Left Ventricular Isovolumic Contraction Research Articles

Usefulness of tissue Doppler-derived left ventricular isovolumic contraction velocity in patients with heart failure with preserved ejection fraction.

Heart failure with preserved ejection fraction (HFpEF) is a group of diseases classified by left ventricular (LV) EF, a measure of pump function. However, LVEF does not reflect LV contractility. Previous studies have shown that tissue Doppler-derived LV isovolumic contraction velocity (IVCv) correlates well with the LV peak dP/dt, an index of LV contractility. We explored whether LV IVCv is associated with 1-year post-discharge outcomes in HFpEF. We enrolled 113 patients (median age, 86 years, 45 male) with HFpEF (EF on admission ≥ 50%) who were admitted to our hospital for the treatment of acute HF. Clinical characteristics including echocardiographic data were obtained before discharge. IVCv was obtained from the tissue Doppler waveforms of both the septal and lateral mitral annulus of the apical 4-chamber view and averaged data were used. Primary outcomes were all-cause death or unplanned hospitalization due to HF within the first year. Among all patients, median LVEF was 61%, left atrial diameter was 47mm, E/e' was 17.5, and IVCv was 4.5cm/sec; mean tricuspid regurgitation velocity was 2.6m/sec. Regarding laboratory data, the median plasma B-type natriuretic peptide level was 185pg/mL. Thirty-four events occurred (15 deaths, 19 unplanned hospitalizations due to HF) within the first year. In multivariate Cox proportional hazards analyses, IVCv was significantly associated with outcomes (hazard ratio .68, 95% confidence interval .50-.89, p=.0095), independent of general characteristics, echocardiographic measures and pertinent laboratory parameters. LV IVCv was independently associated with 1-year outcomes in patients with HFpEF.

Ultrasound Multiparametric Assessment of the Impact of Hypertensive Disorders of Pregnancy on Fetal Cardiac Function and Growth and Development.

ObjectiveTo evaluate the ultrasound multiparametric assessment of the impact of hypertensive disorders of pregnancy (HDP) on fetal cardiac function and growth and development. Methods In this prospective study, 98 cases of HDP treated in our institution were recruited into a study group, and 100 pregnant women with healthy singleton pregnancies were included in a control group. All eligible patients were also assigned to either study group A (HDP fetuses with growth restriction) or study group B (HDP fetuses with normal growth). Fetal echocardiography was performed on all eligible participants to obtain hemodynamic and cardiac function parameters for the evaluation of fetal growth and development, and the impact of HDP on fetal heart function and growth and development was analyzed. Results HDP fetuses were associated with smaller head circumference, biparietal diameter, femoral length, and abdominal circumference versus healthy fetuses. The study group had a higher resistance index (RI) and pulsatility index (PI) of umbilical artery (UA), ductus venous (DV), pulmonary vein (PV), and lower RI and PI of aortic isthmus (AoI) than the control group. The study group showed higher left and right ventricular isovolumic contraction time (IVCT), isovolumic relaxation time (IVRT), and myocardial performance index (MPI) values and lower mitral and tricuspid E wave and E/A values than the control group. The systolic blood pressure was positively correlated with PI, RI of UA, DV, and PV, and left and right ventricular IVCT, IVRT, and MPI and negatively correlated with PI and RI of AoI and mitral and tricuspid E wave and E/A values of HDP fetuses. The peak systolic/diastolic flow rate (S/D), PI, and RI of umbilical blood flow in study group A were higher than those in study group B. Umbilical blood flow S/D showed the highest AUC and specificity for predicting fetal growth restriction, and PI had the highest sensitivity for predicting fetal growth restriction. Conclusion HDP compromises fetal cardiac function and growth, and ultrasound multiparametric assessment provides accurate detection of fetal cardiac function and hemodynamics changes. The patient's condition can be monitored through the assessment of ultrasound parameters of fetal growth and development.

Sympathetic Reinnervation After Heart Transplantation Assessed by Iodine-123 Metaiodobenzylguanidine (123I-MIBG) Imaging and Heart Rate Response to Exercise

<h3>Purpose</h3> The extent of sympathetic reinnervation of transplanted hearts varies among recipients. The purpose of this study is to investigate the relation between the functional response of the left ventricular (LV) myocardium to adrenergic stimulation and the findings of [¹²³I]metaiodobenzylguanidine (MIBG) scintigraphy in cardiac transplant recipients. <h3>Methods</h3> MIBG scintigraphy was performed in 20 heart transplant recipients (mean of 7.6 years after transplantation) and in 20 age-matched individuals with hemodynamically stable (NYHA functional class I) dilated cardiomyopathy (DCM). Heart rate and blood pressure as well as the ECG during exercise- or dobutamine-induced stress tests were measured in all patients. All patients also underwent endomyocardial biopsy, and some of the biopsy specimens were subjected to mRNA analysis. LV isovolumic contraction (<i>dP/dt</i>_max) and relaxation (tau) were measured simultaneously during stress tests in six transplant recipients and five patients with DCM. <h3>Results</h3> MIBG uptake was virtually undetectable in transplant recipients, with the exception of one individual who showed evidence of reinnervation in the anteroseptal region. The heart-to-mediastinum ratio was significantly smaller in transplant recipients than in patients with DCM (1.32 ± 0.6. vs. 2.22 ± 0.3, <i>p</i> < 0.0001). The change in <i>dP/dt</i>_max at peak heart rate during stress tests did not differ significantly between the two groups (83 ± 26 vs. 93 ± 20%, <i>p</i> = 0.335), whereas that in tau was smaller in transplant recipients than in DCM patients (31 ± 8 vs. 42 ± 9%, <i>p</i> < 0.05). RT-PCR analysis revealed that the amount of β-adrenergic receptor kinase-1 mRNA in the ventricular myocardium tended to be smaller in recipients who showed an attenuated response in stress tests than in those with a good response <h3>Conclusion</h3> LV contractility during adrenergic stimulation by dobutamine or exercise was preserved, whereas LV relaxation was attenuated, in transplant recipients. The discrepancy between the responses of LV myocardial contractility and relaxation to adrenergic stimulation and MIBG scintigraphic findings may provide insight into the reinnervation of transplanted hearts.

Concomitant systolic and diastolic alterations during chronic hypertension in pig

The mechanical and cellular relationships between systole and diastole during left ventricular (LV) dysfunction remain to be established. LV contraction-relaxation coupling was examined during LV hypertrophy induced by chronic hypertension. Chronically instrumented pigs received angiotensin II infusion for4weeks to induce chronic hypertension (133 ± 7 mmHg vs 98 ± 5 mmHg for mean arterial pressure at Day 28 vs 0, respectively) and LV hypertrophy. LV function was investigated with the instrumentation and echocardiography for LV twist-untwist assessment before and after dobutamine infusion. The cellular mechanisms were investigated by exploring the intracellular Ca2+ handling. At Day 28, pigs exhibited LV hypertrophy with LV diastolic dysfunction (impaired LV isovolumic relaxation, increased LV end-diastolic pressure, decreased and delayed LV untwisting rate) and LV systolic dysfunction (impaired LV isovolumic contraction and twist) although LV ejection fraction was preserved. Isolated cardiomyocytes exhibited altered shortening and lengthening. Interestingly, contraction-relaxation coupling remained preserved both in vivo and in vitro during LV hypertrophy. LV systolic and diastolic dysfunctions were associated to post-translational remodeling and dysfunction of the type 2 cardiac ryanodine receptor/Ca2+ release channel (RyR2), i.e., PKA hyperphosphorylation of RyR2, depletion of calstabin 2 (FKBP12.6), RyR2 leak and hypersensitivity of RyR2 to cytosolic Ca2+ during both contraction and relaxation phases. In conclusion, LV contraction-relaxation coupling remained preserved during chronic hypertension despite LV systolic and diastolic dysfunctions. This implies that LV diastolic dysfunction is accompanied by LV systolic dysfunction. At the cellular level, this is linked to sarcoplasmic reticulum Ca2+ leak through PKA-mediated RyR2 hyperphosphorylation and depletion of its stabilizing partner.

Left and Right Ventricular Systolic and Diastolic Functional Reserves Are Impaired in Anthracycline-Treated Long-Term Survivors of Childhood Cancers

The aim of this study was to test the hypothesis that left ventricular (LV) and right ventricular (RV) functional reserves are altered in anthracycline-treated long-term survivors of childhood cancers. One hundred three survivors (55% men) aged 25.0±5.8years at 15.2±5.8years after chemotherapy and 61 healthy control subjects (52% men) were studied. Tissue Doppler-derived mitral and tricuspid systolic (s) and early diastolic (e) velocities and LV myocardial acceleration during isovolumic contraction (IVA) were determined at rest and during bicycle exercise. The slope of the LV force-frequency relationship was derived from changes in IVA with heart rate during exercise (ΔIVA/Δ[heart rate]). LV and RV functional reserves were further assessed by the systolic functional reserve index (Δs×[1-1/s at baseline]) and diastolic functional reserve index (Δe×[1-1/e at baseline]). At baseline, mitral annular tissue Doppler indices were similar between survivors and control subjects (P>.05 for all), while tricuspid s and e velocities were significantly lower in survivors (P<.05 for both). The force-frequency relationship slope (P<.001), LV systolic functional reserve index (P<.001), and RV systolic functional reserve index (P=.001) were significantly lower in survivors than control subjects. For diastolic functional reserve, LV but not RV diastolic functional reserve index was significantly lower in survivors (P<.001). Multivariate analysis revealed survivor status (β=-0.39, P<.001) and baseline LV IVA (β=0.15, P<.044) as significant determinants of the LV force-frequency relationship. LV and RV functional reserves during exercise are impaired in anthracycline-treated long-term survivors of childhood cancer.

Erythropoietin alleviates post-resuscitation myocardial dysfunction in rats potentially through increasing the expression of angiotensin II receptor type 2 in myocardial tissues.

Activation of renin-angiotensin system (RAS) is one of the pathological mechanisms associated with myocardial ischemia-reperfusion injury following resuscitation. The present study aimed to determine whether erythropoietin (EPO) improves post-resuscitation myocardial dysfunction and how it affects the renin-angiotensin system. Sprague-Dawley rats were randomly divided into sham, vehicle, epinephrine (EP), EPO and EP + EPO groups. Excluding the sham group, all groups underwent cardiopulmonary resuscitation (CPR) 4 min after asphyxia-induced cardiac arrest (CA). EP and/or EPO was administrated by intravenous injection when CPR began. The results demonstrated that the vehicle group exhibited lower mean arterial pressure, left ventricular systolic pressure, maximal ascending rate of left ventricular pressure during left ventricular isovolumic contraction and maximal descending rate of left ventricular pressure during left ventricular isovolumic relaxation (+LVdP/dt max and -LVdP/dt max, respectively), and higher left ventricular end-diastolic pressure, compared with the sham group following return of spontaneous circulation (ROSC). Few significant differences were observed concerning the myocardial function between the vehicle and EP groups; however, compared with the vehicle group, EPO reversed myocardial function indices following ROSC, excluding-LVdP/dt max. Serum renin and angiotensin (Ang) II levels were measured by ELISA. The serum levels of renin and Ang II were significantly increased in the vehicle group compared with the sham group, which was also observed for the myocardial expression of renin and Ang II receptor type 1 (AT1R), as determined by reverse transcription-quantitative polymerase chain reaction and western blotting. EPO alone did not significantly reduce the high serum levels of renin and Ang II post-resuscitation, but changed the protein levels of renin and AT1R expression in myocardial tissues. However, EPO enhanced the myocardial expression of Ang II receptor type 2 (AT2R) following ROSC. In conclusion, the present study confirmed that CA resuscitation activated the renin-Ang II-AT1R signaling pathway, which may contribute to myocardial dysfunction in rats. The present study confirmed that EPO treatment is beneficial for protecting cardiac function post-resuscitation, and the roles of EPO in alleviating post-resuscitation myocardial dysfunction may potentially be associated with enhanced myocardial expression of AT2R.

Investigating fetal myocardial function in heart anomalies by Doppler myocardial performance indices.

Fetal myocardial performance index are used to assess aspects of systolic and diastolic function in developing fetal heart. The aim of this study was to determine normal values of fetal left ventricular (LV) Tei Index (TI) for measuring systolic performance and K-Index (KI) for diastolic performance in early (<;32 weeks), Mid (32-35 weeks) and late trimester (35-41 weeks) normal fetuses and fetuses with congenital heart diseases (CHD). Simultaneous recordings of Doppler Ultrasound Signal (DUS) of the LV outflow tracts and fetal electrocardiogram signals were obtained in 57 normal and 14 fetuses with CHD. CHDs were categorized in two types (conduction pathway abnormalities [8 cases] and structural anomalies [6 cases]). The LV isovolumic contraction time (ICT), isovolumic relaxation time (IRT), ventricular ejection time (VET) and ventricular filling time (VFT) were measured from amplitudes and peaks of high frequency component of DUS signals by an automated model. The TI and the new index were calculated by using the formula (ICT + IRT)/VET and (ICT + IRT)/VFT respectively. The TI did not show any significant change from CHD (conduction) to CHD (structural) fetuses (0.72± 0.09 vs 0.76±0.02; NS). On the other hand, KI showed significant decline in values (0.82±0.24 vs 0.49±0.34; p<;0.05) during normal development period and CHD with structural anomalies particularly. The correlation of KI with gestational ages was found to be negative and significant (r=- 0.29; p=0.025). Both TI and KI can be easily obtained in the fetus from DUS recording without the need for precise anatomic imaging. In conclusion, KI may be a useful tool to explore the healthy development of fetal myocardial function and identify fetuses with CHD (structural). More research is needed to check if KI could recognize the compromised fetuses from normal ones in future.

Assessing the development of fetal myocardial function by a novel Doppler myocardial performance index.

Doppler-derived myocardial performance index are used to assess aspects of systolic and diastolic function in adult as well as fetal heart. The Tei Index (TI) is a useful and non-invasive tool. The aim of this study was to determine normal values of fetal left ventricular (LV) TI in early (16-32 weeks) and late trimester (35-41 weeks) fetuses and to develop a new myocardial performance index (K-index; KI) which focuses on fetal diastolic interval when oxygenated blood from the placenta filled in the LV. Simultaneous recordings of Doppler Ultrasound Signal (DUS) of the LV outflow tracts and fetal electrocardiogram signals were obtained in 55 early- and late-trimester fetuses. The LV isovolumic contraction time (ICT), isovolumic relaxation time (IRT), ventricular ejection time (VET) and ventricular filling time (VFT) were measured from amplitudes and peaks of high frequency component of DUS signals by an automated model. The TI and the new index were calculated by using the formula (ICT + IRT)/VET and (ICT + IRT)/VFT respectively. The TI did not show any significant change from early-to late trimester fetuses (0.74± 0.057 vs 0.75±0.07; NS). On the other hand, KI showed significant decline in values (1.00±0.24 vs 0.87±0.23; p<;0.05) during this development period. The correlation of KI with gestational ages was found to be negative and significant (r=-0.35; p=0.007). No significant correlation of gestational ages with TI was found. Both TI and KI can be easily obtained in the fetus from DUS recording without the need for precise anatomic imaging. In conclusion, KI may be a useful tool to explore the healthy development of fetal myocardial function. More research is needed to check if KI could recognize the compromised fetuses from normal ones in future.

Exercise Echocardiography Demonstrates Biventricular Systolic Dysfunction and Reveals Decreased Left Ventricular Contractile Reserve in Children After Tetralogy of Fallot Repair

Long-term biventricular systolic performance is a key determinant of clinical outcomes late after tetralogy of Fallot (TOF) repair. A need exists for early indices of both left ventricular (LV) and right ventricular (RV) compromise in this population. Twenty-nine children (age range, 5-18 years) with repaired TOF and 44 healthy controls were prospectively evaluated. M-mode and tissue Doppler data were obtained for each ventricle and the RV outflow tract at rest and during semisupine bicycle exercise. By making measurements of myocardial acceleration during isovolumic contraction during exercise, at increasing heart rates, LV force-frequency curves were constructed. Patients also underwent cardiac magnetic resonance imaging, cardiopulmonary exercise testing, and measurement of serum neurohormonal markers. Children with repaired TOF had dilated right ventricles (RV end-diastolic volume index = 153 ± 37.3 mL/m(2)) but normal ejection fractions as measured on magnetic resonance imaging (LV ejection fraction = 59.3 ± 6.2%, RV ejection fraction = 50.2 ± 8.5%) and normal serum neurohormonal markers. Detailed resting echocardiography detected abnormal ventricular function, worst in the right ventricle and RV outflow tract. Exercise exacerbated these findings and provoked significant decline in LV indices. The LV force-frequency curves of patients were attenuated, with an early plateau and inadequate increase of isovolumic contraction. Correlations were seen between peak exercise LV isovolumic contraction and percentage predicted peak oxygen uptake (r = 0.51, P = .02), LV and RV ejection fractions (r = 0.41, P = .03), and RV and LV long-axis fractional shortening (r = 0.44, P = .02). The postsurgical pathophysiology of TOF begins early after repair. At a time when clinically well and while routine indices of heart function remain normal, children with repaired TOF exhibit RV dilatation and subtle, interlinked biventricular abnormalities on resting echocardiography. Exercise echocardiography provides additional information and reveals abnormal LV excitation-contractile coupling that may be linked to impaired exercise capacity.

Invited Commentary

The report of David and colleagues [1David T.E. David C.M. Manlhiot C. Simplici-T Annuloplasty Band for mitral valve repair for degenerative disease.Ann Thorac Surg. 2014; 98: 1551-1556Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar] using an unmeasured, experience-based approach for mitral annuloplasty is similar to that of Brown and colleagues [2Brown M.L. Schaff H.V. Li Z. Suri R.M. Daly R.C. Orsulak T.A. Results of mitral valve annuloplasty with a standard-sized posterior band: is measuring important?.J Thorac Cardiovasc Surg. 2009; 138: 886-891Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar]. Bothe and colleagues [3Bothe W. Miller C. Doenst T. Sizing for mitral annuloplasty: where does science stop and voodoo begin?.Ann Thorac Surg. 2013; 95: 1475-1483Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar] recently provided an insightful summary of the need for detailed studies of the effects of the various mitral annuloplasty techniques. We also believe that the issues involved are complex and require rigorous investigation using clinical, echo, 2D, 3D, cMRI, cardiac CTA, finite stress analysis, and other engineering data to appreciate fully the effects of different repairs. Our own focus during repair is restoration of the relationships of all the elements whose interrelated structures and dynamic behavior are necessary for normal mitral valve function, starting with normal mitral diastolic locking [4Lawrie G.M. Structure, function, and dynamics of the mitral annulus: importance in mitral valve repair for myxomatous mitral valve disease.Methodist Debakey Cardiovasc J. 2010; 6: 8-14PubMed Google Scholar, 5David D. Michelson E.L. Naito M. Chen C.C. Schaffenburg M. Dreifus L.S. Diastolic locking of the mitral valve: importance of atrial systole and intraventricular volume.Circulation. 1983; 67: 640-645Crossref PubMed Scopus (36) Google Scholar, 6Decloedt A. Verheyen T. Sys S. De Clercq D. Bijnens B. Loon G.V. Influence of atrioventricular interaction on mitral valve closure and left ventricular isovolumic contraction measured by tissue Doppler imaging.Circ Cardiovasc Imaging. 2013; 6: 109-116Crossref PubMed Scopus (12) Google Scholar]. We have reported 100% reparability [7Lawrie G.M. Earle E.A. Earle N.R. Intermediate-term results of a nonresectional dynamic repair technique in 662 patients with mitral valve prolapse and mitral regurgitation.J Thorac Cardiovasc Surg. 2011; 141: 368-376Abstract Full Text Full Text PDF PubMed Scopus (51) Google Scholar], superior durability of the annulus attachment [7Lawrie G.M. Earle E.A. Earle N.R. Intermediate-term results of a nonresectional dynamic repair technique in 662 patients with mitral valve prolapse and mitral regurgitation.J Thorac Cardiovasc Surg. 2011; 141: 368-376Abstract Full Text Full Text PDF PubMed Scopus (51) Google Scholar, 8Spratt J.R. Spratt J.A. Beachley V. Kang Q. Strength comparison of mitral annuloplasty ring and suturing combinations: an in-vitro study.J Heart Valve Disease. 2012; 21: 286-292PubMed Google Scholar], and restoration of near normal annular dynamics [9Little S.H. Ben Zekry S. Lawrie G.M. Zoghbi W.A. Dynamic annular geometry and function in patients with mitral regurgitation: insights from three dimensional annular tracking.J Am Soc Echocardiogr. 2010; 23: 872-879Abstract Full Text Full Text PDF PubMed Scopus (42) Google Scholar, 10Ben Zekry S. Lang R. Sugeng L. et al.Mitral annulus dynamics early after valve repair: Preliminary observations of the effect of resectional versus non-resectional approaches.J Am Soc Echocardiogr. 2011; 24: 1233-1242Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar]. Left ventricular outflow tract dimensions and aortic-mitral angle by cMRI are unchanged postoperatively. Strain analysis showed normal strain distribution in all cases [11Ben Zekry S. Lawrie G. Little S. et al.Comparative evaluation of mitral valve strain by deformation tracking in 3-D echocardiography.Cardiovasc Eng Tech. 2012; 3: 402-412Crossref Scopus (13) Google Scholar]. No patient has undergone reoperation for SAM [7Lawrie G.M. Earle E.A. Earle N.R. Intermediate-term results of a nonresectional dynamic repair technique in 662 patients with mitral valve prolapse and mitral regurgitation.J Thorac Cardiovasc Surg. 2011; 141: 368-376Abstract Full Text Full Text PDF PubMed Scopus (51) Google Scholar]. Preservation of normal annular dynamics eliminates the need for leaflet resection and enables the repair rate to rise to 100%, with 90% durability at 10 years by echo. We believe that optimal annular function is the essential foundation for reproducibly excellent results. Simplici-T Annuloplasty Band for Mitral Valve Repair for Degenerative DiseaseThe Annals of Thoracic SurgeryVol. 98Issue 5PreviewSizing of annuloplasty rings and bands is variably based on intertrigonal or intercommissural distances or estimation of the anterior leaflet area. This study examines the results of mitral valve repair with Simplici-T annuloplasty band without predetermining its length in patients with mitral regurgitation (MR) as a result of degenerative disease. Full-Text PDF

Left ventricular myocardial response to exercise in children after heart transplant

Data on myocardial response to exercise after pediatric heart transplant (HTx) are limited. In this study we used semi-supine bicycle ergometry (SSCE) stress echocardiography to evaluate left ventricular (LV) systolic and diastolic reserve in pediatric HTx recipients. Forty-three HTx patients and 23 controls underwent stepwise SSCE stress echocardiography. Color tissue Doppler imaging (TDI) peak systolic (s') and early diastolic (e') velocities in the LV lateral wall and basal septum, and LV peak global longitudinal and circumferential strain were measured at rest and during different stages of exercise. LV myocardial acceleration during isovolumic contraction (IVA) was measured at incremental heart rates (HRs) to determine the force-frequency relationship (FFR). At rest, compared with controls, HTx patients showed lower TDI velocities in the basal septum (s': 4.7 ± 1.1 vs 5.8 ± 0.8 cm/s, p = 0.002; e': 8.5 ± 2.1 vs 11.3 ± 1.7 cm/s, p < 0.001), whereas in the LV lateral wall only e' was lower (11.2 ± 2.6 vs 13.8 ± 2.3 cm/s, p < 0.001). LV IVA was not different between the groups (p = 0.10). LV peak global longitudinal strain was lower in HTx patients (18 ± 1.9% vs 20 ± 2.2%, p = 0.001), but peak circumferential strain was not different (p = 0.50). At peak, HR was lower in the HTx group (141 ± 12 vs 165 ± 15, p < 0.001), and all systolic and diastolic parameters, except circumferential strain, were lower in HTx recipients. When assessing the increase in TDI and strain values in relation to HR, the slopes were not significantly different between patients and controls. Despite resting differences in myocardial functional parameters, pediatric HTx recipients have preserved LV diastolic and systolic myocardial reserve in response to exercise.

Pulsed Doppler Tei index in the evaluation of pediatric severe pneumonia heart function

Objective To discuss the state of pediatric severe pneumonia heart function using pulsed Doppler Tei index,and provide evidence for clinical diagnosis and treatment.Methods 60 healthy children (normal group) and 33 children with severe pneumonia (pneumonia group) were examined with echocardiography.Left ventricular ejective fraction and fraction shortening were measured by color M-mode Doppler echocardiography; left and right ventricular isovolumic contraction time,isovolumic relaxation time,ejection time and Tei index were measured by pulsed Doppler.The data of two groups were compared and analyzed.Results Left and fight ventricular Tei indexes of pneumonia group were significantly higher than those of normal group,with statistical significant differences between two groups (P ＜ 0.01).Right ventricular Tei index was higher than left ventricular Tei index in pneumonia group,with statistical significant difference (P ＜ 0.01).There were no statistically significant differences in left ventricular ejective fraction and fraction shortening between two groups (P ＞ 0.05).Conclusions Pulsed Doppler Tei index is a new and reliable method in the evaluation of pediatric severe pneumonia heart function.Left and right ventricular Tei indexes of pneumonia group were significantly higher than those of normal group.Heart function in children with pneumonia should be protected during the clinical diagnosis and treatment. Key words: Tei index; Pediatric severe pneumonia; Heart function

A novel approach to assess hemorrhagic shock severity using the arterially determined left ventricular isovolumic contraction period

Recently, the ventilatory variation in pre-ejection period (ΔPEP) was found to be useful in the prediction of fluid-responsiveness of patients in shock. In the present study we investigated the behavior of the ventilation-induced variations in the systolic timing intervals in response to a graded hemorrhage protocol. The timing intervals studied included the ventilatory variation in ventricular electromechanical delay (ΔEMD), isovolumic contraction period (determined from the arterial pressure waveform, ΔAIC), pulse travel time (ΔPTT), and ΔPEP. ΔAIC and ΔPEP were evaluated in the aorta and carotid artery (annotated by subscripts Ao and CA) and were compared with the responses of pulse pressure variation (ΔPPAo) and stroke volume variation (ΔSV). The graded hemorrhage protocol, followed by resuscitation using norepinephrine and autologous blood transfusion, was performed in eight anesthetized Yorkshire X Landrace swine. ΔAICAo, ΔAICCA, ΔPEPAo, ΔPEPCA, ΔPPAo, ΔPPCA, and ΔSV showed significant increases during the graded hemorrhage and significant decreases during the subsequent resuscitation. ΔAICAo, ΔAICCA, ΔPEPAo, and ΔPEPCA all correlated well with ΔPPAo and ΔSV (all r ≥ 0.8, all P < 0.001). ΔEMD and ΔPTT did not significantly change throughout the protocol. In contrast with ΔPEPAo, which was significantly higher than ΔPEPCA (P < 0.01), ΔAICAo was not different from ΔAICCA. In conclusion, ventilation-induced preload variation principally affects the arterially determined isovolumic contraction period (AIC). Moreover, ΔAIC can be determined solely from the arterial pressure waveform, whereas ΔPEP also requires ECG measurement. Importantly, ΔAIC determined from either the carotid or aortic pressure waveform are interchangeable, suggesting that, in contrast with ΔPEP, ΔAIC may be site independent.

Influence of Atrioventricular Interaction on Mitral Valve Closure and Left Ventricular Isovolumic Contraction Measured by Tissue Doppler Imaging

The influence of atrioventricular (AV) interaction on mitral valve closure (MVC) and left ventricular (LV) isovolumic contraction is not fully clarified. We investigated the relationship among AV delay, MVC, and LV isovolumic contraction using a horse model because of the low heart rate and physiologically long AV delay. Six horses were evaluated during sinus rhythm, right ventricular pacing without preceding atrial contraction, and dual-chamber pacing at AV delays of 150 to 350 ms, programmed at a constant rate. Right parasternal 4-chamber views were recorded for simultaneous measurements of MVC from anatomic M-mode and radial tissue Doppler-based LV pre-ejection velocity and isovolumic acceleration. During sinus rhythm and long AV delays (≥300 ms), 2 positive pre-ejection velocity peaks were present. The first peak was identified as LV recoil during atrial relaxation and consistently preceded MVC by 33±17 ms. The second peak was related to LV isovolumic contraction, occurring after MVC. This suggests that MVC was caused by atrial relaxation and followed by true isovolumic contraction. During short AV delays (<300 ms) and right ventricular pacing, MVC occurred significantly later. Only 1 pre-ejection peak was present, of which the end coincided with MVC with a mean difference of -1.5±10 ms. This suggests that LV contraction caused MVC. Peak velocity and isovolumic acceleration were significantly higher (P<0.001) because the mitral valve was open at the onset of LV contraction. Depending on the AV delay, MVC can be atrio- or ventriculogenic, resulting in significant alterations of the LV peak pre-ejection velocity and isovolumic acceleration.

Initiation of ventricular contraction as reflected in the aortic pressure waveform

Prior to aortic valve opening, aortic pressure is perturbed by ventricular contraction. The onset of this pressure perturbation coincides with the onset of the left ventricular (LV) isovolumic contraction, and hence will be referred to as the start of the arterially detected isovolumic contraction (AICstart). In the present study we test the hypothesis that the pressure perturbation indeed has a cardiac origin. In ten Yorkshire–Landrace swine, waveform intensity analysis demonstrated that AICstart was followed by a positive intensity wave (0.3 × 105 ± 0.3 × 105 W (m2 s2)–1). Timing analysis of LV and aortic pressure waveform showed that AICstart was preceded by a LV pressure perturbation (3.8 ± 1.8 ms, p < 0.001). These novel cardiac timing and aortic wave intensity findings reveal the cardiac origin of the pressure perturbation. In 15 Yorkshire–Landrace swine, myocardial motion analysis showed a significantly higher rate of segment shortening during the first part of the LV pressure perturbation. Therefore, both the LV and aortic pressure perturbation are most likely caused by the early phase of myocardial contraction, which also causes mitral valve closure. Consequently, AICstart is useful in the determination of the isovolumic contraction period, a well-known marker to quantify cardiac dysfunction.

Oral Abstract: Understanding the physio-pathology of myocardial mechanics * Friday 9 December 2011, 14:00-15:30 * Location: Kaposvar

Purpose: To evaluate the relationship between atrial contraction, mitral valve closure (MVC) and left ventricular isovolumic contraction. The horse is an ideal model to investigate this mechanism because of the low resting heart rate (25–45 bpm) and long atrioventricular (AV) interval. Methods: Five unsedated horses instrumented with pacing leads in the right atrium and right ventricle were evaluated during sinus rhythm (SR), ventricular pacing without preceding atrial contraction (VP) and dual-chamber pacing at AV delays ranging from 150 to 350 ms, programmed in a random sequence at a constant rate of 40 bpm. Color Doppler myocardial imaging was performed at high frame rates (>100 fps). Modified right parasternal four-chamber views were recorded for simultaneous measurements of MVC by anatomical M-mode and tissue Doppler-based left ventricular pre-ejectional peak velocity spikes and their timing. Results: During SR (AV interval 330–520 ms) and long AV intervals (300 and 350 ms), MVC occurred 12±37 ms after the onset of QRS. Two positive pre-ejectional velocity peaks were present. The first peak was identified as recoil of the left ventricle during atrial relaxation. This peak (2.5±1.1 cm/s) consistently preceded MVC (linear mixed model; P=0.84) by 44±18 ms. The second peak (4.8±1.3 cm/s) was called left ventricular isovolumic contraction and occurred after MVC. This suggests MVC caused by atrial contraction, followed by a true isovolumic contraction. However, during short AV intervals (150 and 200 ms) and VP, MVC occurred significantly later (P=0.002) at 125±5 ms after the onset of QRS. Only one pre-ejectional peak was present and the end of this peak coincided with MVC (linear mixed model; P=0.76). Peak velocity (9.2±2.4 cm/s) was remarkably higher than during SR and long AV intervals (P=0.009). These findings suggest MVC caused by left ventricular myocardial motion, resulting in a high pre-ejectional velocity peak as this contraction is not isovolumic. Conclusions: This study demonstrates the important influence of the atrioventricular interaction on mitral valve closure and pre-ejectional myocardial motion. Depending on the atrioventricular delay, mitral valve closure can be atrio- or ventriculogenic, resulting in high pre-ejectional velocities if the left ventricle is not in a true isovolumic state.

Non-invasive ultrasound-based assessment of ventricular–arterial interaction in vascular Ehlers–Danlos syndrome patients

The role of ventricular–arterial hemodynamic interaction in the occurrence of arterial dissection and rupture in vascular Ehlers–Danlos syndrome (vEDS) is unknown. We recently introduced an ultrasound-based method to extract, from common carotid artery (CCA) diameter waveforms, central arterial properties and left ventricular (LV) systolic time intervals. We obtained CCA diameters, compliance and distensibility coefficients, and LV isovolumic contraction and ejection periods (ICP and EP) of 19 vEDS patients (aged 27–65 yrs) and 19 age-matched healthy controls. CCA distension and compliance tended to be lower in vEDS subjects ( p = 0.062 and p = 0.073), especially in younger patients. ICP (−12 ms) and EP (−24 ms) were shorter ( p < 0.001), while heart rate was increased (+10 bpm; p < 0.001) in vEDS. The ICP/EP ratio and estimated isovolumic d P LV/d t indicated increased LV contractility in vEDS. In conclusion, vascular EDS patients tend to have a lower CCA compliance but a normal pulse pressure, most likely reflecting reduced physical fitness.

Elevated Tricuspid Regurgitation Jet Correlates with Decreased Brachial Artery Relaxivity In Sickle Cell Anemia Patients on Chronic Transfusion Therapy.

AbstractAbstract 1645 Introduction:Vascular disease in both pulmonary and systemic vessels underlies most complications of sickle cell anemia (SCA). Multiple mechanisms contribute to this process, including inflammation, oxidative stress and decreased nitric oxide bioavailability. Chronic transfusion therapy (CTT) is thought to ameliorate some of these factors. Our goal was to determine the relationship between systemic vascular function, as indexed by flow mediated dilation (FMD), and elevated tricuspid regurgitation jet (TRJ) as a surrogate for pulmonary hypertension (PH), in chronically transfused SCA patients. Methods:25 SCA patients on CTT were enrolled in a prospective cross sectional study between August 2008 and June 2010; the protocol was approved by our IRB. Patients were studied on the day of transfusion prior to receiving blood and then again between 24 and 120 hours post transfusion. Echocardiography, brachial artery FMD and blood sampling for CBC, reticulocyte count, LDH, plasma hemoglobin and hs-CRP were performed during each study visit. A TRJ of 2.5 m/s or higher was defined as “pulmonary hypertension” and an FMD of <8% was considered abnormal based on published data for our protocol. Pre and post transfusion data were analyzed using paired T-tests with linear regression used for univariate correlations with FMD and TRJ. Results:Table 1 summarizes pre and post transfusion results. A TRJ > 2.5 m/s was seen in 20% of patients pre-transfusion and in 12% post-transfusion, but this difference did not reach statistical significance. None of the patients with a TRJ < 2.5m/s pre transfusion had a TRJ > 2.5m/s post transfusion. FMD was significantly improved consequent to transfusion (5.4% to 6.8%, p<0.02) and was abnormal in 77% patients pre transfusion and in 64% post transfusion. As expected, transfusion increased Hb and hct and decreased %HbS, reticulocyte count and plasma hemoglobin; LDH and hs-CRP were unchanged. TRJ inversely correlated with FMD (r= -0.21, p=0.0014); all patients with TRJ > 2.5 m/s exhibited blunted FMD response. Abnormal TRJ and FMD correlated with elevated reticulocyte count, LDH, %Hb S, and prolonged left ventricular ejection time and isovolumic contraction time. FMD was directly correlated with hct and Hb and inversely correlated with stroke volume and cardiac output. There was a trend towards an inverse correlation of FMD with plasma hemoglobin, arginine/ ornithine ratio and high sensitivity CRP. Discussion:CTT offers incomplete protection from vascular disease in both the systemic and pulmonary beds. Patients with elevated TRJ > 2.5m/s also had abnormal FMD: both correlated with markers of hemolysis, increased %HbS as well as prolonged cardiac time intervals. Abnormal FMD, but not TRJ, was correlated with decreased Hb and hct and increased cardiac output and stroke volume, suggesting that worsening anemia affects FMD to a greater degree than TRJ. These data support the concept that pulmonary hypertension in SCA is only one manifestation of pan-systemic endothelial disease.Table 1Pre TransfusionPost TransfusionStandard Error95% CIP-ValueTR max value (m/s)223.9218.75.3-16.2 to 5.80.34TR mean (m/s)207204.25.3-13.7 to 8.20.61FMD (%)5.46.810.3 to 2.60.0176Reticulocyte Count12.280.7-5.7 to -2.7<0.0001Hb S%37.131.51.4-8.6 to -2.60.0009Cell free Hb4019.29.7-40.9 to -0.50.04Hemoglobin9.311.50.21.8 to 2.6<0.0001Hematocrit2833.60.64.4 to 6.9<0.0001WBC14.213.20.6-2.2 to 0.30.125LDH1220.4116737.9-132.2 to 25.30.17Hs-CRP6.14.51.7-5.1 to 1.80.33 Disclosures:Coates:Novartis: Research Funding, Speakers Bureau.

Potential use of isovolumic contraction velocity in assessment of left ventricular contractility in man: A simultaneous pulsed Doppler tissue imaging and cardiac catheterization study

Echocardiographic techniques have so far provided suboptimal estimates of myocardial contractility in humans. Longitudinal myocardial motion during the isovolumic contraction (IVC) phase, measured by colour tissue Doppler imaging (TDI), has recently been shown in experimental animal models to reflect the state of myocardial contractility. The aim of the present study was to investigate the relationship between left ventricular (LV) isovolumic contraction velocities (IVCv) using pulsed Doppler tissue imaging (DTI) and global LV contractility as measured during cardiac catheterization. Cardiac catheterization and pulsed DTI were simultaneously performed in 16 consecutive patients (13 males, mean age 55+/-10years) with a variety of cardiac diseases. Relationships between the peak positive IVCv as measured at basal levels of the lateral, septal, anterior and posterior walls and the first derivative of LV pressure (+dP/dt(max)), were investigated. Peak IVCv measurements were obtainable in 81-100% of the four LV wall segments. Statistically significant linear relationships were found between IVCv and +dP/dt(max) at the lateral (r=0.58, P<0.05), septal (r=0.66, P<0.01), anterior (r=0.73, P<0.01) and posterior (r=0.81, P<0.001) segments of the LV. IVCv of the basal four LV walls correlates strongly with peak +dP/dt. IVCv is a readily obtainable non-invasive parameter, which correlates with the classical invasive measurement of global LV contractility. It appears likely that there are regional differences in wall motion when DTI is used to determine state of LV contractility.

The 'TEI-index' is preload dependent and can be measured by transoesophageal echocardiography during mechanical ventilation

Background and objective: The Doppler-derived echocardiographic TEI-index, defined as the sum of the left ventricular isovolumic contraction and isovolumic relaxation times divided by ejection time, quantifies combined systolic and diastolic ventricular functions. The index has been proposed to be independent of arterial pressure and heart rate, implying a broad clinical usefulness. However, it is unclear whether the index is preload independent. We assessed whether and to what degree the TEI-index is altered by left ventricular loading conditions, and the feasibility of measurement by transoesophageal echocardiography during anaesthesia and mechanical ventilation. Methods: We studied 17 anaesthetized mechanically ventilated patients with coronary artery disease during variations in left ventricular preload evoked by head-up and head-down tilt, respectively. Results: A head-down tilt increasing left ventricular end-diastolic area from 18.8 ± 4 to 23.7 ± 4 cm2 (P < 0.05) significantly decreased the TEI-index from 0.5 ± 0.17 to 0.33 ± 0.15 (P < 0.05). In contrast, the TEI-index remained unchanged with decreased left ventricular preload (14.4 ± 3.7 cm2) during head-up tilt. Conclusions: An increase in preload decreases the TEI-index indicating its sensitivity to acute increases in left ventricular preload. The TEI-index can be measured perioperatively by transoesophageal echocardiography.