Sometimes we tend to ignore a family history of cholesterol as a significant risk for heart attacks. So I had a 37-year-old health-conscious executive with a family history of heart disease come to me with furrowed brows. At the age of 35, concerned because of his family history, he underwent a detailed heart evaluation. This included a treadmill stress test and a coronary CT angiogram — a sophisticated scan that looks directly at the arteries of the heart and can detect both hardened plaque and the softer, earlier fatty deposits that can eventually lead to blockages. His arteries appeared clean. There was no visible plaque. No sign of coronary artery disease.
Despite clean reports, he stuck to discipline over the next two years. He remained physically active, walked between 7,000 and 10,000 steps daily, exercised regularly, maintained a healthy weight (his BMI was 24 or normal), did not smoke and generally ate well. Two years later, he had some chest discomfort. From zero, his plaque had crusted in two years although such a pileup is not seen before five years of an angiogram!
What repeat tests showed
Cautious about family history, he did the treadmill stress test, which showed changes that can sometimes suggest reduced blood flow to the heart. Yet he also performed exceptionally well on the test, lasting about 13 minutes and reaching a level of exertion that reflects very strong fitness. Because of this mixed picture, doctors proceeded to an angiogram, an invasive test in which dye is injected directly into the heart’s arteries to look for narrowing.
This test showed that one artery had a 60 percent narrowing and another had a smaller 30 percent narrowing. To determine whether the larger narrowing was seriously restricting blood flow, doctors performed an additional measurement. Think of it as checking water pressure across a partially narrowed pipe. The result showed blood was still flowing well enough and a stent was not needed.
Instead, treatment began with baby aspirin and rosuvastatin, a powerful cholesterol-lowering medication. Knowing him to be meticulous, I checked his clinical history. Although low density lipoprotein (LDL) or bad cholesterol should be less than 100 mg/dL in Indians, given their genetic risk of early heart attack, his LDL had consistently run on the higher side since his early 20s, ranging between 140 and 159 mg/dL. He told me that his doctors had since told him to keep his body weight and activity patterns constant and he had not bothered much, thinking these would keep his LDL in check. Except they didn’t.
How can arteries look completely clean at 35 and then show plaque at 37?
Plaque buildup is often far more complex and far less visible in its early stages than most people realise. Imagine rust slowly forming inside a pipe. For a long time, the inside may still look smooth enough that no scan can detect a problem. But beneath the surface, small changes are already taking place. Over time, enough material builds up so that it finally becomes visible.
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So, a “clean” heart scan means no plaque large enough to be seen at that moment. It does not always mean the underlying reason for plaque formation is absent. This is why a normal scan, while very reassuring, is not an absolute guarantee.
The biggest factor in this case is likely years of elevated cholesterol, which his clinical history showed was high from the 20s. If someone inherits a tendency to elevated LDL cholesterol from childhood or early adulthood, their arteries are essentially exposed to excess cholesterol for decades longer than average. This condition is called familial hypercholesterolemia, and it affects roughly one in 250 people, so it is not rare. If one parent carries a genetic tendency toward high cholesterol, there is roughly a 50% chance of it being passed down to a child.
If untreated, it can dramatically increase the risk of early coronary artery disease because LDL cholesterol is elevated from birth. A person with this condition may have no symptoms at all until plaque has already built up.
Many people inherit more subtle patterns, such as persistently above-average LDL, abnormal cholesterol particle types, elevated Lipoprotein(a), which is a type of lipid or fat in the body that is similar in structure to LDL and is more likely to stick to artery walls. These don’t always produce spectacular cholesterol numbers, but they can still substantially raise heart attack risk. Sometimes elevated triglycerides, another type of fat, may be a problem. When they stick around in the bloodstream for too long, fatty components invade the artery walls. And, like cholesterol, they can build up over time.
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When cholesterol enters the artery wall, the body reacts as though it is responding to an injury. That inflammatory response can accelerate plaque growth. Stress, poor sleep, certain medical conditions, and other hidden biological factors are other triggers.
Different types of cholesterol
Two people can have exactly the same cholesterol number on a blood test, but one may have particles that are far more likely to settle into the artery wall and trigger plaque formation. This is why some outwardly healthy, active people still develop heart disease relatively young.
Plaque growth is also rarely smooth and predictable. It can move in bursts. There may be years of very slow change followed by a period of faster progression. This can make it seem as though disease appeared suddenly, when in reality it had been quietly developing below the radar.
(Dr Shetty is lead cardiologist and medical director, Sparsh Hospital, Bengaluru)
