Atrial Fibrillation Friend or Foe?

Atrial fibrillation and atrial flutter are considered pathologic rhythms. These are arrhythmias characterized by abnormal electrical circuits propagating from the pulmonary veins and upper part of the heart called the atria causing it to fibrillate and flutter. These electrical signals travel to the lower part of the heart called the ventricles causing them to beat rapidly, inefficiently, and irregularly. Atrial fibrillation is a common arrhythmia and a major cause of medical morbidity, decreased quality of life, and stroke. There are few people that don’t have a friend, family member, or personal experience with atrial fibrillation. 

The observation that atrial fibrillation is so common, raises an interesting question. Could atrial fibrillation be a beneficial compensatory mechanism evolved by the heart to protect organs against the stress of acute high blood pressure and fluid overload?

First some background physiology:  

The kidneys release a substance called renin in response to stress, dehydration, low sodium, blood loss, and low blood pressure. Renin causes the secretion of angiotensin and aldosterone constricting blood vessels, elevating the blood pressure, and causing fluid and sodium retention. These compensations can be life-saving in times of extreme stress, but over-corrections can have adverse consequences. Congestive heart failure is an example of overcompensation of the renin-angiotensin system. This is why the treatment of congestive heart failure involves medications (ACE inhibitors, or angiotensin receptor blockers) that counteract the effects of renin and angiotensin.

Now consider the following observations:

1. Athletes with strong hearts and no pre-existing cardiac disease can experience atrial fibrillation. They typically convert back to sinus rhythm within a few days. In fact, the majority of younger patients with new-onset atrial fibrillation will convert back to sinus rhythm within a few days. This is especially true for those without pre-existing hypertension, coronary artery disease, or structural heart disease. (1)

2. Intense exercise can raise blood pressure by causing a spike in renin secretion from cells in the kidney. This in turn leads to fluid retention, sodium retention, and increases in blood pressure. In most cases, this is a normal adaptive response to physical stress. In some cases, there can be an overcorrection leading to a marked increase in sodium and fluid retention and blood pressure. Overcorrection can happen in patients who exercise too aggressively and in patients who have inherited slightly abnormal overactive genes that regulate the renin-angiotensin system.

3. Marked elevation in blood pressure and fluid retention can harm the body's organs.

How possibly could atrial fibrillation be beneficial?

1. Atrial fibrillation can rapidly lower blood pressure that otherwise might damage organs. The loss of the synchronized beating of the atrium with the ventricle and erratic tachycardia beating of the ventricle typically causes a reduction in blood pressure, and interestingly, increased blood flow to the coronary arteries. (2)

2. Atrial fibrillation induces the release of natriuretic peptides from the atria and atrial appendage. These include atrial natriuretic peptide (ANP) and other natriuretic peptides, BNP and CNP. (3,4,5,6) These substances cause water and sodium excretion by the kidneys and decrease sympathetic tone which induces relaxation of blood vessels and lowering blood pressure. Naturitetic peptides counter the renin-angiotensin system. This would be expected if atrial fibrillation evolved as a protective mechanism against an overstressed cardiovascular system

What implications could this have for the management of atrial fibrillation?

1. In young, healthy patients, atrial fibrillation could be considered a benign, physiologic rather than pathologic response to extreme cardiovascular stress. Avoidance of activities that promote atrial fibrillation would be an important part of treatment. This would include less strenuous exercise, not more, and avoiding excess salt and alcohol.

2. Could administering natriuretic factors convert atrial fibrillation back to normal heart rhythm?

3. Since atrial fibrillation is a mechanism that occurs in response to overcorrection of the renin-angiotensin system, long-term treatment with medications that inhibit the effects of renin and angiotensin may help prevent atrial fibrillation.(6)

To be clear, in most cases in the general population, atrial fibrillation has no benefits. Patients with chronic hypertension, valvular heart disease, coronary artery disease, etc, struggle with atrial fibrillation because what may be an adaptive, protective mechanism in the young and healthy, is now dysregulated and behaves aberrantly. 

References

1. 1. Mariani, et al. Incidence and Determinants of Spontaneous Cardioversion of Early Onset Symptomatic Atrial Fibrillation.  Medicina. 2022 Nov; 58(11): 1513.

1. 2.  Kochiadakis, et al. Effect of acute atrial fibrillation on phasic coronary blood flow pattern and flow reserve in humans. Eur Heart J. 2002 May;23(9):734-41. 

1. 3. Goetze, et al. Nat Rev Cardiol. Cardiac natriuretic peptides. 2020 Nov;17(11):698-717. 

1. 4. Wozakowska-Kaplon, et al. Int J Cardiol. Atrial natriuretic peptide level after cardioversion of chronic atrial fibrillation. 2002 May;83(2):159-65. 

1. 5.  Sramko, et al. Independent effect of atrial fibrillation on natriuretic peptide release. Clin Res Cardiol.  2019 Feb;108(2):142-149. 

1. 6. Zeng, et al. Level Of Natriuretic Peptide Determines Outcome In Atrial Fibrillation. J Atr Fibrillation. 2010 Jan-Feb; 2(4): 227.

1. 7. Marott, et al. Eur Heart J. Antihypertensive treatment and risk of atrial fibrillation: a nationwide study. 2014 May;35(18):1205-14.