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Biomedical subjects

Patrick Segers

Publications and source records attributed to Patrick Segers.

At least 19 recordsLinked to original sources
PubMed2007

Thoracic epidural anesthesia impairs the hemodynamic response to acute pulmonary hypertension by deteriorating right ventricular-pulmonary arterial coupling.

OBJECTIVE: Thoracic epidural anesthesia is increasingly used in critically ill patients. This analgesic technique was shown to decrease left ventricular contractility, but effects on right ventricular function have not been reported. A deterioration of right ventricular performance may be clinically relevant for patients with acute pulmonary hypertension, in which right ventricular function is an important determinant of outcome. In the present study, we tested the hypothesis that thoracic epidural anesthesia decreases right ventricular contractility and limits its capacity to tolerate pulmonary hypertension. DESIGN: Prospective, placebo-controlled study using an established model of acute pulmonary hypertension. SETTING: University hospital laboratory. SUBJECTS: A total of 14 pigs (mean weight, 35 +/- 2 kg). INTERVENTIONS: After instrumentation with an epidural catheter, biventricular conductance catheters, a pulmonary flow probe, and a high-fidelity pulmonary pressure catheter, seven pigs received thoracic epidural anesthesia and seven pigs served as control. Hemodynamic measurements were performed in baseline conditions and after induction of pulmonary hypertension via hypoxic pulmonary vasoconstriction (Fio2 of 0.15). MEASUREMENTS AND MAIN RESULTS: Ventricular contractility was assessed using load- and heart rate-independent variables. Right ventricular afterload was characterized with instantaneous pressure-flow measurements. In baseline conditions, thoracic epidural anesthesia decreased left but not right ventricular contractility. In untreated animals, pulmonary hypertension was associated with an increase in right ventricular contractility and cardiac output. Pretreatment with thoracic epidural anesthesia completely abolished the positive inotropic response to acute pulmonary hypertension. As a result, ventriculo-vascular coupling between the right ventricle and pulmonary-arterial system deteriorated, and cardiac output was significantly lower in animals with thoracic epidural anesthesia than in untreated controls during hypoxia-induced pulmonary hypertension. CONCLUSIONS: Thoracic epidural anesthesia inhibits the native positive inotropic response of the right ventricle to increased afterload and deteriorates the hemodynamic effects of acute pulmonary hypertension.

Acute Disease↗
PubMed2006

Cardiovascular haemodynamics and ventriculo-arterial coupling in an acute pig model of coronary ischaemia-reperfusion.

Although reperfusion after coronary occlusion is mandatory for myocardial salvage, reperfusion may trigger a cascade of harmful events (reperfusion injury) adding to myocardial injury. We investigated effects of reperfusion on left ventricular (LV) haemodynamics and ventriculo-arterial (VA) coupling in pigs following acute myocardial ischaemia induced by coronary artery occlusion. Experiments were performed in six animals, with measurements of cardiac and arterial function at baseline, after 60 min of ischaemia (T60) and after 2 (T180) and 4 h of reperfusion (T300). Ventriculo-arterial coupling was assessed using the ventriculo-arterial elastance ratio of paper, as well as using a 'stiffness coupling' and 'temporal coupling' index. Reperfusion following ischaemia (T180 versus T60) induced a progressive decline in cardiovascular function, evidenced by a decrease in mean arterial blood pressure, cardiac output and ejection fraction which was not restored at T300. Although reperfusion also induced an increase in slope of the end-systolic pressure-volume relationship (ESPVR), the ESPVR curve shifted to the right, associated with a depression of contractile function. Histology demonstrated irreversible myocardial damage at T300. The ventriculo-arterial elastance ratio and the 'stiffness coupling' index were unaffected throughout the protocol, but the 'temporal coupling' parameter indicated a relative shift between heart period and the time constant of the arterial system. It is unlikely that these alterations are attributable to ischaemic injury alone. The combination of both the stiffness and temporal coupling index may provide more information when studying ventriculo-arterial coupling than the more commonly used ventricular end-systolic stiffness/effection arterial elastance (E(es)/E(a)) ratio.

Animals↗
PubMed2006

Ventricular-arterial coupling in a rat model of reduced arterial compliance provoked by hypervitaminosis D and nicotine.

The vitamin D(3) and nicotine (VDN) model is one of isolated systolic hypertension (ISH) in which arterial calcification raises arterial stiffness and vascular impedance. The effects of VDN treatment on arterial and cardiac hemodynamics have been investigated; however, a complete analysis of ventricular-arterial interaction is lacking. Wistar rats were treated with VDN (VDN group, n = 9), and a control group (n = 10) was included without the VDN. At week 8, invasive indexes of cardiac function were obtained using a conductance catheter. Simultaneously, aortic pressure and flow were measured to derive vascular impedance and characterize ventricular-vascular interaction. VDN caused significant increases in systolic (138 +/- 6 vs. 116 +/- 13 mmHg, P < 0.01) and pulse (42 +/- 10 vs. 26 +/- 4 mmHg, P < 0.01) pressures with respect to control. Total arterial compliance decreased (0.12 +/- 0.08 vs. 0.21 +/- 0.04 ml/mmHg in control, P < 0.05), and pulse wave velocity increased significantly (8.8 +/- 2.5 vs. 5.1 +/- 2.0 m/s in control, P < 0.05). The arterial elastance and end-systolic elastance rose significantly in the VDN group (P < 0.05). Wave reflection was augmented in the VDN group, as reflected by the increase in the wave reflection coefficient (0.63 +/- 0.06 vs. 0.52 +/- 0.05 in control, P < 0.05) and the amplitude of the reflected pressure wave (13.3 +/- 3.1 vs. 8.4 +/- 1.0 mmHg in control, P < 0.05). We studied ventricular-arterial coupling in a VDN-induced rat model of reduced arterial compliance. The VDN treatment led to development of ISH and provoked alterations in cardiac function, arterial impedance, arterial function, and ventricular-arterial interaction, which in many aspects are similar to effects of an aged and stiffened arterial tree.

Animals↗
PubMed2006

Numerical assessment of the impact of a flow wire on its velocity measurements.

Blood flow velocities can be measured using a Doppler flow wire. This numerical study evaluates the impact of a 0.014" flow wire on the measured frequencies in a straight artery with diameters of 3 mm and 4 mm, under steady and pulsatile flow conditions. Simulations were performed with the wires positioned differently in the artery (perfectly centred and at an offset of 0.5 mm from the wall) and with different types of wire (tilted and straight). Measurements were taken at range gates from 4 mm to 10 mm. During simulations using a 3-mm vessel under pulsatile flow conditions, the relative error between the measured and reference maximum frequency (occurring in absence of the wire) decreased from 17.7% to 11.6% (with a mean value of 14.9%). During simulations using an off-centre 1.5 degree tilted wire, the mean error was approximately 5%. Therefore, our study suggests that that a centrally positioned flow wire is unfavourable for measuring flow velocities.

Arteries↗
PubMed2006

Hemodynamic effects of different lung-protective ventilation strategies in closed-chest pigs with normal lungs.

OBJECTIVE: The benefits of lung-protective ventilation strategies used for acute respiratory distress syndrome in subjects with normal lungs are uncertain. The purpose of this study was to investigate the hemodynamic effects of conventional lung-protective ventilation (CLPV) and high-frequency oscillatory ventilation (HFOV) in a normal lung animal model. DESIGN: Prospective laboratory investigation. SETTING: Animal laboratory in a university medical center. SUBJECTS: Seven landrace pigs (mean weight 41 kg). INTERVENTIONS: Pigs were ventilated at random conventionally with positive end-expiratory pressure 2-3 cm H2O and tidal volume 10-12 mL/kg (control), with CLPV (positive end-expiratory pressure 10 cm H2O, tidal volume 6 mL/kg), or with HFOV. Hemodynamics were analyzed after insertion of biventricular conductance catheters and a pulmonary artery catheter. MEASUREMENTS AND MAIN RESULTS: The protective strategies led to higher mean airway pressures and severe hypercapnia with acidosis, which was only significant with CLPV. Compared with control, oxygenation was worse with CLPV and HFOV. With HFOV and CLPV, mean arterial pressure, cardiac output, and stroke volume decreased significantly; pulmonary arterial elastance increased. The slope of the end-diastolic pressure volume relationship for the left and right ventricle remained unchanged (preserved ventricular function), whereas the intercept increased with both protective strategies (augmented intrathoracic pressure); left and right end-diastolic volumes decreased significantly. CONCLUSIONS: In the absence of a fluid resuscitation strategy, CLPV and HFOV caused decreased mean arterial pressure, cardiac output, and stroke volume and worsened oxygenation in this normal lung animal model. This resulted primarily from a biventricular decrease in preload.

Acidosis↗
PubMed2006

Hemodynamics of a pulsatile left ventricular assist device driven by a counterpulsation pump in a mock circulation.

The BCM (CardialCare, Minneapolis, MN, U.S.A.) is a pusher-plate pulsatile left ventricular assist device (LVAD) that is operated by counterpulsation pumps. The purpose of this work was to assess the fluid dynamics associated with operating the BCM in a mock circulation, and also to examine the similarities between hemodynamic parameters produced by this device in vitro and those produced by the left ventricle (LV) in vivo. The BCM was connected to a true size silicon rubber aorta and operated by an intra-aortic balloon pump. We examined the performance of the device at two system pressures (6.5 and 8 kPa); at three heart rates (60, 80, and 100 bpm); and at three pumping frequencies (1:1, 1:2, 1:3). Pressure and flow were measured in the upper descending aorta, and wave intensity analysis was used to calculate the peak intensity and energy of the compression and expansion waves. Pressure and flow waveforms produced by the BCM LVAD in vitro under different loading conditions were similar to those observed in vivo under similar loadings. Pusher-plate-type LVADs can produce compression and expansion waves similar to those generated by healthy LV in vivo.

Aorta↗
PubMed2006

Hydrodynamic evaluation of kangaroo aortic valve matrices for tissue valve engineering.

We evaluated the hydrodynamic performance of kangaroo aortic valve matrices (KMs) (19, 21, and 23 mm), as potential scaffolds in tissue valve engineering using a pulsatile left heart model at low and high cardiac outputs (COs) and heart rates (HRs) of 60 and 90 beats/min. Data were measured in two samples of each type, pooled in two CO levels (2.1 +/- 0.7 and 4.2 +/- 0.6 L/min; mean +/- standard errors on the mean), and analyzed using analysis of variance with CO level, HR, and valve type as fixed factors and compared to similar porcine matrices (PMs). Transvalvular pressure gradient (DeltaP) was a function of HR (P < 0.001) and CO (P < 0.001) but not of valve type (P = 0.39). DeltaP was consistently lower in KMs but not significantly different from PMs. The effective orifice area and performance index of kangaroo matrices was statistically larger for all sizes at both COs and HRs.

Animals↗
PubMed2006

Assessment of the tilting properties of the human mitral valve during three main phases of the heart cycle: an echocardiographic study.

RATIONALE AND OBJECTIVES: In experimental models of the left heart, the mitral valve (MV) is commonly implanted perpendicular to a central axis of the apex/MV. To adapt this to a more correct anatomical model, as well as for further studies of the left ventricle, we created a database of implantation angles of the MV and annulus during three main phases of the heart cycle, based on standard cardiac ultrasound measurements. MATERIALS AND METHODS: Twenty-eight patients were studied with the standard cardiac ultrasound equipment. From the apical echo window, an anteroposterior (AP) plane and a perpendicular commisure-commisure (CC) plane were generated during three critical moments in the heart cycle: systole (S); diastole early filling (E); and diastole late filling (A). In both planes, the angles between the annular plane and each mitral leaflet, as well as the angle between a theoretical longitudinal axis through the apex and center of the MV orifice and the mitral annulus plane, were measured with a custom-made application of Matlab R14. RESULTS: We observed an inclination of the angle mitral annulus/central left ventricle axis, with its lowest point in the direction of the aortic valve (AP plane) of 85 degrees+/-7 degrees in systole (S), 88 degrees+/-8 degrees in early diastole (E), and 88 degrees+/-7 degrees in late diastole (A). In the CC plane, we observed an almost horizontal implantation of 91 degrees+/-5 degrees in systole (S), 91 degrees+/-8 degrees in early diastole (E), and 91 degrees+/-7 degrees in late diastole (A).

Adult↗
PubMed2005

Evaluation of BM-573, a novel TXA2 synthase inhibitor and receptor antagonist, in a porcine model of myocardial ischemia-reperfusion.

AIMS: To investigate whether BM-573 (N-tert-butyl-N'-[2-(4'-methylphenylamino)-5-nitro-benzenesulfonyl]urea), an original combined thromboxane A2 synthase inhibitor and receptor antagonist, prevents reperfusion injury in acutely ischemic pigs. METHODS: Twelve animals were randomly divided in two groups: a control group (n = 6) intravenously infused with vehicle, and a BM-573-treated group (n = 6) infused with BM-573 (10 mg kg(-1) h(-1)). In both groups, the left anterior descending (LAD) coronary artery was occluded for 60 min and reperfused for 240 min. Either vehicle or BM-573 was infused 30 min before LAD occlusion and throughout the experiment. Platelet aggregation induced by arachidonic acid ex vivo measured was prevented by BM-573. RESULTS: In both groups, LAD occlusion decreased cardiac output, ejection fraction, slope of stroke work--end-diastolic volume relationship, and induced end-systolic pressure-volume relationship (ESPVR) rightward shift, while left ventricular afterload increased. Ventriculo-arterial coupling and mechanical efficiency decreased. In both groups, reperfusion further decreased cardiac output and ejection fraction, while ESPVR displayed a further rightward shift. Ventriculo-arterial coupling and mechanical efficiency remained impaired. Area at risk, evidenced with Evans blue, was 33.2+/-3.4% of the LV mass (LVM) in both groups, and mean infarct size, revealed by triphenyltetrazolium chloride (TTC), was 27.3+/-2.6% of the LVM in the BM-573-treated group (NS). Histological examination and immunohistochemical identification of desmin revealed necrosis in the anteroseptal region similar in both groups, while myocardial ATP dosages and electron microscopy also showed that BM-573 had no cardioprotective effect. CONCLUSIONS: These data suggest that BM-573 failed to prevent reperfusion injury in acutely ischemic pigs.

Animals↗
PubMed2005

Primary impairment of left ventricular function in Marfan syndrome.

BACKGROUND: Cardiovascular involvement in Marfan syndrome is mainly characterized by progressive dilatation of the proximal aorta. Whether left ventricular dysfunction is present in these patients is not clear at present. OBJECTIVES: Assess left ventricular function in patients with Marfan syndrome, free of significant valvular heart disease, using a combination of MRI and Tissue Doppler imaging (TDI). METHODS AND RESULTS: A total of 26 Marfan patients (mean age=32.0+/-10.9, 12 men) without significant valvular heart disease, and 26 age- and sex-matched controls were studied. Left ventricular volumes and ejection fraction were measured with magnetic resonance imaging. Systolic and diastolic function parameters were assessed using conventional echocardiography and TDI. When compared to controls, Marfan patients showed impairment of left ventricular contractile function as expressed by a reduced ejection fraction (53.5+/-9.0% vs. 59.6+/-6.7%, p=0.009), an increased end-systolic volume (36.0+/-9.5 vs. 29.5+/-6.7 ml/m(2), p=0.007), and reduced peak systolic velocities at the basal septal and lateral myocardial wall (5.2+/-1.4 vs. 6.4+/-1.3 cm/s, p=0.003 and 6.0+/-2.2 vs. 7.5+/-2.3 cm/s, p=0.03, respectively). Diastolic function was impaired with an increased deceleration time of the E wave (171+/-41 ms vs. 141+/-36 ms, p=0.006). Peak early diastolic velocity at the mitral valve annulus was significantly lower (9.6+/-2.4 cm/s vs. 11.9+/-3.3 cm/s, p=0.006). CONCLUSION: These data provide evidence for mild, but significant impairment of left ventricular systolic and diastolic function in Marfan patients, not related to valvular heart disease.

Adult↗
PubMed2005

Noninvasive Doppler-derived myocardial performance index in rats with myocardial infarction: validation and correlation by conductance catheter.

The rodent model of myocardial infarction (MI) is extensively used in heart failure studies. However, long-term follow-up of echocardiographic left ventricular (LV) function parameters such as the myocardial performance index (MPI) and its ratio with the fractional shortening (LVFS/MPI) has not been validated in conjunction with invasive indexes, such as those derived from the conductance catheter (CC). Sprague-Dawley rats with left anterior descending coronary artery ligation (MI group, n = 9) were compared with a sham-operated control group (n = 10) without MI. Transthoracic echocardiography (TTE) was performed every 2 wk over an 8-wk period, after which classic TTE parameters, especially MPI and LVFS/MPI, were compared with invasive indexes obtained by using a CC. Serial TTE data showed significant alterations in the majority of the noninvasive functional and structural parameters (classic and novel) studied in the presence of MI. Both MPI and LVFS/MPI significantly (P < 0.05 for all reported values) correlated with body weight (r = -0.58 and 0.76 for MPI and LVFS/MPI, respectively), preload recruitable stroke work (r = -0.61 and 0.63), LV end-diastolic pressure (LVEDP) (r = 0.82 and -0.80), end-diastolic volume (r = 0.61 and -0.58), and end-systolic volume (r = 0.46 and -0.48). Forward stepwise linear regression analysis revealed that, of all variables tested, LVEDP was the only independent determinant of MPI (r = 0.84) and LVFS/MPI (r = 0.83). We conclude that MPI and LVFS/MPI correlate strongly and better than the classic noninvasive TTE parameters with established, invasively assessed indexes of contractility, preload, and volumetry. These findings support the use of these two new noninvasive indexes for long-term analysis of the post-MI LV remodeling.

Animals↗
PubMed2005

Noninvasive assessment of local pulse pressure: importance of brachial-to-radial pressure amplification.

The advocated SphygmoCor procedure uses a radial-to-aorta transfer function with calibration on brachial instead of radial artery pressure to assess the central pulse pressure. We compared these values with carotid artery pulse pressures obtained from a validated calibration method, assuming mean minus diastolic blood pressure constant throughout the large artery tree. From 44 healthy subjects (21 males; 22 to 68 years) pressure waves were obtained at the radial, brachial, and carotid artery with applanation tonometry. Using the calibration method, radial and carotid artery pressures were assessed from brachial artery waves and pressures. The effect of brachial-to-radial pulse pressure amplification, brachial pulse pressure, mean pressure, age, gender, height, body mass index, and smoking on differences between the 2 methods was assessed. Brachial artery pressure was 118+/-12/72+/-10 mm Hg. SphygmoCor central pulse pressure was 9.7+/-4.6 mm Hg lower (P<0.001) than the carotid artery pulse pressure (33.0+/-6.8 versus 42.7+/-8.9 mm Hg). The difference between the 2 methods strongly depended (P<0.001) on brachial-to-radial artery pulse pressure amplification (5.8+/-5.1 mm Hg; 12+/-11%) and less on brachial artery pulse pressure (P=0.005). After calibration of the radial pressure wave with radial instead of brachial artery pressures, the difference between SphygmoCor central pulse pressure and carotid pulse pressure decreased with 4 mm Hg. The advocated SphygmoCor procedure systematically underestimates the central pulse pressure with brachial-to-radial pulse pressure amplification as important determinant. Therefore, calibration of radial artery pressure waves on brachial artery pressures should be avoided. The underestimation of central aortic pulse pressure caused by the radial-to-aorta transfer function itself is much less than previously reported.

Adult↗
PubMed2005

Characterization of an original model of myocardial infarction provoked by coronary artery thrombosis induced by ferric chloride in pig.

BACKGROUND: Great advances have been made in the prevention of thrombotic disorders by developments of new pharmacological and surgical treatments. Animal models of arterial thrombosis have largely contributed to the discovery and to the validation of original treatments. The purpose of the present work was to develop and validate an original model of acute myocardial infarction provoked in pig by thrombosis of the left anterior descending (LAD) coronary artery induced by topical application of ferric chloride solution. METHODS AND RESULTS: Myocardial infarction, resulting from an occlusive and adherent mixed thrombus formed in the LAD coronary artery, was examined at macroscopic level using dual staining technique (Evans blue dye; triphenyltetrazolium chloride) and at microscopic level using conventional histological analyses and immunohistochemical detection of desmin. Biochemical markers (troponin T and ATP), platelet reactivity and standard hemodynamic parameters (such as stroke volume, ejection fraction, stroke work and cardiac output) have also been evaluated. From these analyses, it was demonstrated that each pig developed a transmural area of irreversible damage mainly located in the anteroseptal region of the left ventricle. The more progressive development of coronary artery occlusion, as compared to an abrupt ligation, was accompanied by a correspondingly progressive impairment in hemodynamics. CONCLUSION: We conclude that this original porcine model of myocardial infarction is quite close to clinical pathophysiological conditions, such as thrombus formation occurring after atherosclerotic plaque rupture. This certainly constitutes a further argument in favour of this model to assess pharmaceutical or mechanical support of an acutely ischemic heart.

Adenosine Triphosphate↗
PubMed2005

Carotid tonometry versus synthesized aorta pressure waves for the estimation of central systolic blood pressure and augmentation index.

OBJECTIVE: To assess the interchangeability of carotid tonometry and synthesized aorta pressure waveforms for estimating central systolic blood pressure (SBP) and augmentation index (AIx). METHODS: Tonometry waveforms were acquired with a custom built hardware and software platform in 276 subjects (179 men/97 women; aged 45.5 +/- 5.7 years; mean +/- standard deviation) at the radial (P(wf,ra)), brachial (P(wf,ba)), and carotid artery (P(wf,ca)). The P(wf,ba) was calibrated using systolic (SBP(ba)) and diastolic (DBP(ba)) sphygmomanometer pressure. The DBP(ba) and calculated mean (MAP(ba)) brachial pressure were subsequently used for calibration of P(wf,ra) and P(wf,ca). A central pressure waveform (P(wf,sao)) was synthesized from P(wf,ra) using a generalized pressure transfer function (TFF). The AIx and SBP were measured on P(wf,ra), P(wf,ca), and P(wf,sao). RESULTS: The SBP(ra), SBP(ca), and SBP(sao) were 138.5 +/- 16.8, 130.0 +/- 16.2, and 131.1 +/- 16.6 mm Hg, respectively. The SBP(ra) correlated well with the SBP(ca) (r = 0.93) and the SBP(sao) (r = 0.94), as did the SBP(ca) and the SBP(sao) (r = 0.97) with a mean bias of 1.35 +/- 3.90 mm Hg. The AIx derived from P(wf,ra), P(wf,ca), and P(wf,sao) were -20.8% +/- 14.5%, 12.4% +/- 13.9%, and 20.0% +/- 11.7%, respectively. The correlation between radial and carotid, and radial and central AIx was 0.72 and 0.94, respectively. The correlation between AIx derived from P(wf,ca) and P(wf,sao) was 0.75 with a bias of 11.0% +/- 14% (all correlations P < .001). CONCLUSIONS: The use of a generalized TFF in combination with well-calibrated radial pressure curves yields estimates of SBP in good agreement with carotid tonometry. Although AIx derived from a measured radial pressure curve correlates surprisingly closely with AIx measured on a synthesized aortic pressure curve, the correlation with a directly measured AIx on carotid signals is relatively poor.

Adult↗
PubMed2005

Accuracy of 4 different algorithms for the analysis of tomographic radionuclide ventriculography using a physical, dynamic 4-chamber cardiac phantom.

UNLABELLED: Various automatic algorithms are now being developed to calculate left ventricular (LV) and right ventricular (RV) ejection fraction from tomographic radionuclide ventriculography. We tested the performance of 4 of these algorithms in estimating LV and RV volume and ejection fraction using a dynamic 4-chamber cardiac phantom. METHODS: We developed a realistic physical, dynamic 4-chamber cardiac phantom and acquired 25 tomographic radionuclide ventriculography images within a wide range of end-diastolic volumes, end-systolic volumes, and stroke volumes. We assessed the ability of 4 algorithms (QBS, QUBE, 4D-MSPECT, and BP-SPECT) to calculate LV and RV volume and ejection fraction. RESULTS: For the left ventricle, the correlations between reference and estimated volumes (0.93, 0.93, 0.96, and 0.93 for QBS, QUBE, 4D-MSPECT, and BP-SPECT, respectively; all with P < 0.001) and ejection fractions (0.90, 0.93, 0.88, and 0.92, respectively; all with P < 0.001) were good, although all algorithms underestimated the volumes (mean difference [+/-2 SDs] from Bland-Altman analysis: -39.83 +/- 43.12 mL, -33.39 +/- 38.12 mL, -33.29 +/- 40.70 mL, and -16.61 +/- 39.64 mL, respectively). The underestimation by QBS, QUBE, and 4D-MSPECT was greater for higher volumes. QBS, QUBE, and BP-SPECT could also be tested for the right ventricle. Correlations were good for the volumes (0.93, 0.95, and 0.97 for QBS, QUBE, and BP-SPECT, respectively; all with P < 0.001). In terms of absolute volume estimation, the mean differences (+/-2 SDs) from Bland-Altman analysis were -41.28 +/- 43.66 mL, 11.13 +/- 49.26 mL, and -13.11 +/- 28.20 mL, respectively. Calculation of RV ejection fraction correlated well with true values (0.84, 0.92, and 0.94, respectively; all with P < 0.001), although an overestimation was seen for higher ejection fractions. CONCLUSION: Calculation of LV and RV ejection fraction based on tomographic radionuclide ventriculography was accurate for all tested algorithms. All algorithms underestimated LV volume; estimation of RV volume seemed more difficult, with different results for each algorithm. The more irregular shape and inclusion of a relatively hypokinetic RV outflow tract in the right ventricle seemed to cause the greater difficulty with delineation of the right ventricle, compared with the left ventricle.

Algorithms↗
PubMed2005

Predicting ATS Open Pivot heart valve performance with computational fluid dynamics.

BACKGROUND AND AIM OF THE STUDY: In-vitro studies on the ATS heart valve have indicated that valve opening is less in an expanding conduit than in a straight conduit. METHODS: Bileaflet valve behavior was studied using a new computational fluid-structure interaction model. A three-dimensional model of the ATS valve was studied in two geometries, simulating the valve in a geometry with sudden expansion downstream of the valve, and in a straight conduit. Mitral and aortic flow patterns were simulated. RESULTS: The ATS valve in the expanding geometry showed opening to a maximum angle of 77.5 degrees; this was confirmed in previous clinical and in-vitro studies. The mean and maximum transvalvular Doppler pressure gradients were 1.1 and 4.3 mmHg, respectively. The maximum shear stress calculated on the leaflet was 25 Pa. Maximum opening of the valve was achieved in the straight conduit; with mean and maximum pressure gradients of 2.1 and 4.6 mmHg, respectively. The maximum shear stress calculated on the leaflet was 35 Pa. CONCLUSION: The results of this numerical study confirmed that valve hemodynamics and leaflet motion were dependent on the geometrical conditions of the valve: the presence of a diverging flow influenced the maximum opening angle of the valve leaflets. This model could be used to predict pressure gradients, effective orifice area, performance index and shear stress loading of mechanical heart valves, and in future will serve as a major research tool to characterize the hemodynamics of existing and new mechanical heart valves.

Aortic Valve↗