Key result
Coronary microembolization in swine models induced subtle cardiac systolic dysfunction and dyssynchrony, with Tcs-12SD prolonged from 85.00 ms to 151.30 ms at 1 week (p < 0.01).
Why the study?
Does coronary microembolization induce left ventricular contractile dysfunction or dyssynchrony in swine models?
Does coronary microembolization induce left ventricular contractile dysfunction or dyssynchrony in swine models?
Subtle cardiac systolic dysfunction and dyssynchrony caused by coronary microembolization can be sensitively detected using dipyridamole stress 2D-STI in a swine model.
Provides swine model for microembolization effects; leaves open human translation and clinical detection strategies.
To investigate whether subtle myocardial injury caused by coronary microembolization (CME) can induce left ventricular contractile dysfunction or dyssynchrony on swine models. CME swine models were constructed by the injection of 150,000 microspheres into the left coronary artery compared with the control group. The peak systolic values of longitudinal strain (LS), radial strain (RS), and circumferential strain (CS) by two-dimensional speckle tracking imaging (2D-STI) were measured under resting stage and dipyridamole stress prior to, 6 hours after, and 1 week after CME. The mean standard deviation of 12 segmental time-to-peak longitudinal strain (Tls-12SD), radial strain (Trs-12SD), and circumferential strain (Tcs-12SD) of the left ventricle were calculated as the dyssynchrony index. Postmortem analysis demonstrated 29.76% of the left ventricular segments manifested myocardial necrosis in MCE group compared with the control group (0%, p < 0.01). Left ventricular ejection fraction had no significant differences throughout the entire study (p > 0.05). In the CME group, compared with the baseline, LS on the basal anterior wall deteriorated from −9.72 ± 4.96 % to −6.35 ± 3.75 % (p < 0.05) and Tcs-12SD was prolonged from 85.00 ± 35.74 ms to 151.30 ± 75.14 ms at 1 week (p < 0.01) under resting stage. After dipyridamole infusing, a further decrease of contractility on all CME-related segments occurred at 6 hours and/or 1 week (p < 0.05–0.01). The deterioration of Tls-12SD achieved statistical significance at 1 week (157.66 ± 78.25 ms vs. 112.54 ± 62.52 ms, p < 0.05). Furthermore, Tcs-12SD was progressively delayed from 6 hours to 1 week (148.30 ± 45.53 ms and 162.45 ± 51.67 ms vs. 78.00 ± 40.17 ms, all p < 0.01). Subtle cardiac systolic dysfunction as well as dyssynchrony caused by CME can be detected using dipyridamole stress 2D-STI sensitively. Moreover, left ventricular dyssynchrony could be affected even by slight myocardial injury.
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Cheng et al. (2013) studied Coronary microembolization. Coronary microembolization vs. Control group was evaluated on Left ventricular contractile dysfunction and dyssynchrony. Coronary microembolization in swine models induced subtle cardiac systolic dysfunction and dyssynchrony, with Tcs-12SD prolonged from 85.00 ms to 151.30 ms at 1 week (p < 0.01).
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