Anyone who is familiar with the medical school process, understands that second year is an incredibly stressful time. Looking back, I can say without a doubt that my 2nd year of medical school was the toughest period in my life. Aside from the added stress of board exams looming over my head, life threw me several curve balls all at once. A tough break-up in September, my Mom’s unexpected Multiple Sclerosis diagnosis in October, and roommate conflicts leading to an early-termination of a lease and a move in November. So when my Dad called me with “some news” at the end of November, my first thought was “now what?”.
After going for a Heart Scan, a focused CT to assess for Coronary Artery Disease, my Dad scored in the 88th percentile; meaning he had more calcified atherosclerotic plaques than 88% of people the same age and gender as him. The scan also indicated he had 10 blockages in his coronary vessels, with 5 blockages in his Left Anterior Descending Artery (LAD). The LAD is the major blood supply to the interventricular septum which contains the conducting system that keeps the heart pumping. Because of the large area of heart dependent on the LAD, a blockage in this artery is often referred to as the “widow maker” due to the high rates of mortality.
The news shocked me. My dad is a healthy guy. He had none of the coronary disease risk factors; he has never smoked, he is not overweight, and rarely sways from his healthy diet. In addition to working around the house my dad hits the gym often and is in good shape. He had been on a statin for over 10 years and his cholesterol levels were well within the normal limits. So how could he possibly have 10- blockages in his heart?? His doctor thought the result was surprising and decided to order more tests to investigate. After a series of normal results, one thing stuck out: my dad has elevated lipoprotein (a). (typically referred to as “LP little a”)
Despite being in medical school, when my dad told me about his result my first thought was, “huh??”. I had finished my cardiology block, but for some reason lipoprotein (a) wasn’t ringing any bells. I decided to turn to the pathology bible of medical school, Robbins & Cotran and was shocked to find Lp(a) only got 1 sentence in the entire book:
“Lipoprotein a is an altered form of LDL that contains the apolipoprotein B-100 portion of LDL linked to apo A; Lp(a) levels are associated with coronary and cerebrovascular disease risk, independent of total cholesterol of LDL levels.”
Unsatisfied with the lack of information in my textbooks, I took to the internet to find out more. I stumbled across “The Lipoprotein A Foundation”. I discovered that Lp(a) is a mutated form of LDL that contains an additional protein called apolipoprotein a. The amount of Lp(a) has a strong genetic predisposition and levels are unaffected by diet and exercise. Because levels remain constant throughout one’s life, Lp(a) was not frequently measured. Recent epidemiologic evidence indicates that elevated Lp(a) levels are a strong predictor of coronary vascular disease. The Copenhagen City Heart Study identified a causal association between elevated Lp(a) and an increased risk of having a heart attack. Furthermore this study found people with an elevated Lp(a) have 2-4x greater risk of an early heart attack or cerebrovascular accident. In a study by McGill University Health Center, elevation of Lp(a) are responsible for 1 in 14 heart attacks and 1 in 7 cases of aortic valve disease. Studies have indicated that an elevated lipoprotein A level is an independent risk factor for cardiovascular events, which explains why someone like my dad, who has no coronary artery disease risk factors can be predisposed to forming atherosclerotic plaques. Furthermore Lp(a) is generally inherited and there is no known medication that can lower Lp(a).
So how does Lp(a) increase one’s risk for cardiovascular events? Lp(a), just like LDL (bad cholesterol) accumulate in arteries to form plaques. One study found that Lp(a) has a higher “atherogenic potential” than LDL and binds more firmly to arterial lumens. Both of these factors contribute to the formation of clots. Clot formation is the initial incident in myocardial infarctions (heart attacks) and cerebrovascular events (stroke).
Heart attacks occur when there is a lack of oxygen-rich blood flow to a section of heart muscle. This typically occurs in the setting of coronary heart disease (CHD), when a build up of plaque occurs inside of the artery, known as atherosclerosis. Plaques have a sticky surface, and if an area of the plaque ruptures it can cause a rapid formation of a blood clot at that site. This clot can block blood flow, resulting in cardiac muscle downstream to be deprived of oxygen. If this blockage isn’t reversed quickly the muscle will die. If a significant amount of the heart is oxygen deprived or if the conduction system of the heart is involved, a person may not survive the initial attack. If a patient survives, the dead heart tissue will form a scar. This scar tissue can result in abnormal heart rhythms (arrhythmias) or heart failure. Much like in the heart, a rupture of a plaque in the brain can result in a thrombus (clot) which deprives the affected part of the brain of oxygen and nutrients resulting in a stroke.
During further research of the Lipoprotein (a) foundation, I was utterly shocked to read survival stories about Lp(a) patients who had their first cardiovascular events as early as their 30s. These patients all seemed to be at the peak of health. I began to worry. I had been experiencing chest pains since starting medical school but I wrote it off to stress, anxiety, caffeine or a combination of all three. I decided to ask my family doctor to order me a cholesterol panel and a lipoprotein (a) level. She shrugged it off, saying I was suffering from “med student syndrome” but she finally relented after I told her about my dad. Despite fantastic cholesterol levels, I too had an elevated lipoprotein (a). My doctor was stunned, she had no idea what an elevated Lp(a) meant for a young healthy patient. She referred me to a cardiologist. After consulting a lipoprotein (a) specialist at the Cleveland Clinic I was started on a statin and an 81mg aspirin at the ripe old age of 24.
So the big question is, should you get tested for lipoprotein (a)? With 20% of the population having an elevated Lp(a) level, getting a lipid panel and testing for Lp(a) isn’t an outrageous request. But regardless of the result there are several ways to start living a heart-healthy life.
- Say no to tobacco: smokers are twice as likely to have a heart attack than nonsmokers. There are many resources out there for those looking to quit, here’s a good summary of the various options to kick the habit for good.
- Follow a heart healthy diet. The Mediterranean diet is consistently hailed as the best diet for your heart. The diet is primarily plant based, with the addition of fish and whole grains and healthy fats like olive oil and nuts. This diet also encourages drinking red wine in moderation, something I can definitely get on board with 🙂
- Exercise! The CDC recommends that everyone gets 150 minutes of moderate-intensity aerobic activity per week
- Maintain a healthy weight. Being at a healthy BMI also has the added benefit of decreasing high blood pressure and better management of diabetes for those affected by those conditions.
- Reduce stress: this is easier said than done as a medical student but there are various stress relief tips out there; meditate, breathe deeply, go to yoga, invest in aromatherapy, the options are endless.