Figure 3
Figure 3. Echocardiographic evaluation of cardiac anatomy and cardiac function in WT and PAI-1−/− mice. Representative M-mode images of the short-axis view of the 48-week WT (A) and PAI-1−/− (B) LVs. Substantial LV wall motion irregularities were found in 48-week-old PAI-1−/− mice, demonstrated by severe reductions and odd movements in both systolic and diastolic LV posterior and anterior wall movements. AW indicates anterior wall; and PW, posterior wall. The overall left ventricular function, measured by left ventricle ejection fraction (LVEF; C) and left ventricle fractioning shortening (LVFS; D), was diminished by a PAI-1 deficiency, especially after 36 weeks of age. The internal diameters of LV at diastole and systole were decreased in PAI-1−/− mice, especially after 36 weeks (E-F). The LV posterior wall diameter was increased in PAI-1−/− mice at both systole and diastole (G-H). n ≥ 6 for each age group; *P < .05.

Echocardiographic evaluation of cardiac anatomy and cardiac function in WT and PAI-1−/− mice. Representative M-mode images of the short-axis view of the 48-week WT (A) and PAI-1−/− (B) LVs. Substantial LV wall motion irregularities were found in 48-week-old PAI-1−/− mice, demonstrated by severe reductions and odd movements in both systolic and diastolic LV posterior and anterior wall movements. AW indicates anterior wall; and PW, posterior wall. The overall left ventricular function, measured by left ventricle ejection fraction (LVEF; C) and left ventricle fractioning shortening (LVFS; D), was diminished by a PAI-1 deficiency, especially after 36 weeks of age. The internal diameters of LV at diastole and systole were decreased in PAI-1−/− mice, especially after 36 weeks (E-F). The LV posterior wall diameter was increased in PAI-1−/− mice at both systole and diastole (G-H). n ≥ 6 for each age group; *P < .05.

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