LVESVLeft Ventricular End-Systolic Volume
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In addition, with the reversal of myocardial remodeling, with every 10% reduction in LVESV, the risk of VF was reduced by 21%, and the number of appropriate defibrillations significantly decreased.[5] Schaer et al .[19] and Van Boven et al .[20] showed that patients with cardiac function improvement of LVEF >35% had a significantly reduced number of ICDs.
In conclusion, HFD-induced IR induces cardiac morphological changes, with a higher ejection fraction, smaller LVESV, and thicker end-systolic wall thickness than the control group.
This study confirmed the efficacy of CRT in increasing EF of the left ventricle and decreasing both LVEDV and LVESV. These changes were even greater than reported in previous studies, since we enrolled only patients with substantial QRS prolongation, who obviously gain substantial benefit from CRT.
The LVEDV and LVESV increased and the LVEF decreased after the operation, which indicated cardiac dysfunction.
As shown in Table 1 and Figure 1, treatment with valsartan prevented ventricular dysfunction due to AAC, as evidenced by improvements in LVIDs, LVESV, LVEF, and LVFS (all P [less than or equal to] 0.001); no significant changes were observed in the ACC-surgery rats treated with valsartan relative to the sham-operated, vehicle-treated control animals (P > 0.05).
The objective of the analysis was to evaluate the efficacy of MPC-150-IM in patients with advanced heart failure, as defined by substantial baseline left ventricular (LV) contractile abnormality (LV end systolic volume, LVESV, greater than 100 ml).
* in contrast, no HF-MACE were seen over the entire 36 months in 150 million MPC-treated patients with baseline LVESV greater than 100 ml (p equals 0.0007 when analyzed by KaplanMeier time-to-first-event analysis and p is less than 0.0001 by incidence analysis for total/recurrent HF-MACE, 0 versus 11 events).
LVEF(%) = (LVEDV-LVESV)/LVEDV x 100 where LVEDV and LVESV are the LV end diastolic and end-systolic volumes.
The following parameters were below the level in the control group: left ventricle end-systolic volume (LVESV), left ventricle end-diastolic volume (LVEDV), stroke volume (SV), cardiac output (Q), stroke volume index (SVI), left ventricle end-diastolic volume/left ventricular myocardial mass (LVEDV/LVMM), stroke index (SI), left ventricle diastolic function--maximum later peak velocity (peak A) (LVDF-[V.sub.a]), maximum blood flow velocity--aortic valve ([V.sub.max]-AoV), gradient (difference) of blood pressure--mitral valve ([Pg.sub.max]-MV), gradient (difference) of blood pressure--aortic valve ([Pg.sub.max]--AoV), and gradient (difference) of blood pressure - pulmonary valve ([Pg.sub.max]-PuV).
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