Case Study

In 2009, a 34-year-old man, who had no prior cardiac issues, began training for a half-marathon. He had no history of heart disease, never smoked, and was not on any medications. However, he experienced jaw pain during his training, prompting him to seek medical evaluation, which included a stress test. Abnormal results from the treadmill test led to a coronary angiogram revealing a significant narrowing in his left main coronary artery (LMCA), the heart's largest artery. After consulting various specialists, he received a single coronary stent, which alleviated his jaw pain, and he has not required further invasive treatments or hospital stays since. Post-procedure, he continued on cholesterol-lowering medications along with aspirin.

When he visited my clinic in 2020, he presented laboratory results showing a dramatically elevated Lp(a) level of 431 nmol/L in 2014, where the normal range is below 75 nmol/L. In 2019, his lipid profile was as follows: total cholesterol 152 mg/dl, HDL 35, LDL 85, and triglycerides at 153. He had never been diagnosed with hypertension or diabetes. His ongoing regimen included rosuvastatin 20 mg, ezetimibe 10 mg, fenofibrate 140 mg, and daily doses of aspirin and clopidogrel since the stent placement.

A recent lab assessment in 2020 indicated an HgbA1C of 5.3%, normal thyroid and liver function, total cholesterol at 132 mg/dl, triglycerides at 185, HDL cholesterol at 42, apoB at 92, hs-CRP at 1.0, and a Lp(a) level of 539 nmol/L. Currently, he has transitioned from fenofibrate to a prescription omega-3, is slated for a stress echocardiogram, has embraced a whole-food plant-based diet, and has been referred to the HORIZON trial for an investigational drug aimed at reducing Lp(a).

Discussion

Identifying advanced coronary artery disease in someone in their mid-30s, particularly with a severe lesion in the LMCA, is quite rare. Fortunately, the stent he received has functioned well for ten years, even though it was a relatively new treatment at the time. Given his lack of smoking habits, diabetes, and hypertension, the abnormalities in his cholesterol levels likely contributed to his early CAD. Although his cholesterol profile indicated low HDL and mildly elevated triglycerides, the most alarming aspect was the significantly high Lp(a) level, one of the highest I have encountered.

Lp(a) is a complex cholesterol particle, and its concentration in the bloodstream is largely dictated by genetics. Comprising an LDL-cholesterol particle, a sulfur bridge, and apolipoprotein(a), Lp(a) levels typically plateau around the age of two and remain elevated throughout life in roughly 25% of the population. It stands as the most prevalent inherited risk factor for early cardiovascular disease. Numerous studies have highlighted the significance of elevated Lp(a) levels since they were first identified by Norwegian researchers in 1963. A report from the National Heart, Lung, and Blood Institute in 2018 estimated that 1.4 billion individuals worldwide have elevated Lp(a) levels.

Elevated Lp(a) can lead to various forms of coronary heart disease, including heart attacks, strokes, peripheral arterial disease, aortic valve disease, and heart failure. The risk associated with high Lp(a) levels is further exacerbated in individuals who smoke, have high blood pressure, or are diagnosed with type 2 diabetes.

One notable example is the INTERHEART study conducted in Canada in 2004, which found that individuals with elevated Lp(a) had a 1.5-fold increased risk of heart attacks compared to those with lower levels, even when other known risk factors were considered. An analysis of data from 1970 to 2009 revealed that individuals with Lp(a) levels in the highest third experienced heart disease rates 5.6 times greater than those in the lowest third. Additionally, a 2019 study indicated a direct correlation between high Lp(a) levels and increased cardiac event risks among heart disease patients, suggesting that measuring Lp(a) could help patients and healthcare providers assess cardiovascular risks more accurately.

Despite the widespread availability of Lp(a) testing, it is not yet a routine laboratory assessment in many U.S. clinics. In my preventive clinic, we have routinely tested Lp(a) levels for over a decade, encompassing thousands of patients. The European Society of Cardiology recommended testing Lp(a) levels at least once during a person's lifetime in 2019. Moreover, a clinical trial involving a novel injectable therapy is currently enrolling over 7,500 participants, with results expected in the next 4 to 5 years.

This compelling case study underscores the critical role Lp(a) plays in the onset of CAD, even in younger individuals. Establishing safe and effective strategies to lower Lp(a) is essential for reducing clinical events. Until such therapies are confirmed, measuring Lp(a) levels in patients with CAD and aortic valve disease is advisable. The recommendation to assess Lp(a) levels at least once in a lifetime will become increasingly urgent as definitive treatments become available. For more detailed information on Lp(a), please refer to my new book.

In the video titled "What Your Coronary Artery Calcium Score Means," viewers can learn about the significance of coronary artery calcium scoring in assessing heart health risks.

The video "Left Anterior Descending Coronary Artery Stenosis" provides insights into the implications of stenosis in one of the heart's critical arteries.