Lipoprotein (a)
Before we continue our series discussing more lipid-modulating drugs, I want to talk about another topic that I have been asked about frequently on my message board: What is Lp(a) and what can one do for it?
Lipoprotein (a), which is pronounced "little a", is simply an LDL particle to which a protein called apolipoprotein (a) is attached. As I have discussed before in a previous posting about advanced lipoprotein testing, LDL particles are the vehicles that transport cholesterol through the body.
They "drive" the cholesterol into the arterial wall and then the LDL particle becomes a foam cell which is the hallmark of atherosclerosis. Apolipoprotein (a) can also be attached to triglyceride enriched VLDL particles which can also can accelerate plaque formation. Since 90-95% of all the circulating "bad" particles are LDL-P, they become the most important target to modify in order decrease the number of "cars" that move the cholesterol into the arterial wall. So the question remains: If one has an elevated Lp(a), are they at increased risk of a cardiovascular event?
In most epidemiologic studies, the risk of elevated apolipoprotein (a) depends on the LDL cholesterol level. In the large Physicians Health Study, Lp(a) conveyed no risk unless the LDL-C is > 160mg/dl. In the Women's Health Study, Lp(a) was of no risk unless it was very high (>90th percentile) and the LDL cholesterol was also elevated. Thus, elevated Lp(a) in the face of normal cholesterol is not a risk factor.
The proper treatment of elevated Lp(a) is to lower one's bad cholesterol. That means lowering LDL-P or ApoB (or its surrogates - LDL cholesterol and non HDL cholesterol). Although a statin is the primary drug used to treat high cholesterol, they have not been shown to lower Lp(a).
The reason relates to one of the ways a statin works to lower cholesterol. Statins increase the number of receptors made by the liver to bind to the LDL particles. It seems that when apolipoprotein(a) is attached to an LDL particle, it is "camouflaged" from the LDL receptor. Those particles that do not have the apoliporotein (a) attached are cleared in the usual fashion by binding to the LDL receptors. So statins will lower the LDL cholesterol, ApoB, and LDL particle levels but have little to no effect on Lp(a) levels. Despite this, the lowering of the cholesterol carrying particles would greatly lower the clinical risk of a cardiovascular event.
The best way to increase the number of receptors to remove the particles is with a statin, statin/zetia combination, or a bile acid sequestrant( I have had a prior posting on both zetia and bile acid sequestrants).
There are drugs they inhibit the synthesis of apolipoprotein (a) by the liver. These include fibrates, estrogen, evista, and niacin. It is most important to remember that there are no clinical outcome studies relating event reduction to what a drug does to Lp(a). As we have talked about previously, there are numerous studies that have conclusively shown that lowering LDL-C or LDL-P saves lives.
Some people advocate niacin to lower Lp(a) levels, but there is not one ounce of clinical trial data that outcomes would be affected by using niacin to lower Lp(a). As I have said over and over, the name of the game is to lower the LDL-P or ApoB and is still the best way to reduce risk if one has dyslipidemia and high Lp(a).
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Lipoprotein (a), which is pronounced "little a", is simply an LDL particle to which a protein called apolipoprotein (a) is attached. As I have discussed before in a previous posting about advanced lipoprotein testing, LDL particles are the vehicles that transport cholesterol through the body.
They "drive" the cholesterol into the arterial wall and then the LDL particle becomes a foam cell which is the hallmark of atherosclerosis. Apolipoprotein (a) can also be attached to triglyceride enriched VLDL particles which can also can accelerate plaque formation. Since 90-95% of all the circulating "bad" particles are LDL-P, they become the most important target to modify in order decrease the number of "cars" that move the cholesterol into the arterial wall. So the question remains: If one has an elevated Lp(a), are they at increased risk of a cardiovascular event?
In most epidemiologic studies, the risk of elevated apolipoprotein (a) depends on the LDL cholesterol level. In the large Physicians Health Study, Lp(a) conveyed no risk unless the LDL-C is > 160mg/dl. In the Women's Health Study, Lp(a) was of no risk unless it was very high (>90th percentile) and the LDL cholesterol was also elevated. Thus, elevated Lp(a) in the face of normal cholesterol is not a risk factor.
The proper treatment of elevated Lp(a) is to lower one's bad cholesterol. That means lowering LDL-P or ApoB (or its surrogates - LDL cholesterol and non HDL cholesterol). Although a statin is the primary drug used to treat high cholesterol, they have not been shown to lower Lp(a).
The reason relates to one of the ways a statin works to lower cholesterol. Statins increase the number of receptors made by the liver to bind to the LDL particles. It seems that when apolipoprotein(a) is attached to an LDL particle, it is "camouflaged" from the LDL receptor. Those particles that do not have the apoliporotein (a) attached are cleared in the usual fashion by binding to the LDL receptors. So statins will lower the LDL cholesterol, ApoB, and LDL particle levels but have little to no effect on Lp(a) levels. Despite this, the lowering of the cholesterol carrying particles would greatly lower the clinical risk of a cardiovascular event.
The best way to increase the number of receptors to remove the particles is with a statin, statin/zetia combination, or a bile acid sequestrant( I have had a prior posting on both zetia and bile acid sequestrants).
There are drugs they inhibit the synthesis of apolipoprotein (a) by the liver. These include fibrates, estrogen, evista, and niacin. It is most important to remember that there are no clinical outcome studies relating event reduction to what a drug does to Lp(a). As we have talked about previously, there are numerous studies that have conclusively shown that lowering LDL-C or LDL-P saves lives.
Some people advocate niacin to lower Lp(a) levels, but there is not one ounce of clinical trial data that outcomes would be affected by using niacin to lower Lp(a). As I have said over and over, the name of the game is to lower the LDL-P or ApoB and is still the best way to reduce risk if one has dyslipidemia and high Lp(a).
Related Topics:
15 Comments:
Thank you so much for clarifying this topic. I see so many people on your message board giving what they believe are the facts and really don't know what they are talking about. I also was not sure why my doctor would order this and obviously he did not understand what it meant. I think your postings are outstanding and so is your website. You have helped me and my wife understand this complex topic of cholesterol management. God bless you!
Agree completely, great piece, thanks! Now, can you explain how LP(a) relates to the LP-PLA2 test?
My Lipoprotein a is 206
My Dr. did not seem that concerned.
My Triglycerides were 72
My total Cholesterol was 165
HDL 75
LDL 76
CHOL/HDLC Ratio 2.2
I have been concerned over my Liipoprotein being so high, but I really do not know what to do.
Any suggestions?
Lipoprotein (a) is an independent risk factor due to new research.
Lipoprotein (a) is found in only 4 species in world namely Humans, Chimps, Pig and Fruit Bat. They all have one thing in common - They can not manufacture their own "Vitamin C" as done by all other species.
Vitamin C is a collagen (Binds cells together). Lack of Vitamin C will bring Lipoprotein (a) into picture. It tries to acts like repair the cell walls in some persons but the problem is it acts as a great binder to LDL.
To control Lipoprotein (a) only Niacin works. Niacin is also called as vitamin B3. Slowly increase its value and keep your liver function under test (AST & ALT) under test for every 4 months.
Niacin also causes a harmless flushing and itching. Hence increase it very slowly under guidance of a doctor.
My Lipoprotein is 124 and have a family history of heart disease.My LDL-P is 1164
Small LDL-P 696
LDL-C 132
HDL-C 53
Triglycerides 78
LDL particle size 21.1
Large HDL-P 11.7
Large VLDL-P 0.7
I'm concern about my health because I just lost my Mom at the age of 62.My heart doctor wants to see me in 3 years.What do I do to watch my health.
Why is so much time spent on statins when even Merck's own research yielded mixed results at best? It is the sugar that we need to control. Eliminating sugar in my diet dropped my cholesterol 100 points, mostly on the LDL side.
My Berkeley HeartLab tests results"
Total Chol. - 241
LDL-C - 138
HDL-C - 76
Trig. - 136
IIIa + b - 13.4
LDL IVb - 1.6
HDL2b - 27
Apo B - 116
Lp(a) - 120
Holocysteine - 13.4
Apo E Genotype - 2/4
Lipo-PLA2 - 195
CRP - 0.6
Fibrinogen - 315
Insulin - 8
Should I be concerned about this result. I have lost weight since this test and exercise regularly and eat a heart healthy diet.
What is your theory on the use of Plantsterols/stanols with regards to lowering cholesterol? More manufactures are now adding these compounds into foods as well as supplements. Any benefits?
if i hadn't taken the berkely test (which is new? and I can't help wondering if just some gimmick) i would have never known about this 'new' thing lipoprotein (a) and all the rest..and my cholestrol test would have been 'all normal' range.
\after that test, my doctor suggested i take the generic of zocar and also a fibrate and THEN i read that taking a statin and fibrate 'together' can cause big problems..that the fibrate can cause problems with muscles etc which i sure don't need any more headaches.
I understand that 'all' medicines have 'warnings'but there were several articles about the dangers of taking fibrates together with a statin. so??????? what do you have to say about that? as a p.s. can this be lowered some other way, like thru eating some correct foods etc marilyn
I have a problem with the emphasis on the word “bad” in this discussion. I tell my patients and visitors at my website nomoremedicines.com that if your LDL cholesterol is too high the only thing that is bad is your diet. “Bad” cholesterol is good marketing. The drug companies have demonized cholesterol to benefit their own bottom line. Lipitor (only one of 6 statin drugs) is the best selling drug in history, with annual sales at $11-12 billion.
Statins actually only benefit a tiny minority of patients that take them. Read the medical literature – the study was called “ASCOT-LLA”. Pfizer put the results of this study on the back cover of the Journal of the American Medical Association (JAMA) for the doctors to read and then prescribe Lipitor to their patients. (Pfizer depends on the doctors not reading the fine print in their ads carefully.)
Pfizer showed over a 3.3 year double-blinded, placebo controlled study that Lipitor® only prevented an adverse cardiac event in slightly more than 1% of patients. This is important: all the patients in the study were “high risk”, that is they had multiple risk factors for heart disease, such as high blood pressure, +family history, diabetes, obesity, etc. None of the statins have been shown to benefit patients who only have high cholesterol and no other heart disease risk factors. And remember, this study lasted only 3.3 years. Pfizer has no data that shows Lipitor still benefits patients beyond about 5 years. But when you are given a statin, implied if not actually spoken is the direction, “take this drug everyday for the rest of your life.”
At the bottom of the ad Pfizer admits that Lipitor did not prevent fatal heart attacks. Saving lives with statins is not something that Big Pharma can brag about. One final note: much is made of the strength of statins. Lipitor® was the strongest until Crestor® was developed. These brand name drugs are 7x as expensive as generic pravachol which does the same thing. A 3 month supply of Lipitor® is $336 and of Crestor® is $311. A 3 month supply of generic pravastatin is $50. Do the math. Whether the dose is 20 mg or 50 mg, the pill size is about the same and equally easy to swallow. Stronger is not better, but stronger may lead to more frequent side effects. If you are taking a brand name statin, “ask your doctor if pravachol is right for you”.
my LDL is 82, HDL 120 and that has been since first test that I took in the 80's when Cholesterol concerns began
I am 75 female other wise in good health should I be concerned.??
Kev--Thanks for your question. I will be writing on this topic very soon. It is not possible in a very brief response to fully address your question. Suffice it to say that plant stanols are great and Benecol spread or chews are the only available stanol.
Please explain what htn dyslipidemia is.
My Lp(a) level went from 21 to 51. Am now taking 1000mg. a day. All other bloodwork excellent. Am a Lifetime Weight Watcher.
Would greatly appreciate your comments.
Mary
I just got a call from my DR's nurse. My bloodwork showed my total cholesterol of 209, trygicerides 190, but my small ldl particle # is over 1400. They want to see me on Monday. How worried should I be and can I fix this. Thank you for whatever you can tell me.
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