Abstract
Abstract Funding Acknowledgements Type of funding sources: None. 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 left ventricular (LV) global longitudinal strain (GLS) in patients with CMD. METHODS. 59 patients (39% women, mean age 65.6 ± 6.1 years) with history of chest pain and without obstructive coronary artery disease (CAD) underwent dipyridamole stress echocardiography. Coronary flow was assessed in the left anterior descending coronary artery. Coronary flow reserve (CFR) was determined as the ratio of hyperaemic to baseline diastolic coronary flow velocity. CMD was defined as CFR < 2. GLS was measured at rest and at peak dose, 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. Nineteen patients (32%) among the overall population showed CMD. Baseline GLS was significantly lower in patients with CMD (-16.8 ± 2.7 vs. -19.1 ± 3.1, p < 0.01). A different contractile response to dipyridamole infusion was observed between the two groups: GLS significantly increased up to peak dose in patients without CMD (from -19.1 ± 3.1 to -20.2 ± 3.1, p < 0.01), and significantly decreased in patients with CMD (from -16.8 ± 2.7 to -15.8 ± 2.7, p < 0.01). There was a significant inverse correlation between CFR and DGLS (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 LV myocardium to stress test. It could be assumed that the inverse correlation between CFR and delta GLS reflects a progressive subclinical worsening of LV myocardial function and lack of LV contractile reserve due to underlying myocardial ischemia. Larger studies could confirm our data. Abstract Figure. Abstract Figure.
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