Introduction
Aortic regurgitation (AR) causes left ventricular (LV) volume and pressure overload. Initially, the left ventricle adapts to the volume overload with eccentric hypertrophy to preserve the LV ejection fraction (LVEF).1 2 However, progressive LV dilatation and pressure overload lead to myocardial damage and reduced ejection fraction (EF). Previous studies have reported that myocardial damage becomes irreversible even after aortic valve surgery, whereas some patients show significant improvement in LV function after surgery despite pre-operative LV dysfunction.3-5
The efficacy of aortic valve surgery in high-risk patients with severe AR and low LVEF is not well established. A recent study revealed that AVR was associated with lower mortality than medical therapy.6 This finding suggests that some of the pathophysiological changes in LVEF imposed by chronic severe AR are better tolerated than previously thought and that reverse remodeling can be achieved even in the late stages. Another study reported that post-operative and pre-operative reduced LVEF were associated with poor long-term outcomes.7 Therefore, there is a clinical need to predict LV reverse remodeling after aortic valve surgery.
Dobutamine stress echocardiography (DSE) is an established tool for detecting myocardial viability,8 and DSE has often been used to predict outcomes in various diseases.9-11 However, few reports have investigated the myocardial viability by DSE in patients with severe AR. Therefore, we performed low-dose DSE (LDSE) in patients with severe AR and reduced LVEF and examined the relationship with reverse remodeling after surgery.