Left Ventricular Systolic Dysfunction Due to Atrial Fibrillation: Clinical and Echocardiographic Predictors

Abstract

Background: Diagnosis of AF-induced cardiomyopathy can be challenging and relies on ruling out other causes of cardiomyopathy and, after restoration of sinus rhythm, recovery of left ventricular (LV) function. The aim of this study was to identify clinical and echocardiographic predictors for developing cardiomyopathy with systolic dysfunction in patients with atrial tachyarrhythmia. Methods: This retrospective study was conducted in a large tertiary care centre and compared patients who experienced deterioration of LV ejection fraction (EF) during paroxysmal AF, demonstrated by precardioversion transoesophageal echocardiography with patients with preserved LV function during AF. All patients had documented preserved LVEF at baseline (EF >50%) while in sinus rhythm. Results: Of 482 patients included in the final analysis, 80 (17%) had reduced and 402 (83%) had preserved LV function during the precardioversion transoesophageal echocardiography. Patients with reduced LVEF were more likely to be men and to have a more rapid ventricular response during AF or atrial flutter (AFL). A history of prosthetic valves was also identified as a risk factor for reduced LVEF. Patients with reduced LVEF also had higher incidence of tricuspid regurgitation and right ventricular dysfunction. Conclusion: In ‘real-world’ experience, male patients with rapid ventricular response during paroxysmal AF or AFL are more prone to LVEF reduction. Patients with prosthetic valves are also at risk for LVEF reduction during AF/AFL. Finally, tricuspid regurgitation and right ventricular dysfunction may indicate relatively long-standing AF with an associated reduction in LVEF.

New-onset atrial fibrillation following arteriovenous fistula increases adverse clinical events in dialysis patients with end-stage renal disease

“…AF and heart failure are mutually causative, and atrial excitation during AF cannot be transmitted to the ventricle in a normal rhythm, resulting in abnormal ventricular filling and impaired diastolic function, ultimately leading to AF cardiomyopathy and inducing heart failure (19). When heart failure occurs, acute and chronic LA pressure increase, and increased atrial pressure and enlargement promote scar formation and fibrosis, ultimately leading to conduction abnormalities and inducing AF.…”