Skip to main content
. Author manuscript; available in PMC: 2022 Mar 30.
Published in final edited form as: Circulation. 2021 Jan 21;143(13):1317–1330. doi: 10.1161/CIRCULATIONAHA.120.051517

Figure 1. Antagonism of 5-HT2B preserves cardiac structure and function following myocardial infarction (MI) and prevents deterioration of myocardial contractile capability.

Figure 1.

A, Experimental approach. 12-week-old mice were subjected to MI surgery and coincidentally treated with dimethyl sulfoxide (DMSO) control or the 5-HT2B antagonist, SB204741 (SB). Treatment was ceased three weeks following injury, and serial echocardiography was performed at times shown. B, Left ventricular ejection fraction (LV EF). C, Left ventricular fractional shortening (LV FS). D,E, Left ventricular internal dimension at end-diastole (LVID;d) and end-systole (LVID;s). F,G, Left ventricular volume at end-diastole (LV Vol;d) and end-systole (LV Vol;s). H, Vector diagram showing magnitude and direction of myocardial deformation in systole and quantified global longitudinal strain (GLS). B-H, Mean ± SEM, *P<0.05, **P<0.01, ***P<0.001 between DMSO and SB treatments, #P<0.05 between timepoints within treatment group following 2-way ANOVA and Holm-Sidak post hoc test. Number of mice denoted in B applies to subsequent groups except H where explicitly labeled.