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Lp(a): The cardiovascular time bomb that evades traditional screening


I think most health-conscious people are aware that heart disease is the leading cause of death in this country and outpaces cancer even further when you add in strokes. But what too many people – and frankly, too many doctors – aren’t aware of is that it need not be this way.


Cancer can sneak up on you. Atherosclerosis, the progressive injury to the arterial walls that may lead to myocardial infarction or ischemic stroke, cannot. It is the snail of pathologies, usually requiring decades to develop before it reaches life-threatening proportions. Unfortunately, our standard lipid tests often miss the early signs of the disease process, and in particular, overlook one very nasty particle circulating in the blood called lipoprotein(a) or Lp(a), spoken shorthand, “LP little a.”.


In my judgment, elevated Lp(a) levels, which are associated with increased risk of stroke, aortic stenosis, and can triple the risk of myocardial infarctions, explain many of the heart attacks suffered by people, especially younger, middle-aged people, who don’t have the usual cardiac risk factors that we typically look for. The shocking, “out of left field” kind. To take one example, fitness expert and Biggest Loser host Bob Harper only discovered his high Lp(a) numbers after he endured the heart attack that almost killed him in 2017.


The estimated percentage of people with these elevated Lp(a)levels? About 20%. The percentage of people who get their levels tested? Fewer than 1%. Let me go on record: order up a Lp(a) test. It probably won’t be covered by insurance but shouldn’t cost much more than $50. If your doctor won’t cooperate, order up a new doctor.


So, stepping back a minute, how does atherosclerosis, the snail, manage, all too frequently, to slither through our standard tests for detecting elevated risk for heart attack? One reason is that the HDL/LDL ratio that doctors invest such trust in only gives an indication of how much cholesterol is circulating in the system, high-density (HDL) and low-density (LDL). But cholesterol itself isn’t the problem – after all, your liver makes most of your body’s supply of cholesterol and it’s an essential building block of cell membranes and hormones. The potential problem is what carries the cholesterol around the bloodstream and delivers it to the tissues that need it. They are “lipoproteins,” part lipid (fats, basically), part protein. The lipoproteins, these miniature cargo ships, are covered in large molecules. In the case of HDL, it’s the apoA protein, in the case of LDL, apoB. In simplest terms, apoA is “good,” allowing HDL to move inside and outside the artery wall. ApoB is, if not bad, at least problematic, prone to getting stuck inside the wall where its cargo of cholesterol and phospholipids can become oxidized, setting in motion the process that results in the creation of atherosclerotic plaques.

 

The apoB test your doctor should give you gives us an idea of how many of these apoB-tagged lipoprotein cargo ships are navigating your bloodstream – the more ships, the more potential for disaster. Which, finally, brings us back to Lp(a). This is a special type of LDL particle (which includes the apo-B protein), draped in loops of amino acids called “kringles” (named after a Danish pastry!). The kringles snag oxidized lipid molecules from the bloodstream and, when Lp(a) gets stuck inside the arterial wall, dumps it there. The toxic payload promotes inflammation and clot-formation, hastening the growth of plaque. It also contributes to stenosis in the aortic valve.

 

Deciding to get the Lp(a) test should be the easy part. Because the tests haven’t been standardized, interpreting the results can be somewhat more challenging. But here’s a cheat sheet: a desirable, optimal range, is less than 14 mg/dl (or <35 nmol/L) ; 14-30 mg/dl (or 35-75 nmol/L) is borderline; over 30 mg/dl( or >75 nmol/L) is high risk.  

 

If your numbers are higher than the optimal range, what to do then?  Lp(a) levels are mostly genetically determined and the same lifestyle upgrades that can effectively drive LDL down don’t have much effect here. There is a class of drugs, called PCSK9 inhibitors, that has been shown to push down Lp(a) but we’ve yet to see any evidence that it actually reduces heart attacks or strokes, the real-world measure of efficacy. A handful of drugs are currently in clinical trials so the therapeutic landscape may change over the next few years. But, for now, the best strategy is to do what we know works to reduce LDL, and hence overall cardiovascular disease risk, as much as possible: plenty of exercise, a sensible high-fiber, lower-carb diet, and when appropriate, first-line anti-cholesterol drugs like statins (e.g., Crestor and Lipitor) and/or a cholesterol absorption blocker like ezetimibe (Zetia). If you are intolerant of statins, then ask your doctor for one of the alternatives such as bempedoic acid or the PCSK9 inhibitors (e.g., Repatha).


How aggressive do we want to be to drive down cardiac risk when we find elevated Lp(a) levels? That depends on whether there’s any evidence that the atherosclerotic process has already begun, that we’re dealing with some measurable, visible amount of arterial plaque. To know that, I turn to advanced imaging tests like the coronary calcium scan and the CT angiogram. More on that in my next post.  

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