Background: Excessive fibrosis can alter the electrical conduction in the atrial tissue leading to atrial fibrillation (AFib). However, the underlying mechanisms driving atrial fibrosis and the development of AFib remain incompletely understood. We hypothesized that atrial fibrosis could result due to coronary microvascular vasodilator dysfunction.

Methods: Right human atrial appendages were collected during cardiac surgeries. Coronary arterioles (~100 µm) were dissected, cannulated, and pressurized (80 mmHg). Using video-microscopy, endothelium-dependent vasodilation was assessed by bradykinin (BK) and smooth muscle-dependent vasodilation was measured using sodium nitroprusside (SNP). Atrial tissue was then paraffin embedded and, via Masson’s Trichrome staining, the collagen content was quantified by ImageJ.

Results: When submitted to cumulative increases of bradykinin, AFib patients showed a significant reduced maximum vasodilation compared to the control patient with sinus rhythm (p=0.021), whereas no significant changes were recorded in SNP-induced vasodilator response. This decrease in BK-induced vasodilatory response was accompanied by a trend in increasing collagen content in the AFib patients, when compared to the control group (p=0.133).

Conclusion: The collected data shows that patients with AFib have an increased collagen content in association with impaired endothelium-dependent vasodilatory response. Together, these data show that coronary microvascular dysfunction is accompanied by increased fibrosis, which may lead to hypoxia and AFib.

Relevance for Patient Care: These data show a possible link between coronary microvascular dysfunction and Afib, which allows us to better understand AFib.

Strengths/limitations: Limitations of this study include small sample size (n=8). The strength of these data is that these are samples taken from patients.

Ethical Permissions: Ethical Approval was obtained for biological sample use.