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.