Research Square
Impaired Myocardial Reserve Unmasked by High-frequency Speckle-Tracking Stress Echocardiography During Late Recovery From Experimental Kawasaki Disease
By Wang H, Zhou Y, Wang D and 1 others.
Abstract
Abstract Background Residual myocardial injury after Kawasaki disease (KD) may not be detected by resting left ventricular ejection fraction (LVEF). Whether stress deformation imaging unmasks impaired myocardial reserve linked to residual fibrosis remains uncertain. Methods Forty male C57BL/6 mice were assigned to independent rest and stress cohorts, each comprising control and Lactobacillus casei cell-wall extract (LCWE)-treated groups (n = 10 per group). Eight weeks after LCWE or vehicle administration, the rest cohort underwent high-frequency echocardiography followed by histology; the stress cohort underwent paired baseline and peak-dobutamine speckle-tracking echocardiography followed by histology. Contractile reserve was calculated as peak stress minus baseline. The primary functional endpoint was global longitudinal strain (GLS) reserve. Strain values are reported as absolute magnitudes. Myocardial collagen volume fraction (CVF) was quantified by Masson trichrome staining. Results In the stress cohort, LVEF reserve was preserved after LCWE exposure (control, 14.5 ± 2.8%; LCWE, 14.1 ± 2.8%; P = 0.764), whereas GLS reserve was lower (7.9 ± 1.6% vs 4.5 ± 1.3%; P < 0.001). Global circumferential strain reserve and longitudinal and circumferential strain-rate reserves did not differ between groups. CVF was higher after LCWE exposure in both cohorts (both P < 0.001). Within LCWE-exposed animals, GLS reserve correlated inversely with CVF (r = − 0.876; P = 0.001). In an exploratory analysis of the full stress cohort, GLS reserve remained associated with CVF after adjustment for resting GLS (B = − 0.717 per percentage point; 95% CI, − 1.005 to − 0.428; standardized β = −0.754; P < 0.001). Conclusions High-frequency speckle-tracking stress echocardiography is a feasible and sensitive approach for detecting myocardial contractile reserve dysfunction in KD mice during recovery phase.






