As part of the BEAT-AFib study, participants undergo a blood draw during their in-person visits. We collect blood for both clinical and research laboratory measurements.
What are we looking for with the clinical laboratory measurements?
There are several risk factors for atrial fibrillation (AFib), including age (65 and older), high blood pressure, diabetes, obesity, and heart failure. To determine whether we can predict some of these risk factors, we collect several clinical labs including: a fasting lipid panel, hemoglobin A1c, and C-Reactive protein.
Fasting Lipid Panel
A fasting lipid panel involves a series of tests that measure your cholesterol levels and can be used to determine your risk of heart disease. With high cholesterol levels, plaque (fats) can build up in your blood vessels, which can make them more narrow over time and restrict blood flow to the heart.1 We also know that high cholesterol can also lead to inflammation in the blood vessel wall and in the heart itself.
Hemoglobin A1c measures your average blood sugar levels in the past 3 months and can be used to diagnose prediabetes/diabetes or to monitor blood sugar levels in those who are diabetic. In patients with diabetes, elevated blood sugar levels can lead to damage to blood vessels and nerves in the heart, increasing the risk of heart disease.2 While the relationship between diabetes and AFib is still being studied, diabetes is thought to be linked to changes in the structure and electrical activity of the heart as well as the autonomic nervous system, which controls heart rhythm. Diabetes and pre-diabetes are thought to be one of the causes of fibrosis (increased scar tissue) in the heart. These changes may play a role in AFib.3
The C-Reactive protein blood test is used as a measure of inflammation in the body. Inflammation is thought to be associated with changes in electrical activity of the heart and the structure of the atria (the top chambers of the heart), which can lead to the development or progression of AFib. Prior research has found that C-reactive protein levels are higher in those with AFib.4-5
What are we looking for with the research laboratory measurements?
In AFib, we know that in addition to the irregular heartbeat, there are some functional changes that occur in the atria. One such change is atrial fibrosis. Atrial fibrosis is the thickening or scarring of atrial tissue. Dr. Jeffrey Olgin’s (BEAT-AFib’s lead investigator) basic science lab has previously conducted studies in models of atrial fibrillation and has looked at cells that cause fibrosis (scarring) in the atria. These studies found a series of novel proteins that serve as unique markers of atrial fibrosis and atrial fibrillation. Building on this research, we plan to run large-scale protein analyses in the BEAT-AFib blood samples to identify these potential markers of atrial fibrosis early and before its progression. This will aid in our study’s goal of identifying patients who are at risk for developing AFib or progressing to experience more frequent episodes of AFib. In addition, we plan to use these blood samples for future genetic studies to determine if we can identify genes related to atrial fibrillation.
- High cholesterol: Causes, symptoms and how it affects the body. Cleveland Clinic. https://my.clevelandclinic.org/health/articles/11918-cholesterol-high-cholesterol-diseases. Accessed November 16, 2022.
- Diabetic heart disease. MedlinePlus. https://medlineplus.gov/diabeticheartdisease.html. Accessed November 17, 2022.
- Grisanti LA. Diabetes and Arrhythmias: Pathophysiology, Mechanisms and Therapeutic Outcomes. Front Physiol. 2018;9:1669. Published 2018 Nov 26. doi:10.3389/fphys.2018.01669
- Chung MK, Martin DO, Sprecher D, et al. C-reactive protein elevation in patients with atrial arrhythmias: inflammatory mechanisms and persistence of atrial fibrillation. Circulation. 2001;104(24):2886-2891. doi:10.1161/hc4901.101760
- Galea R, Cardillo MT, Caroli A, et al. Inflammation and C-reactive protein in atrial fibrillation: cause or effect?. Tex Heart Inst J. 2014;41(5):461-468. Published 2014 Oct 1. doi:10.14503/THIJ-13-3466