Lp(a) increases the risk of heart disease through several mechanisms. (File Photo)This 48-year-old man was a fitness fanatic, doing everything right. At 174 cm, he weighed 67 kg, was a swimmer and had a resting heart rate — the number of times your heart beats per minute (bpm) while at rest — of around 48. Which means his heart was not under extra stress and was functioning healthy. He didn’t smoke, ate mostly whole foods and had no apparent reason to worry. Till he voluntarily signed up for routine heart function tests. He cleared electrocardiogram (ECG), echocardiogram (Echo) and stress tests. But one test result looked problematic.His calcium score test, which is a non-invasive CT scan that measures the amount of calcified plaque in the heart’s arteries, showed a high count of 30 (1-10 being safe) indicating plaque deposition. A lipid profile test didn’t seem too worrying; his low-density lipoprotein (LDL) or bad cholesterol was below 60 mg/dL. To be doubly sure given his age, we did a lipoprotein(a) or Lp(a) test and found that to be high at 70 mg/dL (normal is less than 30 mg/dL). Problem is Lp(a) is the clingy, sticky component of cholesterol that claws on to artery walls, raising the risk of heart disease and stroke. People of Indian and South Asian descent have a higher prevalence of elevated Lp(a) compared to other ethnic groups, with approximately 25 per cent having elevated levels.What is Lp(a)?This is a cholesterol-carrying lipoprotein in your blood. Its levels are mostly inherited. Lp(a) has an additional protein attached to it known as apolipoprotein(a). This extra protein changes how the particle behaves in the body and makes it more harmful to the cardiovascular system than ordinary LDL. Unlike typical cholesterol, its levels are not easily changed by diet or exercise. So, a person can be physically fit, eat well and maintain excellent standard cholesterol numbers, yet still have a high Lp(a) level simply because of inherited DNA.How does Lp(a) damage the heart?Lp(a) increases the risk of heart disease through several mechanisms. First, like LDL, it carries cholesterol into the walls of arteries. Over time, this cholesterol accumulates and forms fatty deposits known as plaques. These narrow the arteries and restrict blood flow, raising the risk of chest pain, heart attacks and other cardiovascular problems.Second, the apolipoprotein(a) component makes Lp(a) unusually sticky and inflammatory. It promotes irritation within the lining of blood vessels and accelerates plaque growth. Plaques influenced by Lp(a) also tend to be more unstable, meaning they are more likely to rupture suddenly and trigger acute cardiac events.Third, Lp(a) interferes with the body’s natural system for dissolving blood clots. As a result, blood clots may form more easily and persist longer, increasing the risk of heart attack and stroke. These effects explain why Lp(a) can endanger even people who appear exceptionally healthy.Who should get tested for Lp(a)?The test requires a simple blood sample, and because levels remain fairly stable over time, repeated testing is usually unnecessary. It is affordable too. Testing is important if a person has a family history, heart disease despite normal cholesterol, has very high LDL cholesterol or suspected familial hypercholesterolemia and has recurrent heart events despite treatment.Story continues below this adCan normal cholesterol-lowering medications work for Lp(a)?Medications like statins are highly effective at lowering LDL cholesterol and remain one of the most important strategies for preventing heart attacks and strokes. However, research has shown that they may increase Lp(a) by about 10–20% on average. This increase does not cancel the heart-protective benefits of statins, so doctors generally do not stop statins solely because of a higher Lp(a). When Lp(a) levels are at 20, it doesn’t matter because they will go up to 25.But when Lp(a) is too high, it is like a matchbox, the gas or fuel being the LDL. So in such patients we push LDL levels further down to less than 30 mg/dL. Cardiologists may then give a low dose statin along with PCSK9 inhibitors, which are currently the most effective approved drugs for lowering Lp(a). These are injectables that lower LDL by up to 70% and reduce Lp(a) by roughly 20–30 per cent.An oral daily pill is being trialled currently to reduce Lp(a) and has been found to lower it by up to 65-85% in studies. It will be available in the end of 2026 or early 2027. Till then there must be aggressive management of other modifiable risks, including stricter LDL targets, blood pressure control, diabetes prevention, smoking avoidance and regular exercise.(Dr Shetty is lead cardiologist and medical director at Sparsh Hospital, Bengaluru) © The Indian Express Pvt LtdTags:cholesterol