Abstract

Abstract Background Coronary microvascular dysfunction (CMD) is a potential cause of myocardial ischemia and may affect myocardial function at rest and during stress. 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, and can be impaired in both obstructive CAD and CMD. The aim of this study was to investigate the dipyridamole-induced changes of global longitudinal strain (GLS) in patients with CMD. Methods 43 patients (29M, 14F; mean age 68±7 years) without obstructive CAD, assessed by invasive coronary angiogram, underwent dipyridamole stress echocardiography. Coronary flow was assessed in the left anterior descending coronary artery (LAD) and was identified as the colour signal directed from the base to the apex of the left ventricle, containing the characteristic biphasic pulsed-Doppler flow signals. CFR were determined as the ratio of hyperaemic to baseline diastolic coronary flow velocity. CMD was defined as CFR <2. GLS was measured using automated function imaging, through the positioning of three endocardial markers (two markers at the mitral annulus and one at the apex) in each apical view. Subsequently, the obtained segmental values of GLS were visualized as a bull's-eye map in a quick and feasible manner. We had optimal left ventricular endocardial tracking in the overall population. 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 Thirteen 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 (−16.9±3.78 vs. −17.8±3.77 – 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 −17.8±3.77 to −19.3±4.09 – p<0.01), whereas on the other hand, a significant decrease from rest to peak dose was observed in patients with CMD (from −16.9±3.78 to −15.5±4.18 – p<0.01). There was a significant inverse correlation between CFR and delta GLS measured at rest and after dipyridamole peak dose (r=−0.82 – p<0.01). Conclusions GLS analysis, particularly 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. Funding Acknowledgement Type of funding source: None

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