Effective Ejection Fraction Research Articles

The Partial Support of the Left Ventricular Assist Device Shifts the Systemic Cardiac Output Curve Upward in Proportion to the Effective Left Ventricular Ejection Fraction in Pressure-Volume Loop.

Left ventricular assist device (LVAD) has been saving many lives in patients with severe left ventricular (LV) failure. Recently, a minimally invasive transvascular LVAD such as Impella enables us to support unstable hemodynamics in severely ill patients. Although LVAD support increases total LV cardiac output (COTLV) at the expense of decreases in the native LV cardiac output (CONLV), the underlying mechanism determining COTLV remains unestablished. This study aims to clarify the mechanism and develop a framework to predict COTLV under known LVAD flow (COLVAD). We previously developed a generalized framework of circulatory equilibrium that consists of the integrated CO curve and the VR surface as common functions of right atrial pressure (PRA) and left atrial pressure (PLA). The intersection between the integrated CO curve and the VR surface defines circulatory equilibrium. Incorporating LVAD into this framework indicated that LVAD increases afterload, which in turn decreases CONLV. The total LV cardiac output (COTLV) under LVAD support becomes COTLV = CONLV+EFe · COLVAD, where EFe is effective ejection fraction, i.e., Ees/(Ees+Ea). Ees and Ea represent LV end-systolic elastance (Ees) and effective arterial elastance (Ea), respectively. In other words, LVAD shifts the total LV cardiac output curve upward by EFe · COLVAD. In contrast, LVAD does not change the VR surface or the right ventricular CO curve. In six anesthetized dogs, we created LV failure by the coronary ligation of the left anterior descending artery and inserted LVAD by withdrawing blood from LV and pumping out to the femoral artery. We determined the parameters of the CO curve with a volume-change technique. We then changed the COLVAD stepwise from 0 to 70–100 ml/kg/min and predicted hemodynamics by using the proposed circulatory equilibrium. Predicted COTLV, PRA, and PLA for each step correlated well with those measured (SEE; 2.8 ml/kg/min 0.17 mmHg, and 0.65 mmHg, respectively, r2; 0.993, 0.993, and 0.965, respectively). The proposed framework quantitatively predicted the upward-shift of the total CO curve resulting from the synergistic effect of LV systolic function and LVAD support. The proposed framework can contribute to the safe management of patients with LVAD.

Left heart chambers reverse remodeling after combined CABG and mitral repair

Results The mean effective ejection fraction increased from 18 ± 6% to 39 ± 13% (p << 0.05) at the follow-up. Left ventricular end-systolic volume index decreased from 44 ± 24 ml/m2 to 39 ± 26 ml/m2 (p = 0.002). Significant left ventricular reverse remodeling (≥ 15% reduction of LVESVI) was observed in 55 % of all survivors. Recurrent IMR was detected in only 2.8% (2/71) of the evaluated patients. Left atrial volume index decreased from 43 ± 15 ml/m2 to 36 ± 14 ml/m2 (p = 0.000003) and left atrial reverse remodeling was significant for 57 % of all survivors.

Effect of isolated cabg on mild-to-moderate ischemic mitral regurgitation and cardiac remodeling

Results At follow-up 56 % of all survivors showed improvement in IMR grade, 32 % presented with the unchanged valve function and in only 12 % IMR grade was more severe than preoperative. Preoperative effective ejection fraction increased from 26 ± 8% to 32 ± 14% (p = 0.002) at the follow-up. Left ventricular end-systolic volume index (LVESVI) decreased from 35 ± 16 ml/m2 to 30 ± 14 ml/m2 (p = 0.001). Significant left ventricular reverse remodeling (≥ 15% reduction of LVESVI) was observed in 45 % of all survivors. In 21 % of all survivors significant left atrial reverse remodeling was present although mean left atrial volume index did not change significantly. Conclusions Isolated surgical revascularization improves the valve function in ischemic mitral regurgitation. It also triggers significant left ventricular reverse remodeling in half of the patients. It remains unclear how the persisting or advancing remodeling process seen in the other half changes the prognosis of these individuals.

Abstract 8453: 2D Speckle Tracking Strain for Functional Characterization of Right Ventricular Wall Motion

Background: Left ventricular (LV) twist appears to play an important role in effective ejection fraction (EF). MRI based tagging methods are limited for tracking right ventricular (RV) free wall motion, especially for the normal thin free wall. We used a new motion analysis program based on tracking speckles in B-mode echo images to study RV motion. Methods: For our study, 6 small (2-3kg) piglets were intubated and anesthetized; median sternotomy was done to expose the heart. We used a 10MHz sector probe and a 13MHz linear probe to acquire 2D and tissue Doppler images of the RV from the surface of the heart, using liver as a standoff to improve extent and clarity of the RV free wall images. Short axis views were acquired on a GE Vivid 7 Dimension ultrasound system at frame rates &gt;100/sec. The study was conducted at 3 hemodynamic states of baseline and after 10% and 20% volume loading. Data was later analyzed offline in EchoPac using 2D speckle tracking. Results: There was a minimal component of rotation in the free wall of the RV (1°-2°) but more in the septum (5°-8°), which was similar to the rotation of the LV free wall for that level. Strain values were similar in both free wall and the RV side of the septum. With volume loading, there was an increase in the septum (mean 2° ± 1°) amplitude of twist and a decrease in time to peak twist, but the RV free wall showed no significant change. Conclusions: These findings are consistent with observations that the septum plays an important role in RV dynamic function.

Congestive heart failure: Systolic and diastolic function

There is increasing recognition that disorders of both left ventricular systolic and diastolic function can result in congestive heart failure. As such, consideration of both the filling and emptying characteristics of the left heart is needed to evaluate the hemodynamic abnormalities present in this syndrome. Consideration of the systolic (emptying) and diastolic (filling) pumping characteristics of the left heart also provides a conceptual basis to classify and understand the pathophysiology of congestive heart failure. In this context, systolic dysfunction can be defined as impaired emptying of the LV, apparent as a decreased (<50%) effective ejection fraction (forward stroke volume divided by end-diastolic volume). Systolic dysfunction may result from impaired myocardial contractile function, increased left ventricular afterload, and/or structural abnormalities of the left heart. Diastolic dysfunction can be defined as a condition in which filling of the LV sufficient to produce an adequate cardiac output requires an elevated pulmonary venous pressure. Thus, diastolic dysfunction is clinically manifested as pulmonary congestion. Defined in this manner, the most common cause of diastolic dysfunction is systolic dysfunction. In fact, the most common symptom of patients with systolic dysfunction is dyspnea from the resulting diastolic dysfunction. Diastolic dysfunction in the setting of normal systolic function may be due to obstruction of left ventricular filling, impaired left ventricular distensibility, or extensive external compression of the LV. Treatment of diastolic dysfunction can be accomplished by relieving myocardial ischemia, improving systolic function, lowering arterial systolic pressure, and decreasing cardiac distention.