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“We’re trying to bring that awareness to the public to get Congress to start taking action,” he said. “We have an understanding with the families — we ARE the families. We are the victims, the families of victims, and we are the comrades of those we’ve watched go from perfectly healthy to getting sick and dying.”
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).