CardioNerds Dan Ambinder, Dr. Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), and episode lead, Dr. Teodora Donisan (CardioNerds Academy fellow and incoming Chief fellow and Beaumont Health Internal Medicine resident) join Dr. Matthew Budoff (professor of medicine at David Geffen School of Medicine at UCLA and the Endowed Chair of Preventive Cardiology at Harbor-UCLA Medical Center) for a discussion about triglycerides from pathophysiology to clinical outcomes. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC).
Triglyceride (TG) metabolism can produce a by-product called remnant lipoproteins, which can be atherogenic. Most guidelines consider hypertriglyceridemia to start at values ≥ 150 mg/dl. It is the most common dyslipidemia, as it can occur in 30% of the general population. Although fasting levels are usually obtained per the current US protocol, there is evidence that non-fasting TG levels might be a better indicator of cardiovascular (CV) risk as these levels may better reflect the usual levels that the body is exposed to. There are multiple primary (genetic) causes of elevated TG, but these are rarer than lifestyle factors, medical conditions, or medications. Genetic association studies are helping better define the level of CV risk stemming from elevated TG-levels, which will impact how we target lifestyle and treatment interventions in the future.
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Relevant disclosures: Dr. Matthew Budoff has funding from General Electric.
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Pearls - Triglycerides - Pathophysiology to Clinical Outcomes
In the process of metabolizing TG, remnant lipoproteins are formed, which have been shown to promote atherogenesis. TG themselves have not been directly linked to this process and have not been studied in large population studies, and so are considered risk enhancing factors, and not risk factors per se. Elevated triglyceride levels measured on our traditional lipid panels act as a proxy for the Apo-B rich lipoproteins, such as VLDL, which directly cause atherogenesis.Hypertriglyceridemia is defined as TG values of ≥150 mg/dl, although there is emerging evidence that even high-normal values (100-140 mg/dl) can still be associated with increased CV risk. You can think of TG in a similar fashion to glucose values (patients with prediabetes are still at higher CV risk than those with normal glycemic level). These are continuous and not binary variables!Fasting lipid levels are not necessarily a better predictor of CV events than non-fasting lipid levels. A non-fasting TG level can potentially provide information on the body’s metabolism similarly to how we interpret glucose tolerance tests, although there isn’t such a standardized approach in the lipid world yet.Before testing for genetic causes, make sure you review secondary causes of elevated TG. Don’t forget to evaluate for lifestyle factors and medical causes (diabetes, alcohol abuse, hypothyroidism, pregnancy) and to review the medication list (pay attention to thiazides, non-selective beta blockers, antipsychotics and others).TG values of ≥ 175 mg/dl are considered a risk enhancing factor and can aid in the decision to be more aggressive with lifestyle changes or starting treatment.Although treatment will be reviewed in depth in future episodes, Dr. Budoff suggests we “back away from using fibrates for CV event protection.” Even though they are efficient at lowering TG levels,
