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The indices of LV systolic function, i.e., stroke volume (SV), cardiac output (CO), and ejection fraction (EF), were decreased by 66%, 51% and 46% respectively, in WT.Tc (vs. WT) mice (Fig 7A–7C, all, p<0.01). The systolic dysfunction prolonged the pre-ejection isovolumic contraction time (IVCT, 74% increase, Fig 7D, p<0.05) and shortened the LV ejection time (LVET, Fig 7E, p<0.05) in chagasic mice. Further, 40–67% changes in the early (E) and late (A) diastolic filling velocities indicated diastolic dysfunction in chagasic WT mice (Fig 7F & 7G, all, p<0.05). Both systolic and diastolic dysfunction contribute to abnormality in myocardial relaxation that was presented by 50% increase in isovolumic relaxation time (IVRT, Fig 7H, p<0.05) in WT.Tc mice. In comparison to WT.Tc mice, PARP1+/-.Tc and PARP1-/-.Tc mice exhibited a partial-to-full control of systolic and diastolic dysfunction, and myocardial contraction and relaxation indices, the maximal benefits of PARP1 deletion being observed in PARP1-/- mice (Fig 7A–7H).


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