Short Circuits in the Heart: A Look at Atrial Fibrillation

Short Circuits in the Heart: A Look at Atrial Fibrillation

Last month my hot water went out so we called the plumber. They came by and plumbed (or whatever it is they do), but it didn’t fix the issue - except to drain my wallet of a paycheck or two. After some detective work, we discovered the real problem wasn’t the plumbing at all -  it was the electrical system. This can happen in the body, too. The heart is a big muscle that pumps blood throughout the body, but one of the most common heart problems happens in the heart’s electrical system!

Muscles are told to contract when they receive an electrical signal. In a healthy heart, electrical circuits coordinate the pumping action. However, atrial fibrillation disrupts these electrical signals, firing too early and too frequently. This causes abnormal, rapid, and chaotic beating of the upper chambers of the heart. These chambers aren’t the main drivers of the heart’s pumping action, but you can still land in hot water when they get out of rhythm. The major complication of atrial fibrillation is a five times increase in the chance of stroke. The lack of coordinated contractions causes blood to pool in the atria, and stagnant blood increases the risk of clot formation. The heart pumps less blood, which creates problems. 

Atrial fibrillation is the most common form of arrhythmia, affecting around six million Americans. There is around a one-in-four lifetime risk of developing atrial fibrillation after age 40. White Americans and males are at an increased risk, but the chance of developing atrial fibrillation really heats up with age. Cardiovascular problems, including high blood pressure and heart disease, increase the odds of developing atrial fibrillation. Other risk factors include smoking, nutrition imbalances, thyroid disease, immune system changes, and metabolic syndrome.

Normal symptoms of atrial fibrillation include a feeling of fluttering in the chest, shortness of breath, and fatigue. The symptoms may seem minor at first, but the progressive nature of the abnormal heart rhythm can make them really boil over. Doctors typically measure the progression of atrial fibrillation by how long each arrhythmia affects individuals.  It can start as paroxysmal fibrillation, lasting less than a week, progressing to long-standing persistent fibrillation lasting over a year, and eventually become chronic or permanent arrhythmia. In the early stages, veins near the atria - especially those coming from the lungs - may send accidental signals to the atria, causing them to start firing. These triggers can eventually cause changes to the electrical system, muscle function, and tissue changes in the heart. These electrical and tissue changes - which may include a scarring called fibrosis or an expansion of the atria called dilation - can eventually cause the wayward electrical signals to bounce around in the atria even without outside interference.

Doctors find it challenging to treat atrial fibrillation due to its varied causes. Different triggers affect different patients and even the same patient can have varying triggers at different times! Underlying problems like nutrition deficiencies and lifestyle changes are foundational. Treating conditions like high blood pressure, obesity, and sleep apnea are vital, but Dr. Sanghvi on the MedEvidence! Podcast states, “the biggest challenge is us being successful at it.” Beyond lifestyle changes, therapies need to be targeted to each patient. Doctors rely on monitoring to find a way to chill out a specific arrhythmia. For patients with a high risk of stroke, a doctor may prescribe anticoagulants, though these increase the chances of bleeding events. Other medications may be prescribed to manipulate the electrical signals. Some patients may benefit from device therapies, including destroying or isolating the electrical signal from a problematic trigger or implanting a small device to prevent stroke-causing blood clots. In the future, clinical trials may heat the way for better, more targeted therapies to help tank atrial fibrillation. Water you waiting for? Call your local research office to see what clinical trials you can participate in today!

 

 

Creative Director Benton Lowey-Ball, BS, BFA

 

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References:

 

Heijman, J., Voigt, N., Nattel, S., & Dobrev, D. (2014). Cellular and molecular electrophysiology of atrial fibrillation initiation, maintenance, and progression. Circulation research, 114(9), 1483-1499. https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.114.302226

Lip, G. Y., Fauchier, L., Freedman, S. B., Van Gelder, I., Natale, A., Gianni, C., ... & Lane, D. A. (2016). Atrial fibrillation (Primer). Nature Reviews: Disease Primers, 2(1). https://www.proquest.com/scholarly-journals/atrial-fibrillation-primer/docview/2711094799/se-2?accountid=14690

Lloyd-Jones, D. M., Wang, T. J., Leip, E. P., Larson, M. G., Levy, D., Vasan, R. S., ... & Benjamin, E. J. (2004). Lifetime risk for development of atrial fibrillation: the Framingham Heart Study. Circulation, 110(9), 1042-1046. https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000140263.20897.42

Munger, T.M., Wu, L.Q., Shen, W.K..(2013).  Atrial fibrillation. J Biomed Res.28(1):1-17. doi: 10.7555/JBR.28.20130191. https://pmc.ncbi.nlm.nih.gov/articles/PMC3904170/

Koren, M.J., & Sanghvi, N. (14 June, 2023). Two docs talk A-fib. On MedEvidence! Truth Behind the Data. [Podcast]. https://medevidence.com/two-docs-talk-a-fib-1

Wijesurendra, R. S., & Casadei, B. (2019). Mechanisms of atrial fibrillation. Heart, 105(24), 1860-1867. https://heart.bmj.com/content/105/24/1860.abstract

Yao, Y., Yang, M., Liu, D., & Zhao, Q. (2022). Immune remodeling and atrial fibrillation. Frontiers in Physiology, 13, 927221. https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2022.927221/full