the study does establish is scale. Roughly one in five adults carries clinically meaningful lipoprotein(a), most have never been tested, and in this population the risk it carries did not stop climbing.
Actionable Insights
Get tested once. Lipoprotein(a) is more than 90 percent genetically fixed and stable across adult life, so a single measurement in nmol/L settles the question permanently. It is not part of a standard lipid panel and you have to ask.
Understand the magnitude honestly. Over 5.4 years, 14.0 percent of people with lipoprotein(a) below 15 nmol/L had a repeat cardiovascular event, versus 19.9 percent of those above 300 nmol/L. That is a gap of 5.9 percentage points, meaning about 1 additional event for every 17 high-lipoprotein(a) people over five years. Expressed as a standardized effect size, this is a Cohen’s d of roughly 0.18, which statisticians call small. Small effects still matter at population scale, and this one applies to a fifth of adults.
Roughly, each additional 100 nmol/L is associated with about 11 percent more relative risk, with no plateau observed. Note the units: nmol/L and mg/dL are not interchangeable and cannot be reliably converted.
If yours is high, your siblings, parents, and children each have roughly a 50 percent chance of also being high. Cascade testing of first-degree relatives is the highest-yield thing you can do with the result.
There is no approved drug that lowers it. If yours is high, the practical response is to drive everything else down harder: LDL cholesterol, blood pressure, smoking, glycemic control. This study is consistent with that approach helping, but does not prove it.
Context and Source
- Open Access Paper: Lipoprotein(a) and recurrent atherosclerotic cardiovascular events: the US Family Heart Database
- Institutions: Family Heart Foundation (Fernandina Beach, FL); Copenhagen University Hospital Rigshospitalet and University of Copenhagen; Stanford University; BIA Clinical Group (Ann Arbor, MI); Flourish Research (Apex, NC); Copenhagen University Hospital Herlev and Gentofte
- Countries: United States and Denmark
- Journal: European Heart Journal (Oxford University Press, on behalf of the European Society of Cardiology), 2025;46:4762-4775, doi 10.1093/eurheartj/ehaf297. Published in the FastTrack Clinical Research section.
- Impact evaluation: The impact score of this journal is 45.3, evaluated against a typical high-end range of 0 to 60+ for top general science, therefore this is an Elite impact journal.
