Tag: lipid

  • Why ApoB Matters For Your Heart Health

    Why ApoB Matters For Your Heart Health

    If you care about your heart, then you’ve probably been told to keep an eye on your cholesterol. For decades, low-density lipoprotein cholesterol (LDL-C) has been the poster child for cardiovascular risk. The higher your LDL-C, the higher your risk of heart attack and stroke. So we measure it, we target it, and we try to lower it.

    However, it is little known that LDL-C is just a proxy. What actually damages arteries is not the cholesterol floating around your blood, but the particles that carry it. Each of those particles has, on it’s surface, a protein called apolipoprotein B (apoB). The more apoB particles you have, the more chances they have to burrow into your artery walls and trigger atherosclerosis.

    ApoB is, in effect, a headcount of all the atherogenic particles in your blood. For years, evidence has been mounting that it is a better marker of risk than LDL-C. In 2019, European guidelines even stated that apoB was more accurate, easier to measure, and more precise. And yet LDL-C still reigns supreme in clinical practice.

    Why isn’t ApoB used more in clinical practice?

    The reason Apob is not used more frequently in current clinical practice is partly inertia. It is also partly habit. And it is partly the argument that LDL-C and apoB are so highly correlated, it makes no practical difference. If you lower one, you lower the other. So many cardiologists and primary care doctors would argue, why bother changing the guidelines?

    A new UK Biobank study has put that argument to bed.

    What this new study found about ApoB

    Researchers followed nearly 300,000 healthy adults for 11 years. They looked at LDL-C, non-HDL cholesterol, triglycerides and apoB, and tracked how each one related to future heart attacks and strokes.

    Yes, LDL-C and apoB were highly correlated. But the correlation was not perfect. At any given LDL-C level, individual apoB levels varied widely. Two people could have the same LDL-C, but one might have far more apoB particles quietly driving up their cardiovascular risk.

    Across every LDL-C or non-HDL-C level, people with higher apoB levels had significantly more cardiovascular events. ApoB gave extra risk information that LDL-C or non-HDL-C simply missed.

    When the researchers ran adjusted statistical models, apoB consistently came out on top as the stronger predictor of risk. LDL-C added no meaningful information once apoB was taken into account.

    Triglycerides too? Same story. ApoB still won.

    Some guidelines only recommend testing apoB if your triglycerides are high. The idea is that apoB might only be useful in those cases, when cholesterol particles are small and harder to measure accurately using standard tests. But this study found no support for that.

    In fact, apoB was consistently useful regardless of triglyceride levels. Even when triglycerides were taken into account, apoB still gave meaningful extra information about risk. The reverse wasn’t true. Once you knew someone’s apoB, their triglyceride level didn’t add much.

    This suggests apoB is giving us more useful insight, across the board, not just in people with high triglycerides.

    Because in clinical practice, we are treating individual patients, not population averages. Knowing your apoB level helps tailor your treatment far more accurately. Without it, there is too much guesswork. Two patients with the same LDL-C could have very different numbers of atherogenic particles, and very different risk.

    We now have safe and powerful therapies, from statins to PCSK9 inhibitors. But they are costly and need to be used wisely. ApoB is the best tool we have to target those therapies to the right people.

    Why has ApoB not been widely adopted yet?

    One argument that is frequently given is cost. But measuring apoB is inexpensive. In the US, it would raise lipid testing costs by about 1 percent. And in reality, once apoB is used, there is little need to keep measuring LDL-C or non-HDL-C, so the total cost of care need not rise.

    Another barrier is familiarity. Doctors and labs are used to ordering LDL-C. Changing habits takes time. But with evidence like this, the argument for change is becoming hard to ignore.

    ApoB is the best available measure of atherosclerotic risk. LDL-C and non-HDL-C are imperfect stand-ins. If you want the most accurate picture of your cardiovascular risk, you should know your apoB.

    If you are already on treatment, it is the best way to know if your therapy is working. If you are not yet on treatment but considering it, it can help you and your doctor make a better-informed decision.

    If guidelines and clinical practice catch up to the evidence, we will prevent more heart attacks and strokes. And that, surely, is the whole point.

    British Association of Sports and Exercise Medicine  ·  European Atherosclerosis Society  · 
    Independent Doctors Federation

    As seen in The Independent, The Daily Mail and Tatler

    For educational purposes. This article is written by a practising GP and is intended to inform, not replace a consultation with your own doctor. It does not constitute medical advice. A note on clinical guidelines: Coyne Medical is an independent private clinic. Our approach is guided by the best available evidence, tailored to each individual. This may go beyond standard NHS or NICE guidance, which is designed for population-level care and weighted by resource constraints.

  • Lipoprotein(a) – the bad guy of lipids

    Lipoprotein(a) – the bad guy of lipids

    In a previous blog, I tried to explain how dyslipidaemia (abnormal levels of blood lipids) causes atherosclerosis (plaques forming in the arteries) using the analogy of a stag-do. In this blog, I’m going to stretch this analogy even further. 

    In the stag do analogy, low-density lipoprotein (LDL) particles are members of the stag do. This is because it is LDL that causes all the trouble in the wall of the artery. In the same way, stag-dos cause trouble in bars the world over. The way to think of lipoprotein(a) is as the really bad, malevolent guy on a stag do. The guy with an evil streak that everyone else is a little bit wary of. 

    Lipoprotein (a) is a type of LDL particle. It is made up of a glycoprotein (a sugar linked to a protein), an apolipoprotein B molecule that is linked to an apolipoprotein (a). 

    Lipoprotein (a) isn’t all bad. It does have an important role in acute inflammation and wound healing. In our stag-do analogy, our protagonist can be thought of as a guy who is edgy, who brings a sense of excitement, a certain frisson. But this guy is one of those people who are best in small doses. On a stag-do, this bad dude is the type of person who would buy the stag 8 shots of gin to render him comatose, cheat on his partner, start a fight in a bar and get everyone kicked out. In the body, lipoprotein (a) causes problems by:

    • Interfering with the breakdown of clots.
    • Interfering with the functioning of the lining of the artery. 
    • Increasing inflammation in the wall of the artery.
    • Accelerating the formation of foam cells which leads to atherosclerotic plaque formation. 

    The main determinant of our levels of lipoprotein (a) is our genes. Levels can be measured using a standard blood test. Unfortunately, Lp(a) is not routinely measured on standard blood tests. Generally, the levels of Lp(a) remain stable over time although they can be affected to some extent by reduced levels of oestrogen and due to inflammation. 

    High levels of Lp(a) are associated with increased risk of heart and vascular disease as well as narrowing of the aorta. People who have a condition known as Familial Hypercholesterolaemia have a higher likelihood of having high levels of Lp(a). In these people, high Lp(a) further increases their already high risk of developing cardiovascular disease. 

    The European Society of Cardiology recommends that everyone should have their levels of Lp(a) checked at least once in their lifetime. Certainly, the following groups of people should have their Lp(a) levels checked:

    • Those with premature cardiovascular disease. 
    • People with a family history of premature cardiovascular disease (<55 years of age in men and <65 years of age in women).
    • People with a family history of elevated Lp(a).
    • People with a history of Familial Hypercholesterolaemia. 
    • People with a history of recurrent cardiovascular disease despite optimum treatment. 

    In addition, Lp(a) measurement can be useful for people with borderline cardiovascular risk scores who doctors are considering treatment with a statin and in people whose LDL cholesterol has not lowered as expected despite statin treatment. 

    So what can be done with elevated levels of Lp(a)? Currently, there is only limited scientific evidence to suggest that lowering Lp(a) reduced the risk of heart and vascular disease. Therefore, our focus of treatment is to reduce other risk factors for heart disease as much as possible. This includes lowering the levels of LDL as much as possible, usually with one or more medications. These medications include statins and another cholesterol-lowering medication called ezetimibe. 

    For some people, it is not possible to achieve optimum levels of LDL even with a statin at the maximum tolerated dose and ezetimibe, another cholesterol-lowering drug. For these patients, a medication called a PCSK9 inhibitor is required. These medications have been shown to reduce Lp(a) in some people and reduce the risk of heart disease independent of levels of LDL.  

    Some doctors use Nicotinic acid to reduce Lp(a). This medication has side effects that make it difficult to tolerate. Medical studies have shown that it does reduce Lp(a). However, these studies have not demonstrated that Nicotinic acid reduces the risk of heart disease. Another treatment called apheresis can reduce levels of Lp(a) temporarily but it is not clear yet whether this reduces the risk of heart disease. 

    A new promising therapy for elevated Lp(a) is antisense therapy. This is a type of gene therapy that intercepts the message from the body’s genetic code to make one of the key components of Lp(a). Trials in this treatment are ongoing. 

    Although there is no really effective current treatment to lower Lp(a) it is still very worth having levels checked at some stage of your life. Knowing your Lp(a) means that if they are elevated you can take steps that significantly reduce your risk of heart disease. 

    British Association of Sports and Exercise Medicine  ·  European Atherosclerosis Society  · 
    Independent Doctors Federation

    As seen in The Independent, The Daily Mail and Tatler

    For educational purposes. This article is written by a practising GP and is intended to inform, not replace a consultation with your own doctor. It does not constitute medical advice. A note on clinical guidelines: Coyne Medical is an independent private clinic. Our approach is guided by the best available evidence, tailored to each individual. This may go beyond standard NHS or NICE guidance, which is designed for population-level care and weighted by resource constraints.