General anesthesia and positive pressure ventilation suppress left and right ventricular myocardial shortening in patients without myocardial disease - a strain echocardiography study.

BACKGROUND: Myocardial deformation imaging using speckle-tracking echocardiography to assess global longitudinal strain (GLS) is today considered a more sensitive measure of left ventricular (LV) systolic function than ejection fraction. General anesthesia and positive pressure ventilation (PPV) are known to change the right ventricular (RV) and LV loading conditions. However, little is known about the effects of anesthesia and PPV on RV free wall and LV GLS. We studied the influence of general anesthesia and PPV on RV and LV longitudinal strain in patients without myocardial disease. METHODS: Twenty-one patients scheduled for non-cardiac surgery were included. The baseline examination was performed on the un-premedicated patients within 60 min of anesthesia. The second examination was performed 10-15 min after induction of anesthesia (propofol, remifentanil), intubation and start of PPV. The examinations included apical four-, two- and three-chamber projections, mitral and aortic Doppler flow velocities and tissue Doppler velocities of tricuspid and mitral annulus. LV end-systolic elastance (Ees) and aortic elastance were determined (Ea). RESULTS: General anesthesia and PPV reduced the mean arterial blood pressure (- 29%, p <  0.0019), stroke volume index (- 13%, p <  0.001) and cardiac index (- 23%, p <  0.001). RV end-diastolic area index and LV end-diastolic volume index decreased significantly, while systemic vascular resistance was not significantly affected. Ees decreased significantly with the induction of anaesthesia (- 23%, p = 0.002), while there was a trend for a decrease in Ea (p = 0.053). The ventriculo-arterial coupling, Ea/Ees, was not significantly affected by the anesthetics and PPV. The LV GLS decreased from - 19.1 ± 2.3% to - 17.3 ± 2.9% (p <  0.001) and RV free wall strain decreased from - 26.5 ± 3.9% to - 24.1 ± 4.2% (p = 0.001). One patient (5%) had at baseline a LV GLS > - 16% compared with 6 patients (28%) during general anesthesia and PPV. Three patients (14%) had a RV free wall strain > - 24% compared to 8 patients (38%) during general anesthesia and PPV. CONCLUSIONS: General anesthesia and PPV reduces systolic LV and RV function to levels considered indicating dysfunction in a substantial proportion of patients without myocardial disease.

Noninvasive evaluation of left ventricular elastance according to pressure-volume curves modeling in arterial hypertension.

End-systolic left ventricular (LV) elastance (Ees) has been previously calculated and validated invasively using LV pressure-volume (P-V) loops. Noninvasive methods have been proposed, but clinical application remains complex. The aims of the present study were to 1) estimate Ees according to modeling of the LV P-V curve during ejection ("ejection P-V curve" method) and validate our method with existing published LV P-V loop data and 2) test the clinical applicability of noninvasively detecting a difference in Ees between normotensive and hypertensive subjects. On the basis of the ejection P-V curve and a linear relationship between elastance and time during ejection, we used a nonlinear least-squares method to fit the pressure waveform. We then computed the slope and intercept of time-varying elastance as well as the volume intercept (V0). As a validation, 22 P-V loops obtained from previous invasive studies were digitized and analyzed using the ejection P-V curve method. To test clinical applicability, ejection P-V curves were obtained from 33 hypertensive subjects and 32 normotensive subjects with carotid tonometry and real-time three-dimensional echocardiography during the same procedure. A good univariate relationship (r2 = 0.92, P < 0.005) and good limits of agreement were found between the invasive calculation of Ees and our new proposed ejection P-V curve method. In hypertensive patients, an increase in arterial elastance (Ea) was compensated by a parallel increase in Ees without change in Ea/Ees In addition, the clinical reproducibility of our method was similar to that of another noninvasive method. In conclusion, Ees and V0 can be estimated noninvasively from modeling of the P-V curve during ejection. This approach was found to be reproducible and sensitive enough to detect an expected increase in LV contractility in hypertensive patients. Because of its noninvasive nature, this methodology may have clinical implications in various disease states.NEW & NOTEWORTHY The use of real-time three-dimensional echocardiography-derived left ventricular volumes in conjunction with carotid tonometry was found to be reproducible and sensitive enough to detect expected differences in left ventricular elastance in arterial hypertension. Because of its noninvasive nature, this methodology may have clinical implications in various disease states.

Insights into cardiac alterations after pre-eclampsia: an echocardiographic study.

OBJECTIVES: To investigate cardiovascular (CV) performance status several years after early-onset (EO) or late-onset (LO) pre-eclampsia (PE), using echocardiography to assess myocardial strain and left ventricular (LV) torsional mechanics and ventricular-arterial coupling (VAC). METHODS: Thirty non-pregnant women with a previous singleton pregnancy complicated by EO-PE, 30 who had experienced LO-PE and 30 controls underwent echocardiography with two-dimensional (2D) speckle tracking between 6 months and 4 years after delivery and their findings were compared. All women were free from CV risk factors. VAC was defined as the ratio between aortic elastance (Ea) and LV end-systolic elastance (Ees). RESULTS: Women in the EO-PE group showed a persistent subclinical impairment in LV systole and a slight alteration in right ventricular function, with reductions in LV 2D strain (circumferential, radial and longitudinal) and right ventricular 2D strain and impairment of LV torsional mechanics, when compared both with women in the LO-PE group and with healthy controls. Although VAC was within the normal range in the whole study cohort, its individual components Ea and Ees were significantly altered more often in the EO-PE group than in both the LO-PE group and controls. All parameters investigated (except right ventricular 2D strain) were associated independently with gestational age at the time of diagnosis of PE. CONCLUSIONS: Women with a history of EO-PE are more likely to have subclinical impairment of systolic biventricular function than are those with a history of LO-PE and controls. The components of VAC (Ea and Ees) show subclinical alterations which are more significant in women with a history of EO-PE than in those with a history of LO-PE and controls, although VAC itself is maintained. Our study supports the use of closer CV monitoring in previously pre-eclamptic women, particularly those in whom PE was preterm. Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.

Cardiovascular hemodynamics in mice with tumor necrosis factor receptor-associated factor 2 mediated cytoprotection in the heart.

Introduction: Many studies in mice have demonstrated that cardiac-specific innate immune signaling pathways can be reprogrammed to modulate inflammation in response to myocardial injury and improve outcomes. While the echocardiography standard parameters of left ventricular (LV) ejection fraction, fractional shortening, end-diastolic diameter, and others are used to assess cardiac function, their dependency on loading conditions somewhat limits their utility in completely reflecting the contractile function and global cardiovascular efficiency of the heart. A true measure of global cardiovascular efficiency should include the interaction between the ventricle and the aorta (ventricular-vascular coupling, VVC) as well as measures of aortic impedance and pulse wave velocity. Methods: We measured cardiac Doppler velocities, blood pressures, along with VVC, aortic impedance, and pulse wave velocity to evaluate global cardiac function in a mouse model of cardiac-restricted low levels of TRAF2 overexpression that conferred cytoprotection in the heart. Results: While previous studies reported that response to myocardial infarction and reperfusion was improved in the TRAF2 overexpressed mice, we found that TRAF2 mice had significantly lower cardiac systolic velocities and accelerations, diastolic atrial velocity, aortic pressures, rate-pressure product, LV contractility and relaxation, and stroke work when compared to littermate control mice. Also, we found significantly longer aortic ejection time, isovolumic contraction and relaxation times, and significantly higher mitral early/atrial ratio, myocardial performance index, and ventricular vascular coupling in the TRAF2 overexpression mice compared to their littermate controls. We found no significant differences in the aortic impedance and pulse wave velocity. Discussion: While the reported tolerance to ischemic insults in TRAF2 overexpression mice may suggest enhanced cardiac reserve, our results indicate diminished cardiac function in these mice.

Overcoming the Limits of Ejection Fraction and Ventricular-Arterial Coupling in Heart Failure.

Left ventricular ejection fraction (LVEF) and ventricular-arterial coupling (VAC) [VAC = Ea/Ees; Ea: effective arterial elastance; Ees: left ventricle (LV) elastance] are both dimensionless ratios with important limitations, especially in heart failure setting. The LVEF to VAC relationship is a divergent non-linear function, having a point of intersection at the specific value of 0.62, where V0 = 0 ml (V0: the theoretical extrapolated value of the volume-axis intercept at end-systolic pressure 0 mmHg). For the dilated LV, both LVEF and VAC are highly dependent on V0 which is inconclusive when derived from single-beat Ees formulas. VAC simplification should be avoided. Revisiting the relationship between systolic time intervals (STI), pressure, and volumes could provide simple-to-use guiding formulas, affordable for daily clinical practice. We have analyzed by echocardiography the hemodynamics of 21 patients with severe symptomatic heart failure with reduced ejection (HFrEF) compared to 12 asymptomatic patients (at risk of heart failure with mild structural disease). The groups were unequivocally separated by 'classic' measures (LVEF, LV end-systolic volume (ESV), LV mass, STI). Chen's Ees formula was weakly correlated with LVEF and indexed ESV (ESVi) but better correlated to the pre-ejection period (PEP); PEP/total ejection time (PEP/TET); systolic blood pressure/PEP (SBP/PEP) (P < 0.001). Combining the predictability of the LVEF to the determinant role of SBP/PEP on the Ees variations, we obtained: (SBP*LVEF)/PEP mm Hg/ms, with an improved R 2 value (R 2 = 0.848; P < 0.001). The strongest correlations to VAC were for LVEF (R = -0.849; R 2 = 0.722) and PEP/TET (R = 0.925; R 2 = 0.857). By multiple regression, the VAC was strongly predicted (N = 33): (R = 0.975; R 2 = 0.95): VAC = 0.553-0.009*LVEF + 3.463*PEP/TET, and natural logarithm: Ln (VAC) = 0.147-1.4563*DBP/SBP*0.9-0.010*LVEF + 4.207*PEP/TET (R = 0.987; R 2 = 0.975; P = 0) demonstrating its exclusive determinants: LVEF, PEP/TET, and DBP/SBP. Considering Ea as a known value, the VAC-derived Ees formula: Ees_d ≈ Ea/(0.553-0.009*LVEF+3.463*PEP/TET) was strongly correlated to Chen's Ees formula (R = 0.973; R 2 = 0.947) being based on SBP, ESV, LVEF, and PEP/TET and no exponential power. Thus, the new index supports our hypothesis, in the limited sample of patients with HFrEF. Indices like SBP/PEP, (SBP*LVEF)/PEP, PEP/TET, and DBP/SBP deserve further experiments, underlining the major role of the forgotten STI.