Figure 1. In vivo signs of hypertrophy... | Rockefeller University Press

Figure 1.

$In vivo signs of hypertrophy and diastolic heart failure in AOB. 16 wk following AOB (n = 8 hearts), signs of cardiac hypertrophy were evident from increases in the weights of the LV (A; P = 0.0006), right ventricle (B; P = 0.045), and atria (left and right auricles combined; C; P = 0.0009). Pulmonary congestion was evident from a trending increase in lung wet weight (D; P = 0.124). All weights were normalized to body weight and expressed as mg/gram. Diastolic LV dysfunction was evidenced by a pseudo-normalized E/A ration (E; P = 0.94) with an increase in the Doppler echocardiography E/E′ ratio (F; P = 0.014). In contrast, echocardiography-derived fractional shortening was not affected by AOB (G; P = 0.83). Sham-operated animals (n = 8 hearts) served as controls. Additional echocardiography data are presented in Fig. 2. Sham control, open bars; AOB, closed bars. *P = 0.05 by unpaired t test.$

In vivo signs of hypertrophy and diastolic heart failure in AOB. 16 wk following AOB (n = 8 hearts), signs of cardiac hypertrophy were evident from increases in the weights of the LV (A; P = 0.0006), right ventricle (B; P = 0.045), and atria (left and right auricles combined; C; P = 0.0009). Pulmonary congestion was evident from a trending increase in lung wet weight (D; P = 0.124). All weights were normalized to body weight and expressed as mg/gram. Diastolic LV dysfunction was evidenced by a pseudo-normalized E/A ration (E; P = 0.94) with an increase in the Doppler echocardiography E/E′ ratio (F; P = 0.014). In contrast, echocardiography-derived fractional shortening was not affected by AOB (G; P = 0.83). Sham-operated animals (n = 8 hearts) served as controls. Additional echocardiography data are presented in Fig. 2. Sham control, open bars; AOB, closed bars. *P = 0.05 by unpaired t test.

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