Difference in left atrial appendage remodeling between diabetic and nondiabetic patients with atrial fibrillation

Abstract

BackgroundDiabetes mellitus (DM) is a common and increasingly prevalent condition in patients with atrial fibrillation (AFib). The left atrium appendage (LAA), a small outpouch from the LA, is the most common location for thrombus formation in patients with AFib.HypothesisIn this study, we examined LAA remodeling differences between diabetic and nondiabetic patients with AFib.MethodsThis retrospective study analyzed data from 242 subjects subdivided into two subgroups of 122 with DM (diabetic group) and 120 without DM (nondiabetic group). The study group underwent real‐time 3‐dimensional transesophageal echocardiography (RT3DTEE) for AFib ablation, cardioversion, or LAA device closure. The LAA dimensions were measured using the “Yosefy rotational 3DTEE method.”ResultsThe RT3DTEE analysis revealed that diabetic patients display larger LAA diameters, D1‐lengh (2.09 ± 0.50 vs 1.88 ± 0.54 cm, P = .003), D2‐width (1.70 ± 0.48 vs 1.55 ± 0.55 cm, P = .024), D3‐depth (2.21 ± 0.75 vs 1.99 ± 0.65 cm, P = .017), larger orifice areas (2.8 ± 1.35 and 2.3 ± 1.49 cm2, P = .004), and diminished orifice flow velocity (37.3 ± 17.6 and 43.7 ± 19.5 cm/sec, P = .008).ConclusionsAdverse LAA remodeling in DM patients with AFib is characterized by significantly LAA orifice enlargement and reduced orifice flow velocity. Analysis of LAA geometry and hemodynamics may have clinical implications in thrombotic risk assessment and treatment of DM patients with AFib.

Diabetes induces remodeling of the left atrial appendage independently of atrial fibrillation in a rodent model of type-2 diabetes

“…These findings suggest remodeling of the LAA in the diabetic animal but not in the other groups, that evolved in parallel to the development of diabetes. Our murine diabetic model thus successfully reproduced the LAA alterations described by Yosefy et al [ 10 ] in diabetic humans with atrial fibrillation. Since remodeling of the LAA occurred solely in the diabetic CDs/y-DD strain, it was unrelated to strain differences (as it did not appear in CDr/y-DD), to diet (as it did not appear in CDs/y-RD) nor to the presence of atrial fibrillation (as all our animals were in sinus rhythm throughout all stages of the study).…”

“…The phenotype of our model, the Cohen diabetic rat, has been extensively described [ 15 , 17 ]. One important difference between our model and the human subjects reported by Yosefy et al [ 10 ] is that all the animals in our study were in sinus rhythm, whereas the patients in Yosefy’s study were all in atrial fibrillation. This difference allowed us to differentiate between the role of diabetes mellitus and atrial fibrillation in LAA remodeling.…”

“…Our specific target was the LAA, which plays a major role in such events. We went from humans to the animal, seeking to reproduce in a murine model of diabetes mellitus the findings reported by Yosefy et al [ 10 ] in the heart of diabetic patients. We reasoned that such model would lend support to a cause-effect relationship between diabetes and remodeling of the heart in general, and of the LAA in particular.…”

“…Does diabetes by itself predispose to LAA remodeling, unrelated to atrial fibrillation? This question could not be answered in Yosefy’s study [ 10 ], as both diabetic and non-diabetic groups were in atrial fibrillation. Other studies focusing on the LAA have also been carried out primarily in patients with atrial fibrillation [ 14 ].…”

“…The high incidence of atrial fibrillation in diabetics appears to be a major inciting factor, and yet additional factors may be involved. Yosefy et al [ 10 ] recently studied a cohort of patients in atrial fibrillation and reported in diabetics, but not in non-diabetics, the occurrence of remodeling of the LAA, which increases the risk for clot formation and thromboembolism. Remodeling of the LAA has previously been attributed to atrial fibrillation [ 11 – 13 ].…”