This study tested the hypothesis that one mechanism of action of antifailure therapy (Rx) is to improve left ventricular (LV) function by decreasing aortic impedence (AI). Six paediatric patients (mean age 12.5y) with severe congestive failure (mean shortening fraction (SF) =.18) had 11 echocardiograms pre Rx (Gp1) and 18 post Digoxin, Lasix, and Captopril Rx(Gp2). A simplified method of obtaining AI was used. AI was calculated from the fundamental impedence, ie. of the 1st harmonic, from AI = pulse flow(PF)/pulse pressure (PP). An ascending aorta Doppler recording was performed, and PF was derived from peak velocity × aortic cross sectional area/BSA; PP = systolic-diastolic BP. Echo wall stress (σ) and shortening fraction(SF) were obtained. 22 normal children acted as controls (C) and compared to Gp1 and 2 by ANOVA and t-test. Table

Table 1
Full size table

AI for Gp2 vs C, p <.0001 and Gp1, p <.0003. SF for C vs Gp1 and 2, p<.0001 and 1 vs 2 NS. σ for C vs Gp1 and 2, p <.001 and 2 vs 1, p<.006. BP did not fall in Gp2 but clinical responders showed a fall in AI independent of a change in SF.

Thus, the decrease in AI with Rx indicates an important mechanism of action of these agents improving LV performance.