Abstract 12727: Microvascular Coronary Dysfunction Affects Global Longitudinal Strain After Dipyridamole Stress Echocardiography

Abstract

Introduction: Coronary microvascular dysfunction (CMD) is a potential cause of myocardial ischemia and may affect myocardial function. CMD can be identified, in patients with non-obstructive coronary artery disease (CAD), by a reduced transthoracic Doppler-derived coronary flow reserve (CFR), which is an index of coronary arterial reactivity. Hypothesis: The aim of this study was to investigate the dipyridamole-induced changes of global longitudinal strain (GLS) in patients with CMD. Methods: fiftythree patients (35M, 18F; mean age 67±8 years) without obstructive CAD, assessed by invasive coronary angiogram, underwent dipyridamole stress echocardiography. CFR were determined as the ratio of hyperaemic to baseline diastolic coronary flow velocity. CMD was defined as CFR < 2. GLS was visualized as a bull’s-eye map in a quick and feasible manner. In each patient, we used a frame rate of 70 frames/sec for adequate 2D strain analysis. We analyzed GLS at each step of stress test and compared peak-dose values with baseline. Results: Sixteen patients (30%) among the overall population showed CMD. There were no significant differences in baseline characteristics between patients with or without CMD. GLS, at baseline, was significantly lower in patients with CMD (-16.7±3.77 vs. -17.9±3.75 - p<0.01). We observed a different response to dipyridamole stress echocardiography, between the two groups: GLS significantly increased up to peak dose in patients without CMD (from -17.9±3.75 to -19.5±4.12 - p<0.01), whereas on the other hand, a significant decrease from rest to peak dose was observed in patients with CMD (from -16.7±3.77 to -15.4±4.21- p<0.01). There was a significant inverse correlation between CFR and delta GLS measured at rest and after dipyridamole peak dose (r = -0.83 - p<0.01). Conclusions: GLS analysis, performed by comparing dipyridamole peak-dose with baseline values, shows that in patients with CMD there is a different response of left ventricular myocardiim to stress test. It could be assumed that the inverse correlation between CFR and delta GLS reflects a progressive subclinical worsening of left ventricular myocardial function in these patients. Larger studies could confirm our data.