Exercise stress testing is preferred over pharmacological stress testing to evaluate myocardial ischemia as physiologic responses are preserved during exercise.1 Stress echocardiography and nuclear perfusion imaging share similar diagnostic sensitivity for coronary artery disease (CAD), but stress echocardiography carries a higher specificity.2, 3, 4 Normal responses to exercise include increase in left ventricular (LV) ejection fraction (LVEF), decrease in end-systolic volume, and moderate increase in systolic blood pressure. Left ventricular hypokinesis with increased ventricular volumes are abnormal responses and most commonly are indicative of significant CAD.1

“False-positive’ stress echocardiography has been reported in the absence of significant epicardial CAD on angiography and has been attributed to intermediate-grade CAD, abnormal motion due to wall tethering, and a hypertensive response during stress.5,6 An abnormal exercise stress echocardiogram (ESE) in the absence of significant CAD may also be attributed to coronary microvascular dysfunction (CMD).7 However, there are limited data describing markedly abnormal false-positive stress echocardiography tests.8,9 Previous studies defined such markedly abnormal false-positive stress echocardiogram (dobutamine or exercise) as an abnormal change in LV end-systolic volume and ≥5 abnormal segments at peak stress and included patients with normal peak stress LVEF and a hypertensive response to stress.

In patients who present with dyspnea on exertion with normal resting LVEF and without CAD, ESE allows evaluation of peak stress LVEF, which if abnormal, could provide an explanation for their symptoms. This phenomenon has not been comprehensively described, and the outcomes of these patients are unknown. The aim of this study was to clinically characterize patients without significant CAD who at baseline have preserved LVEF and during peak ESE develop transient systolic dysfunction (LVEF <50%).