Interactions Among Vitamin D, Atrial Fibrillation, and the Renin-Angiotensin-Aldosterone System

• Published in: The American journal of cardiology Vol. 122; no. 5; pp. 780 - 784
• Main Authors: Turin, Alexander, Bax, Jeroen J., Doukas, Demetrios, Joyce, Cara, Lopez, John J., Mathew, Verghese, Pontone, Gianluca, Shah, Falak, Singh, Sanjay, Wilber, David J., Rabbat, Mark G.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.09.2018; Elsevier Limited
• Subjects: 25-Hydroxyvitamin D; Aldosterone; Angiotensin; Angiotensin-converting enzyme inhibitors; Binomial distribution; Cardiac arrhythmia; Cardiovascular disease; Chromatography; Chronic obstructive pulmonary disease; Confidence intervals; Coronary vessels; Diabetes; Enzyme inhibitors; Fibrillation; Heart failure; Hypertension; Inhibition; Laboratory tests; Mass spectrometry; Medical records; Morbidity; Patients; Peptidyl-dipeptidase A; Ratios; Renin; Scientific imaging; Sleep apnea; Statistical analysis; Statistical models; Stroke; Vitamin D; Vitamin deficiency
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/j.amjcard.2018.05.013

Blockade of the renin-angiotensin-aldosterone system (RAAS) with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARB) has been shown to decrease incident atrial fibrillation (AF). Vitamin D deficiency has been implicated but associations between vitamin D and AF are inconsistent. However, vitamin D deficiency results in renin and angiotensin upregulation. This study seeks to determine the relation between vitamin D deficiency and incident AF and characterize this relation in the setting of RAAS inhibition. A total of 47,062 patients with 25-hydroxyvitamin D [25(OH)D] laboratory testing were retrospectively identified. Clinical information was extracted from the medical record. The primary outcome was incidence of AF. Given significant patient variation, propensity score matching was used to select comparable groups of those who initiated ACEI/ARB (“AI”) versus those who did not (“NAI”). Odds ratios (ORs) for incident AF associated with ACEI/ARB initiation and 25(OH)D level were estimated using generalized linear mixed models. AI patients had less incident AF than NAI patients (OR 0.36, 95% confidence interval [CI] 0.32 to 0.39) consistent with previous studies, but 25(OH)D deficiency was not associated with incident AF (OR 1.08, 95% CI 0.95 to 1.22). When stratified by 25(OH)D, there was a statistically significant decreased rate of AF in AI patients. Interestingly, this benefit was attenuated in 25(OH)D deficiency (deficient: OR 0.48, 95% CI 0.38 to 0.60 vs normal: OR 0.34, 95% CI 0.30 to 0.37). In conclusion, 25(OH)D deficiency was not associated with incident AF, and the benefit of ACE/ARB use was attenuated in 25(OH)D deficiency; this suggests that 25(OH)D may act as a cofactor in the mitigation of AF by RAAS inhibition.