BIRMINGHAM, UNITED KINGDOM. In January 2003 I hypothesized that high aldosterone levels could precipitate AF episodes. Please see the Conference Room Proceedings Session 2. I further elaborated on this hypothesis in the March 2003 issue of The AFIB Report. In November 2006 researchers at the Veterans Affairs Medical Center in Minneapolis reported on the case of a 58-yar-old man whose weekly afib episodes were clearly related to low serum levels of potassium (2.7 mEq/L – normal range is 3.5 to 5.5 mEq/L) associated with Conn's syndrome (primary hyperaldosteronism). At the time of hospitalization the patient's plasma renin activity (PRA) was 0.07 ng/mL/hr (normal range is 0.7 to 5.0 ng/mL/hr) and his plasma aldosterone (PA) level was 82.7 ng/dL (normal range is 4.0 to 31.0 ng/dL). He was discharged with a prescription for 25 mg/day of spironolactone (Aldactone) and 10 mEq/day (390 mg/day) of potassium chloride. At the time of writing the report the patient had been afib-free for a year.[1]

More recently (July 2009) Timothy Watson and colleagues at the Birmingham City Hospital reported on six cases in which a clear association between hyperaldosteronism (elevated levels of PA and reduced PRA) and lone atrial fibrillation was evident.

Case 1 – A 39-year-old man admitted to hospital with AF was found to have a serum potassium level of 3.3 mmol/L (3.3 mEq/L), a PRA of 0.16 nmol/L/hr, and a PA of 31 ng/dL (845 pmol/L). A CT scan revealed a 10 mm nodule on the right adrenal gland. It was removed resulting in normalization of potassium levels and no recurrence of afib. NOTE: This patient continued treatment for hypertension with 10 mg/day of lisinopril (Zestril).

Case 2 – A 33-year-old male presented with afib which converted spontaneously after 24 hours. His potassium level was 3.3 mmol/L, his PRA 0.7 nmol/L/hr, and his PA 79 ng/dL. A CT scan revealed a 16 mm nodule on the right adrenal gland. It was removed resulting in normalization of potassium levels and no further afib episodes. NOTE: This patient continued treatment with amlopidine (Norvasc) and losartan (Cozaar) for elevated blood pressure.

The Birmingham researchers report on four more cases where a clear association was found between lone AF (no underlying heart disease), low serum potassium levels and hyperaldosteronism. They point out that an elevated aldosterone level has been shown to induce cardiac fibrosis which in turn is a plausible mechanism to promote the development of AF, possibly by disruption of the normal intra-cardiac conduction system.

Watson, T, et al. Atrial fibrillation in primary aldosteronism. Journal of the Renin-Angiotensin-Aldosterone System, Vol. 10, No. 4, December 2009, pp. 190-94
[1] Aloul, BA, et al. Atrial fibrillation associated with hypokalemia due to primary hyperaldosteronism (Conn's syndrome). PACE, Vol. 29, November 2006, pp. 1303-05

Editor's comment: Although hyperaldosteronism is usually associated with high blood pressure (hypertension) there are cases where it is not and there are also many cases where elevated PA is not caused by a tumor on the adrenal gland (idiopathic hyperaldosteronism). I am one such case having undergone a CT scan and since no tumor was found and I do not have hypertension, I was diagnosed with idiopathic hyperaldosteronism. See Conference Room Proceedings Session 26. I would urge any afibber with hypertension or regularly spaced episodes to have their aldosterone and renin levels determined (blood test sitting upright). If they are abnormal then a CT scan should follow in order to rule out a tumor on the adrenal gland the removal of which may eliminate future afib episodes. Even if no tumor is found it may be possible to effectively manage hyperaldosteronism-related AF with eplerenone (Inspra) and/or ACE inhibitors such as lisinopril (Zestril).