Who has had his/her Lp(a) measured?

What value/values did you get?
Is it associated with heart disease for you? (gosh I HATE to type those two words!)

My Lp(a) last month was 50...and yes: coronary artery disease.

I had mine measured, but with the VAP test, which has 10 as the recommended level rather that 30. Mine came out as 14, so if I converted that to the other test results, maybe it would be about 42? I don't have any heart disease.

I think Lp(a) is perhaps the most important measurement to know. Inflammation is also important. Maybe if inflammation is not present, Lp(a) would not do so much damage. I haven't had my CRP or homocysteine measured, though I intend to do so. I do have a fairly high HDL and low LDL.

Lenin,

08/2002: 12.2
07/2003: 4.2
01/2005: 12.0

I have no explanation for the dropoff in 2003--not like that much has changed with me since then and 2005. There should have been a much larger discrepancy between 02 and 03/05....

My MI was 03/2002, so I don't have any values for these novel risk factors prior to the August 2002 measurement.

The Lp(a) values do not correlate at all to the changes in my total C, LDL, HDL, particle sizes of those latter two, nor two VLDL/TG levels and the particle sizes. About the only values that do follow this same trend were my homocysteine and hs-CRP, in that order below.

08/2002: 6.7 0.93
07/2003: 5.8 0.11
01/2005: 8.7 0.4

No correlation for me between the high 50.1 Lp(a) and either of the two LOW inflammatory markers: homocycsteine (8) and CRP (always 0.1)

Jacqueline,
What are the units for the VAP test Lp(a) that you had? Mine are reported in mg./dL.

Of interest from the BRITISH MEDICAL JOURNAL:

Alcohol lowers Lp(a) - heart disease risk

By: Thomas Pickering, MD, DPhil, FRCP, Director of Integrative and Behavioral Cardiology Program
of the Cardiovascular Institute at Mount Sinai School of Medicine, New York.

Lp(a) is one of the lipoproteins involved in the metabolism of cholesterol, and is a risk factor for coronary heart disease. Little is known about the influence of diet on its level in the blood.

A study of 300 Finnish men has related Lp(a) levels to alcohol consumption. The men were divided into four groups: abstainers, and three groups of drinkers: one to four drinks a week, five to 20 drinks a week, and more than 20. Men who drank no alcohol had higher levels of Lp(a) than any of the three groups of drinkers; there were no differences in Lp(a) between the three groups of drinkers.

Doctor's comments

This study shows that drinking minimal amounts of alcohol can lower Lp(a) levels and may help to explain why light alcohol consumption decreases the risk of coronary heart disease. The usual explanation for alcohol's beneficial effects is that it raises HDL cholesterol, but this only occurs in people who drink relatively large amounts (20 drinks a week).

Lenin,
The VAP test is also in mg/dL. They use a different method that measures cholesterol content of Lp(a) rather than an immunoassay and is considered more reliable. This was explained in a thread last month. The report I got also includes a LOT of information on subclasses and percentages of large bouyant to small dense.

Thanks Jacqueline,
It also seems that what SOME tests view as Lp(a), others (presumably the VAP) see a grouping of things like Lp (A1), Lp(A2), and Lp (A1+B) ...confusing and DISTINCTLY unamusing! So therefore your test probably was measuring only a fraction of what mine were.

Here's a study indicating that Lp(a) is quite dangerous ...of course people undergoing angiography are not exactly a sample of men on the street. Probably a GOOD sample might remove something like 40, 50, or 60% from all those percentages. I guess the biblical "Mark of Cain" was nothing more or less than the Lp(a) gene!

Lipoprotein (a) [Lp(a)] levels have been correlated with angiographically defined coronary artery disease (CAD). Pattern of Lp(a) distribution in various racial groups is different. To study this relationship in Indian patients, plasma levels of Lp(a) and other lipid values were assessed in 101 patients undergoing coronary arteriography. Lp(a) concentration was higher in CAD group (n = 77) compared to normal coronary artery group (n = 24) (26.83 +/- 22.09 mg/dl vs. 15.07 +/- 14.61 mg/dl, P < 0.05). Lp(a) values had graded association with CAD. In Lp(a) quartile of < 5 mg/dl, 66.7% patients had CAD; in Lp(a) quartile of 5-25 mg/dl, 69.0% had CAD; Lp(a) quartile of 26-75 mg/dl, 87.5% had CAD; and in Lp(a) quartile of > or = 76 mg/dl, all patients had CAD. High density lipoprotein (HDL) cholesterol was higher in the normal coronary artery group as compared to CAD group (45.25 +/- 8.26 mg/dl vs. 41.83 +/- 16.47 mg/dl; NS). In HDL quartile of < 35 mg/l, 88.9% patients had angiographically defined CAD. Plasma values of total cholesterol, triglycerides (TG), apolipoprotein-A1 (Apo-A1), apolipoprotein-B (Apo-B), low density lipoprotein (LDL) cholesterol, LDL/HDL cholesterol ratio and Apo A1/B ratio were not significantly different in the groups with normal coronary arteries and CAD. Our results indicate that the measurement of Lp(a) provides a better marker for predicting the presence of angiographically defined CAD as compared to traditional measures.

It would seem that, since 3/4 of the group had CAD, then those levels below 75% (Lp(a) < 25 and some undefined amount above 25 that is healthy but somewhere between 26 and 75 (could it be BROADER???) one crosses the "extra" CAD incidence. So it seems that chosen level of 30 as the upper normal of my test might be pretty close to true (using tha standards employed in this study.) Oy, that correlation of 100% CAD with Lp(a) over 76 mg/dL is a DOOZY of a finding though, isn't it?

[url]http://www.clinchem.org/cgi/content/full/48/9/1454[/url]

This study says asprin lowers it

Though I greatly value laboratory assessments, numbers remain just that...numbers. The true significance of Lp(a) is still clouded by conflicting information. The New England Journal (Nov. 27 2003) concluded that among older adults, an elevated level may be a predictor of stroke and vascular disease and "death from any cause" in men but not in women. As a woman, I am not sure that information gives me comfort.

Aspirin lowered serum Lp(a) concentrations to 80% of the baseline values in patients with high Lp(a) concentrations (>300 mg/L). The percentage of decrease in serum Lp(a) was larger in patients with high Lp(a) than in patients with low Lp(a) (<300 mg/L), irrespective of apo(a) isoform size. The decreases in serum Lp(a) in high Lp(a) patients with both the high-molecular-weight and the low-molecular-weight isoforms were positively correlated with the baseline Lp(a) concentrations.

Of course, madox, that is a sample of DEAD MEN WALKING with through the roof Lp(a) of over 300 mg/dL <shudder>.
If 80 mg. aspirin does lower Lp(a) I am in worse trouble than I thought because I've taken AT LEAST 650 mg. aspirin a day for a LONG time.

bigdobe,
That report you cited seems a bit "skewed" from most of the many other studies. I've read at least 30 that STRONGLY suggest that Lp(a) is a VERY WELL CORRELATED marker for CAD. Women and their estrogen levels DO seem to be somewhat more protected.

at age 62 with lpa of 50.1 you have done well i think.