Measure Of Left Ventricular Contractility Research Articles

Myocardial work as an independent predictor of postoperative NT-proBNP after transcatether aortic valve replacement

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): SUPPORTED BY THE ÚNKP-22-3-I NEW NATIONAL EXCELLENCE PROGRAM OF THE MINISTRY FOR CULTURE AND INNOVATION FROM THE SOURCE OF THE NATIONAL RESEARCH, DEVELOPMENT AND INNOVATION FUND. Introduction Aortic valve stenosis is one of the most prevalent valvular disease with significant clinical burden. Its treatment has been revolutionized by transcatether aortic valve replacement (TAVR). Left ventricular function is key element of preprocedural patient assessment, however, conventional echocardiographic parameters are substantially influenced by the increased afterload associated with the valvular disease. Myocardial work index is a novel echocardiographic parameter that quantifies myocardial deformation in the context of the concomitant left ventricular pressure, therefore, it may be a reliable measure of left ventricular contractility even with increased afterload. Purpose Our aim was to evaluate the left ventricular function of the TAVR patients using conventional echocardiographic parameters and myocardial work index, and examine their association with the clinical characteristics of the patients. Methods 84 TAVR candidates were enrolled (age 79±6 years; 48% female). Conventional and advanced echocardiographic measurements were performed prior to the procedure and at 12 months as a part of a follow-up visit. We measured ejection fraction (EF), and also global longitudinal strain (GLS) by speckle-tracking echocardiography, then using left ventricular volume curves estimated from systolic blood pressure and mean transaortic gradient, we quantified global myocardial work index (GWI). Detailed medical history, symptomatic status and as a marker of congestion, NT-proBNP levels were also obtained. Results EF did not change significantly (53±13 vs. 55±10 %; p = 0.172), while the absolute value of GLS increased substantially (−13.5±4.5 vs. −15.3±3.6 %; p<0.001). GWI significantly decreased (1914±787 vs. 1666±594 mmHg%; p = 0.001) compared to the preprocedural values (Figure 1). TAVR significantly reduced the NT-proBNP levels of the cohort (1057 [586–3037] vs. 627 pg/mL [376–1198]; p<0.001). Using multivariate regression analysis, examining relevant preprocedural clinical and echocardiographic parameters, the presence of atrial fibrillation (β=0.31; p<0.01), and the preprocedural GWI value (β=-0.32; p<0.01) proved to be significant independent predictors of postprocedural NT-proBNP (R²=0.30; p<0.001). Conclusions In our study population global longitudinal strain and myocardial work changed significantly after the procedure. The GWI value and the presence of atrial fibrillation proved to be independent predictors of NT-proBNP measured during the postprocedural follow-up. Accordingly, GWI may help in the improvement of patient selection and the estimation of the clinical prognosis in this complex population.

Indicators of haemodynamic instability and left ventricular function in a porcine model of esmolol induced negative inotropy

To investigate if the Hypotension Prediction Index was an early indicator of haemodynamic instability in a negative inotropy porcine model, and to assess the correlation of commonly measured indicators of left ventricular systolic function. Eight anaesthetised pigs were volume resuscitated and then underwent an incremental infusion of esmolol hydrochloride (0-3000 mg/hr), following which it was then reduced in a stepwise manner. Full haemodynamic measurements were taken at each stage and measurements of left ventricular systolic function including left ventricular stroke work index, ejection fraction and peripheral dP/dT were obtained. At an infusion rate of 500 mg/hr of esmolol there were no significant changes in any measured variables. At 1000 mg/hr MAP was on average 11 mmHg lower (95% CI 1 to 11 mmHg, p = 0.027) with a mean of 78 mmHg, HPI increased by 33 units (95% CI 4 to 62, p = 0.026) with a mean value of 63. No other parameters showed significant change from baseline values. Subsequent increases in esmolol showed changes in all parameters except SVV, SVR and PA mean. Correlation between dP/dt and LVSWI was 0.85 (95% CI 0.77 to 0.90, p < 0.001), between LVEF and dP/dt 0.39 (95% CI 0.18 to 0.57, p < 0.001), and between LSWI and LVEF 0.41 (95% CI 0.20 to 0.59, p < 0.001). In this model haemodynamic instability induced by negative inotropy was detected by the HPI algorithm prior to any clinically significant change in commonly measured variables. In addition, the peripheral measure of left ventricular contractility dP/dt correlates well with more established measurements of LV systolic function.

Left ventricular global longitudinal strain is superior to ejection fraction for prognostication in ebstein anomaly

Abstract Background Certain factors such as left ventricular (LV) geometry and loading conditions affect the validity and reliability of LV ejection fraction (LVEF) as a true measure of LV contractility. LV global longitudinal strain (LVGLS) is less sensitive to these factors, and it has superior prognostic performance in patients with acquired heart disease. The purpose of this study was to determine the clinical implications of using LVGLS (instead of LVEF) as the measure of LV systolic function in adults with Ebstein anomaly given the inherent abnormalities of LV geometry and preload in this population. Methods Retrospective cohort study of 673 adults with Ebstein anomaly (2003–2018). We hypothesized that LVGLS had a stronger correlation with heart failure indices and transplant-free survival compared to LVEF. Results Compared to LVEF, LVGLS had stronger correlations with cardiac index (r=0.46 vs r=0.21, p=0.007), glomerular filtration rate (r=0.57 vs r=0.19, p&amp;lt;0.001), and NT-proBNP (r=−0.64 vs r=−0.41, p=0.01). Of 673 patients, 514 (76%) had normal LV systolic function (LVGLSNormal-LVEFNormal), 87 (13%) had subclinical LV dysfunction (LVGLSLow-LVEFNormal) and 66 (10%) had overt LV dysfunction (LVGLSLow-LVEFLow). Compared to the overt LV dysfunction group, the subclinical LV dysfunction group had similar 10-year transplant-free survival (64% vs 63%, p=0.6), but were less likely to be on heart failure therapy (12% vs 82%, p&amp;lt;0.001). LVGLS (but not LVEF) was the independent predictor of transplant-free survival Conclusions LVGLS provided more robust risk stratification and prognostication than LVEF in patients with Ebstein anomaly, and patients with low LVGLS had reduced transplant-free survival regardless of LVEF. The use of LVGLS (rather than LVEF) as the measure of LV systolic function has important clinical implications with regards to initiation of medical and surgical therapies. Funding Acknowledgement Type of funding sources: None.

Post-exertional increase in first-phase ejection fraction in recreational marathon runners.

ObjectivesRunning a marathon has been equivocally associated with acute changes in cardiac performance. First-phase ejection fraction is a novel integrated echocardiographic measure of left ventricular contractility and systo-diastolic coupling which has never been studied in the context of physical activity. The aim of this study was to assess first-phase ejection fraction following recreational marathon running along with standard echocardiographic indices of systolic and diastolic function.Design and participants: Runners (n = 25, 17 males), age (mean ± standard deviation) 39 ± 9 years, were assessed before and immediately after a marathon race which was completed in 4 h, 10 min ± 47 min.Main outcome measuresCentral hemodynamics were estimated with applanation tonometry; cardiac performance was assessed using standard M-mode two-dimensional Doppler, tissue-doppler imaging and speckle-tracking echocardiography. First-phase ejection fraction was calculated as the percentage change in left ventricular volume from end-diastole to the time of peak aortic blood flow.ResultsConventional indices of systolic function and cardiac performance were similar pre- and post-race while aortic systolic blood pressure decreased by 9 ± 8 mmHg (P < 0.001) and first-phase ejection fraction increased by approximately 48% from 16.3 ± 3.9% to 22.9 ± 2.5% (P < 0.001). The ratio of left ventricular transmitral Doppler early velocity (E) to tissue-doppler imaging early annular velocity (e′) increased from 5.1 ± 1.8 to 6.2 ± 1.3 (P < 0.01).ConclusionIn recreational marathon runners, there is a marked increase in first-phase ejection fraction after the race despite no other significant change in cardiac performance or conventional measure of systolic function. More detailed physiological studies are required to elucidate the mechanism of this increase.

The reliability of cardiogenic impedance and correlation with echocardiographic and plethysmographic parameters for predicting CRT time intervals post implantation

Encouraging data have been reported on the use of cardiogenic impedance (CI) in cardiac resynchronization therapy (CRT) optimization. The purposes of this study were to: evaluate the stability of certain CI vectors 24 h postimplantation, study the correlation between these CI signals and selected echocardiographic parameters, and examine the possibility of non-invasive calibration of the patient-specific impedance-based prediction model. Thirteen patients received a CRT-defibrillator device with monitor capability of the dynamic impedance between several electrodes. At implantation, a patient-specific impedance-based prediction model was created for identification of optimal atrioventricular and interventricular (VV) delays and calibrated on invasive measurements of left ventricular contractility (LV dP/dtmax). Simultaneously, non-invasive measurements of LV dP/dtmax and stroke volume (SV) were obtained using a finger plethysmograph. Patients were re-evaluated with echocardiography and new CI measurements the day after implantation. The hemodynamic benefit achieved by optimal VV setting according to the patient-specific impedance-based prediction model at follow-up was not as large as the one obtained at implantation. In a multivariate partial least square regression analysis, a correlation was found between aortic velocity time integral (VTI) and a generic linear combination of CI features (P < 0,005). No correlation was found between the patient-specific impedance-based prediction models and the non-invasive measurements of LV dP/dtmax and SV. Cardiogenic impedance signals can be used to optimize CRT settings but seem less feasible as an ambulatory tool since calibration is required. The positive correlation between aortic VTI and CI measurements seems promising, although a larger cohort is required to create an echocardiography-based patient-specific model.

Altered ventriculo-arterial coupling during exercise in athletes releasing biomarkers after endurance running

Exercise can lead to release of biomarkers such as cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP), a poorly understood phenomenon proposed to especially occur with high-intensity exercise in less trained subjects. We hypothesised that haemodynamic perturbations during exercise are larger in athletes with cTnT release, and studied athletes with detectable cTnT levels after an endurance event (HIGH; n=16; 46±9years) against matched controls whose levels were undetectable (LOW; n=11; 44±7years). Echocardiography was performed at rest and at peak supine bicycle exercise stress. Left ventricular (LV) end-systolic elastance (E (LV) a load-independent measure of LV contractility), effective arterial elastance (E (A) a lumped index of arterial load) and end-systolic meridional wall stress were calculated from cardiac dimensions and brachial blood pressure. Efficiency of cardiac work was judged from the ventriculo-arterial coupling ratio (E (A)/E (LV): optimal range 0.5-1.0). While subgroups had similar values at rest, we found ventriculo-arterial mismatch during exercise in HIGH subjects [0.47 (0.39-0.58) vs. LOW: 0.73 (0.62-0.83); p<0.01] due to unopposed increase in E (LV) (p<0.05). In LOW subjects, a greater increase occurred in E (A) during exercise (+81±67% vs. HIGH: +39±32%; p=0.02) which contributed to a maintained coupling ratio. Subjects with higher baseline NT-proBNP had greater systolic wall stress during exercise (R (2)=0.39; p<0.01) despite no correlation at rest (p=ns). In conclusion, athletes with exercise-induced biomarker release exhibit ventriculo-arterial mismatch during exercise, suggesting non-optimal cardiac work may contribute to this phenomenon.

Comparison of Low-Energy Versus High-Energy Biphasic Defibrillation Shocks Following Prolonged Ventricular Fibrillation

Introduction. Since the initial development of the defibrillator, there has been concern that, while delivery of a large electric shock would stop fibrillation, it would also cause damage to the heart. This concern has been raised again with the development of the biphasic defibrillator. Objective. To compare defibrillation efficacy, postshock cardiac function, and troponin I levels following 150-J and 360-J shocks. Methods. Nineteen swine were anesthetized with isoflurane and instrumented with pressure catheters in the left ventricle, aorta, and right atrium. The animals were fibrillated for 6 minutes, followed by defibrillation with either low-energy (n = 8) or high-energy (n = 11) shocks. After defibrillation, chest compressions were initiated and continued until return of spontaneous circulation (ROSC). Epinephrine, 0.01 mg/kg every 3 minutes, was given for arterial blood pressure < 50 mmHg. Hemodynamic parameters were recorded for four hours. Transthoracic echocardiography was performed and troponin I levels were measured at baseline and four hours following ventricular fibrillation (VF). Results. Survival rates at four hours were not different between the two groups (low-energy, 5 of 8; high-energy, 7 of 11). Results for arterial blood pressure, positive dP/dt (first derivative of pressure measured over time, a measure of left ventricular contractility), and negative dP/dt at the time of lowest arterial blood pressure (ABP) following ROSC were not different between the two groups (p = not significant [NS]), but were lower than at baseline. All hemodynamic measures returned to baseline by four hours. Ejection fractions, stroke volumes, and cardiac outputs were not different between the two groups at four hours. Troponin I levels at four hours were not different between the two groups (12 ± 11 ng/mL versus 21 ± 26 ng/mL, p = NS) but were higher at four hours than at baseline (19 ± 19 ng/mL versus 0.8 ± 0.5 ng/mL, p < 0.05, groups combined). Conclusion. Biphasic 360-J shocks do not cause more cardiac damage than biphasic 150-J shocks in this animal model of prolonged VF and resuscitation.

Chronic intermittent hypoxia increases left ventricular contractility in C57BL/6J mice

Intermittent hypoxia (IH) commonly occurs in patients with obstructive sleep apnea and can cause a wide range of pathology, including reduced left ventricular (LV) ejection fraction in rats as determined by echocardiography, in rodent models. We utilized echocardiography and pressure-volume (PV) loop analyses to determine whether LV contractility was decreased in inbred C57BL/6J mice exposed to IH and whether blockade of beta-adrenergic receptors modified the response to hypoxia. Adult male 9- to 10-wk-old mice were exposed to 4 wk of IH (nadir inspired O(2) 5-6% at 60 cycles/h for 12 h during the light period) or intermittent air (IA) as control. A second group of animals were exposed to the same regimen of IH or IA, but in the presence of nonspecific beta-blockade with propranolol. Cardiac function was assessed by echocardiography and PV loop analyses, and mRNA and protein expression in ventricular homogenates was determined. Contrary to our expectations, we found with PV loop analyses that LV ejection fraction (63.4 +/- 3.5 vs. 50.5 +/- 2.6%, P = 0.015) and other measures of LV contractility were increased in IH-exposed animals compared with IA controls. There were no changes in contractile proteins, atrial natriuretic peptide levels, LV posterior wall thickness, or heart weight with IH exposure. However, cAMP levels were elevated after IH, and propranolol administration attenuated the increase in LV contractility induced by IH exposure. We conclude that, contrary to our hypothesis, 4 wk of IH exposure in C57BL/6J mice causes an increase in LV contractility that occurs independent of ventricular hypertrophy and is, in part, mediated by activation of cardiac beta-adrenergic pathways.

Abstract 718: Head-to-Head Comparison of Apical Rotation versus Mitral Annular Systolic Velocity for Estimation of Global Left Ventricular Contractility

We sought to test whether mitral annular systolic velocity by tissue Doppler (S′) and apical rotation by speckle tracking echocardiography (AR) can represent global left ventricular (LV) contractility. We measured AR and S′ in nine open chest anesthetized mongrel dogs under eight different inotropic stages before and after ligation of left anterior descending (LAD, n=6) or circumflex coronary artery (LCX, n=3). We measured LV pressure simultaneously with a high-fidelity pressure catheter and calculated LV ejection fraction (EF) with the biplane Simpson’s method. Maximal positive dP/dt (dP/dt max ) was used as the gold standard measurement of LV contractility. We compared AR and S′ and EF against dP/dt max by linear regression. Both S′ and AR showed dose-dependent increases and decreases following dobutamine and esmolol infusion, respectively. There was a stronger association between dP/dt max and AR (r=0.820, P &lt;0.001) and S′ (r=0.784, P &lt;0.001) than between dP/dt max and EF (r=0.567, P &lt;0.001), and this trend was more apparent with coronary ligation. There was also a good correlation between AR and S′ with (r=0.690, P &lt;0.001) and without (r=0.740, P &lt;0.001) coronary ligation. Both AR and S′ are effective noninvasive indices of global LV contractility irrespective of coronary ligation and have better accuracy than LV EF.

The Initial Tangent of the Aortic Pressure Increase is an Estimate of Left Ventricular Contractility in Pigs

The aim was, to identify an estimate of left ventricular contractility derived from the aortic pressure wave without load changing manoeuvres. For this purpose, left ventricular contractility was assessed with several aortic pressure wave form derived parameters and was compared to standard parameters of left ventricular contractility (conductance technique) in an experimental study. Measurements were taken during baseline, after beta-stimulation and after injection of a beta-antagonist. The initial and the secondary tangent, the area under the aortic pressure, and the stroke volume were correlated with the endsystolic elastance, a mainly load independent measure of left ventricular contractility: The initial tangent of the aortic pressure increase correlated significantly with the endsystolic elastance (r = 0.54, P < 0.05). The initial tangent of the aortic pressure increase was significantly increased from baseline at beta-stimulation (from 20.2 +/- 4.7 to 36.4 +/- 6.8 mmHg s(-1), P < 0.05) and decreased after injection of a beta-antagonist (from 20.2 +/- 4.7 to 12.3 +/- 2.0, P < 0.05). Thus, we conclude that the initial tangent of the aortic pressure increase is a valid estimate of left ventricular contractility in piglets.

Measuring Stress Velocity Index Using Mean Blood Pressure: Simple yet Accurate?

The stress velocity index, or the relationship of the rate-corrected mean velocity of circumferential shortening (VCFc) to the end systolic wall stress (ESWS), is a sensitive, load-independent measure of left ventricular contractility. ESWS is technically difficult to obtain and requires simultaneous blood pressure measurement, carotid artery tracing, and phonocardiogram. We report our comparison of two simpler methods of measuring ESWS and, therefore, stress velocity index. Patients with normal cardiac anatomy who had completed anthracycline chemotherapy were evaluated. ESWS as measured by the standard method using a carotid artery tracing (ESWScar) was compared to ESWS obtained using mean arterial pressure (ESWSmap) or systolic blood pressure (ESWSsbp). The cohort included 63 patients, with 37 (59%) males and a median age of 13.1 years. The mean (+/-SD) ESWScar was 53.3+/-15.3 g/cm(2) (range, 26.3-94 g/cm(2)); ESWSmap, 53 +/-13.4 g/cm(2) (range, 27.1-86.1 g/cm(2)); and ESWSsbp, 72.9 +/- 18.2 g/cm(2) (range, 40.8-117.2 g/cm(2)). ESWSmap and ESWSsbp closely correlated with ESWScar (coefficient correlation r = 0.88 and r = 0.87, respectively). Using ESWSmap, all patients were correctly classified as having normal or abnormal contractility as defined by stress velocity index, whereas ESWSsbp detected only two of the six patients with impaired contractility. We conclude that ESWSmap is a simple, highly sensitive and specific method for assessing left ventricular contractility. ESWSmap correlates closely with ESWScar and can be incorporated into the monitoring of cardiac dysfunction in the anthracycline-treated population. Further studies are needed to determine if this simplified measure accurately assesses the ESWS in other cardiac disease states.

Cardiac ICAM-1 mediates leukocyte-dependent decreased ventricular contractility in endotoxemic mice☆

Binding of ICAM-1 expressed on cardiomyocytes decreases cardiomyocyte contractility in vitro by altering the intracellular Ca2+ transient. We tested the hypothesis that signaling via ICAM-1 contributes to decreased left ventricular contractility in an in vivo model of systemic inflammation. C57B6 wild-type mice and ICAM-1 knock-out mice were treated with intraperitoneal lipopolysaccharide (LPS) then left ventricular contractility was measured 6 h later using a volume-conductance micromanometer catheter. We repeated this experiment in chimeric mice lacking ICAM-1 expression in bone marrow-derived cells (M-) and/or lacking ICAM-1 expression in the heart and other tissues (H-). In C57B6 wild-type mice LPS injection significantly increased cardiac ICAM-1 expression and decreased in vivo measures of left ventricular contractility (end-systolic elastance, Ees decreased 58 +/- 4%, p < 0.05, [dP/dtmax]/EDV decreased 60 +/- 6%, p < 0.05). Cyclophosphamide pretreatment to decrease leukocyte count prevented the LPS-induced decrease in contractility. In ICAM-1 knock-out mice LPS did not decrease any measure of contractility. LPS did not decrease left ventricular contractility in M+/H- mice but decreased contractility in M+/H+ and M-/H+ mice to the same extent as in C57B6 wild-type mice implicating the importance of cardiac ICAM-1. We conclude that signaling via cardiac ICAM-1 is necessary to mediate leukocyte-dependent decreases of left ventricular contractility in endotoxemic mice.

Echocardiographic ejection fraction in patients with acute heart failure: correlations with hemodynamic, clinical, and neurohormonal measures and short‐term outcome

Although echocardiographic ejection fraction (EF) is frequently used for the estimation of left ventricular contractility in patients with acute heart failure, its exact role and correlations with clinical, hemodynamic, and neurohormonal variables of cardiac contractility is not known. Patients (343) with acute heart failure, enrolled into two prospective placebo-controlled hemodynamic studies of tezosentan, and in whom EF was available at baseline, were included. Outcome was evaluated in a subset of 94 patients who were enrolled in the placebo arms of the studies. Higher echocardiographic EF was correlated with older age, increased incidence of hypertension and atrial fibrillation, and female gender. We observed weak correlation between EF and cardiac output or cardiac power and no correlation with wedge pressure, and the change in hemodynamic variables over time. Higher EF was correlated with more baseline leukocytosis and higher plasma levels of endothelin-1 and blood urea nitrogen, while lower EF was related to higher baseline B-type natriuretic peptide (BNP). We observed no overall correlations between EF and outcome. In patients with acute heart failure, echocardiographic EF is weakly correlated with hemodynamic measures of left ventricular contractility and outcome; hence, it should be interpreted cautiously when evaluating patients admitted due to acute heart failure.

Echocardiographic ejection fraction in patients with acute heart failure: weak correlations with cardiac contractility and short-term outcome

In patients admitted with acute heart failure median left ventricular EF is 40% and in small studies there was no change in EF during admission. Methods: The present study includes 349 patients enrolled into 2 prospective hemodynamic studies of patients with acute heart failure in whom EF was available at baseline. We examined the correlation between EF and clinical, hemodynamic and neurohormonal (BNP and endothelin-1) variables at baseline. The predictive value of EF on short-term outcome (recurrent worsening heart failure at 30 days and death at 6 months from recruitment) was evaluated in a subset of 94 patients enrolled in the placebo arms of the studies. Results: Higher echocardiographic EF was correlated with older age, increased incidence of hypertension and atrial fibrillation and female gender. We observed weak correlation between EF and cardiac output or cardiac power. There were no correlation between EF and wedge pressure, vascular resistance and the change in hemodynamic variables over time. Higher EF was correlated with more baseline leukocytosis, and higher plasma levels of endothelin-1 and blood urea nitrogen, while lower EF was related to lower baseline BNP. We observed no overall correlations between EF and outcome, however, patients with very low EF (<20%) had a higher incidence of worsening heart failure at 30 days. Conclusions: Echocardiographic EF is weakly correlated with hemodynamic measures of left ventricular contractility and short-term outcome in patients admitted with acute heart failure. It is possible that other factors such as renal failure (higher BUN), endothelial activation (higher endothelin-1) and inflammation (more leukocytosis) are important in the pathogenesis of acute heart failure with preserved EF.

Afterload corrected fractional area change (FaCac): A simple, relatively load independent measurement of left ventricular contractility in humans

Afterload corrected fractional area change (FACac) is a simple measurement of contractility which can be acquired during surgery without the need to acutely alter volume. We have validated it against the load-independent measurement, stroke force / end-diastolic area relationship (SF/EDA) in patients undergoing cardiac surgery. SF/EDA regressions were analysed before and after cardiopulmonary bypass in 39 patients and compared with simultaneously acquired FACac data. End-systolic and end-diastolic areas (ESA and EDA) were measured by transesophageal echocardiography and substituted for ventricular volumes. Pulmonary capillary wedge pressure was substituted for end-diastolic pressure and peak-systolic pressure for end-systolic pressure. Stroke force is the integral of the pressure-area loop and a square shape was assumed for calculation. FACac = FAC x log 10(SVRI) x 100%, where SVRI is calculated without multiplication by 80. Comparison of the methods was done by ordinary least products regression analysis where SF/EDA = a+b (FACac). a = 0.004 (95% CI -5.46 to 5.46). b = 0.857 (95% CI 0.777 to 0.936). Agreement between SF/EDA and FACac was identified by the absence of fixed bias. Both SF/EDA and FACac identified a reduction in contractility following cardiopulmonary bypass of similar magnitude suggesting load-independence of FACac. In contrast, the load-dependent indexes, cardiac index and FAC, increased in value but in the presence of reduced afterload. FACac may be used as a simplified index to reflect a relatively load-independent index of left ventricular contractility. Its simplicity offers promise of clinical utility.

Echocardiographic markers for mitral valve surgery to preserve left ventricular performance in mitral regurgitation

Background The timing of mitral valve (MV) surgery to preserve left ventricular (LV) contractility in patients with mitral regurgitation (MR) has been defined by complex cardiac catheterization techniques. Whether noninvasive methods can identify patients with MR, a normal LV ejection fraction, and early LV contractile impairment is unknown. We hypothesized that echocardiographic measures would separate patients with MR and a normal LV ejection fraction into those with and without contractile dysfunction and, thus, prospectively predict the response of LV size and performance to MV surgery. Methods and Results We studied 27 patients with micromanometer LV pressures and radionuclide angiography to obtain a determination of LV volumes and ejection fraction and calculate chamber elastance, a measure of LV contractility, before MV surgery. Echocardiographic studies were performed before MV surgery and repeated at 3 and 12 months after surgery. Age, New York Heart Association class, LV plus maximum pressure per unit change in time, LV systolic and end-diastolic pressures, and echocardiographic posterior wall thickness and radius to wall thickness ratio did not identify preoperative LV contractile dysfunction. However, other echocardiographic measures were related to LV contractility, including LV end-diastolic dimension (r = –0.50, P <.005), LV end-systolic dimension (r = –0.60, P <.0001), and LV fractional shortening (r = 0.50, P =.005). From analysis of receiver operator characteristic curves, an LV end-systolic dimension of ≥40 mm was identified as most predictive for separating patients with MR before surgery into those with and without LV contractile dysfunction (sensitivity of 82% and specificity of 100%). The patients with MR and impaired preoperative LV contractility showed a dramatic deterioration in LV fractional shortening at 3 months after MV surgery (P =.01), which recovered to within the normal range for fractional shortening at 12 months (P =.02) from a progressive reduction in LV end-systolic dimension. This response in LV size and performance temporally differed from that in the patients with MR and normal contractility (2-way analysis of variance P <.0001). However, at 12 months after MV surgery, LV end-diastolic dimension, end-systolic dimension, and fractional shortening were normal in both groups of patients with MR. Conclusion We conclude that echocardiographic measures, particularly an end-systolic dimension of ≥40 mm, may be useful for identifying patients with MR before surgery with early, occult LV contractile dysfunction in whom MV surgery may be recommended to preserve LV systolic performance. (Am Heart J 2000;140:476-82.)

Changes in left ventricular contractility with the phase of respiration

The end-systolic wall stress ( σ es)–velocity of circumferential fiber shortening ( V cfsc) relation was defined during the respiratory cycle, in order to obtain a totally noninvasive measure of left ventricular contractility. Eight young, healthy subjects were studied with echocardiography and calibrated carotid pulse tracings, while performing slow paced breathing. Left ventricular σ es vs. V cfsc relation was determined by fitting linear regression line to data points obtained at different times during the respiratory cycle. Data are given as mean±1SD. Left ventricular σ es and V cfsc exhibited small but significant changes during the respiratory cycle: σ es was highest in late inspiration (56.9±4.8 g/cm 2) and lowest in late expiration (49.2±3.7 g/cm 2); inversely, V cfsc was lowest during late inspiration (1.18±0.17 circ/s) and highest during late expiration (1.34±0.20 circ/s). The relation was significant in each subject ( r=−0.64±0.13) and remained inverse and significant, when it was determined separately for inspiration and expiration ( r=−0.61±0.17 and −0.68±0.12, respectively). At identical end-systolic wall stress, the velocity of shortening was greater during inspiration then expiration, suggesting that contractility was reduced during the expiratory phase. The reduced expiratory contractility might reflect increased vagal influence on the ventricular myocardium.

Normal High Energy Phosphate Ratios in “Stunned” Human Myocardium

Objectives. We sought to investigate whether alterations in cardiac high energy phosphates occur in postischemic “stunned” human myocardium.Background. Transient postischemic myocardial dysfunction is a common phenomenon that occurs in a variety of clinical settings in the absence of necrosis, and its pathogenesis is still unclear. Cardiac high energy phosphates are reduced during ischemia, and persistently altered myocardial high energy phosphate metabolism has been suggested as a mechanism contributing to stunning.Methods. We studied 29 patients with a first anterior myocardial infarction (MI) who underwent successful reperfusion within 6 h of the onset of chest pain. These patients underwent 31P magnetic resonance spectroscopy (MRS) a mean of 4 days after MI for measurement of left ventricular contractility and relative high energy phosphate metabolites. Twenty-one patients underwent a second 31P MRS study a mean of 39 days after MI. Eight volunteers served as control subjects.Results. Global and infarct area wall motion scores improved significantly between the early and late studies. No difference was found between early cardiac phosphocreatine (PCr)/beta-adenosine triphosphate (beta-ATP) ratios in patients and control subjects ([mean ± SD] 1.51 ± 0.17 vs. 1.61 ± 0.18, respectively, p = 0.17) or between early and late study results in patients (1.51 ± 0.17 vs. 1.53 ± 0.17, respectively, p = 0.6). For alpha of 0.05, the study had a 90% power to detect a 9% difference.Conclusions. The results of this study demonstrate normal myocardial PCr/ATP ratios in patients with myocardial stunning after reperfusion and suggest that relative cardiac high energy phosphates are not depleted in stunned human myocardium.

Elevated blood pressure and enhanced myocardial contractility in mice with severe IGF-1 deficiency.

To circumvent the embryonic lethality of a complete deficiency in insulin-like growth factor 1 (IGF-1), we generated mice homozygous for a site-specific insertional event that created a mutant IGF-1 allele (igf1m). These mice have IGF-1 levels 30% of wild type yet survive to adulthood, thereby allowing physiological analysis of the phenotype. Miniaturized catheterization technology revealed elevated conscious blood pressure in IGF-1(m/m) mice, and measurements of left ventricular contractility were increased. Adenylyl cyclase activity was enhanced in IGF-1(m/m) hearts, without an increase in beta-adrenergic receptor density, suggesting that crosstalk between IGF-1 and beta-adrenergic signaling pathways may mediate the increased contractility. The hypertrophic response of the left ventricular myocardium in response to aortic constriction, however, was preserved in IGF-1(m/m) mice. We conclude that chronic alterations in IGF-1 levels can selectively modulate blood pressure and left ventricular function, while not affecting adaptive myocardial hypertrophy in vivo.

Totally non-invasive pressure-area measurements of left ventricular contractility during non-invasive preload reduction in humans

Totally non-invasive pressure-area measurements of left ventricular contractility during non-invasive preload reduction in humans