Biomedical subjects

Patrick Segers

Publications and source records attributed to Patrick Segers.

At least 37 records · Page 2Linked to original sources

PubMed2004

Echocardiographic assessment of aortic elastic properties with automated border detection in an ICU: in vivo application of the arctangent Langewouters model.

We studied whether combined pressure and transesophageal ultrasound monitoring is feasible in the intensive care unit (ICU) setting for global cardiovascular hemodynamic monitoring [systemic vascular resistance (SVR) and total arterial compliance (C(PPM))] and direct estimation of local ascending and descending aortic mechanical properties, i.e., distensibility and compliance coefficients (DC and CC). Pressure-area data were fitted to the arctangent Langewouters model, with aortic cross-sectional area obtained via automated border detection. Data were measured in 19 subjects at baseline, during infusion of sodium nitroprusside (SNP), and after washout. SNP infusion lowered SVR from 1.15 +/- 0.40 to 0.80 +/- 0.32 mmHg.ml(-1).s (P < 0.05), whereas C(PPM) increased from 0.87 +/- 0.46 to 1.02 +/- 0.42 ml/mmHg (P < 0.05). DC and CC increased from 0.0018 +/- 0.0007 to 0.0025 +/- 0.0009 l/mmHg (P < 0.05) and from 0.0066 +/- 0.0028 to 0.0083 +/- 0.0026 cm2/mmHg (P < 0.05), respectively, at the descending, but not ascending, aorta. The Langewouters model fitted the descending aorta data reasonably well. Assessment of local mechanical properties of the human ascending aorta in a clinical setting by automated border detection remains technically challenging.

Aged↗

PubMed2004

Conductance catheter-based assessment of arterial input impedance, arterial function, and ventricular-vascular interaction in mice.

Global assessment of both cardiac and arterial function is important for a meaningful interpretation of pathophysiological changes in animal models of cardiovascular disease. We simultaneously acquired left ventricular (LV) and aortic pressure and LV volume (V(LV)) in 17 open-chest anesthetized mice (26.7 +/- 3.2g) during steady-state (BL) and caval vein occlusion (VCO) using a 1.4-Fr dual-pressure conductance catheter and in a subgroup of eight animals during aortic occlusion (AOO). Aortic flow was obtained from numerical differentiation of V(LV). AOO increased input impedance (Z(in)) for the first two harmonics, increased characteristic impedance (0.025 +/- 0.007 to 0.040 +/- 0.011 mmHg x microl(-1) x s, P < 0.05), and shifted the minimum in Z(in) from the third to the sixth harmonic. For all conditions, the Z(in) could be well represented by a four-element windkessel model. The augmentation index increased from 116.7 +/- 7.8% to 145.9 +/- 19.5% (P < 0.01) as well as estimated pulse-wave velocity (3.50 +/- 0.94 to 5.95 +/- 1.62 m/s, P < 0.05) and arterial elastance (E(a), 4.46 +/- 1.62 to 6.02 +/- 1.43 mmHg/microl, P < 0.01). AOO altered the maximal slope (E(max), 3.23 +/- 1.02 to 5.53 +/- 1.53 mmHg/microl, P < 0.05) and intercept (-19.9 +/- 8.6 to 1.62 +/- 13.51 microl, P < 0.01) of the end-systolic pressure-volume relation but not E(a)/E(max) (1.44 +/- 0.43 to 1.21 +/- 0.37, not significant). We conclude that simultaneous acquisition of Z(in) and arterial function parameters in the mouse, based solely on conductance catheter measurements, is feasible. We obtained an anticipated response of Z(in) and arterial function parameters following VCO and AOO, demonstrating the sensitivity of the measuring technique to induced physiological alterations in murine hemodynamics.

Animals↗

PubMed2004

Effect of BM-573 [N-terbutyl-N'-[2-(4'-methylphenylamino)-5-nitro-benzenesulfonyl]urea], a dual thromboxane synthase inhibitor and thromboxane receptor antagonist, in a porcine model of acute pulmonary embolism.

The aim of this study was to evaluate the effect of BM-573 [N-terbutyl-N'-[2-(4'-methylphenylamino)-5-nitro-benzenesulfonyl]urea], a dual thromboxane A2 synthase inhibitor and receptor antagonist, on the hemodynamic response to acute pulmonary embolism. Six anesthetized pigs were infused with placebo (placebo group) and compared with six other pigs receiving a continuous infusion of BM-573 (BM group). Pulmonary embolization with 0.3 g/kg autologous blood clots was carried out 30 min after the start of the infusion. Right ventricular pressure-volume loops were recorded using a conductance catheter, and end-systolic ventricular elastance was periodically assessed by varying right ventricular preload. Pulmonary vascular properties were studied by use of a four-element windkessel model. Hemodynamic data, including assessment of right ventricular-arterial coupling, were collected at baseline and every 30 min for 4 h. Blood samples were collected to assess gas exchange, thromboxane A2, and prostacyclin plasma levels and to evaluate platelet aggregation. Mean pulmonary arterial pressure in the placebo group increased significantly more than in the BM group, mainly because of an additional increase in pulmonary vascular resistance. Arterial and end-systolic ventricular elastances increased also more in the placebo group, whereas right ventricular efficiency decreased. BM-573 prevented both platelet aggregation induced by U-46619 (9,11-dideoxy-11alpha,9alpha-epoxymethanoprostaglandin F2alpha) or by arachidonic acid, and thromboxane A2 overproduction, whereas prostacyclin liberation was preserved. Oxygenation, however, was not significantly improved. We conclude that in this animal model of acute pulmonary embolism, infusion of BM-573 reduced pulmonary vasoconstriction. As a result, right ventricular-vascular coupling values were maintained at a maximal efficiency level.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2004

Pharmacological characterization of N-tert-butyl-N'-[2-(4'-methylphenylamino)-5-nitrobenzenesulfonyl]urea (BM-573), a novel thromboxane A2 receptor antagonist and thromboxane synthase inhibitor in a rat model of arterial thrombosis and its effects on bleeding time.

The present study was undertaken to characterize the antiplatelet and antithrombotic effects of BM-573 [N-tert-butyl-N'-[2-(4'-methylphenylamino)-5-nitrobenzenesulfonyl]urea], an original combined thromboxane receptor antagonist and thromboxane synthase inhibitor in rats, and to determine its effects on mice bleeding time. Intraperitoneal injection of a single dose of 5 mg/kg BM-573 to rats inhibited U-46619 (9,11-dideoxy-9,11-methanoepoxy-prostaglandin F(2))-induced washed platelet aggregation 30 min and 1, 2, and 4 h after drug administration with a maximum antiplatelet effect observed after 1 and 2 h. In a rat model of thrombosis induced by ferric chloride application on the abdominal aorta, BM-573 significantly reduced the thrombus weight by 92.53, 80.20, 64.75, and 18.21% at doses of 5, 2, 0.5, and 0.2 mg/kg, respectively. Time to occlusion of abdominal aorta in the BM-573-treated group (41.50 +/- 5.21 min) was significantly prolonged compared with the vehicle-treated rats (16.16 +/- 0.79 min). Like furegrelate, seratrodast, and acetylsalicylic acid, BM-573 did not affect the tail bleeding time induced by tail transection in mice compared with vehicle-treated mice. Moreover, BM-573, a close derivative of the loop diuretic torasemide, failed to induce a significant increase in diuresis in rat and did not produce a decrease in blood glucose concentration as observed with the sulfonylurea glibenclamide. In conclusion, we have demonstrated that the nitrobenzenic sulfonylurea BM-573, an original combined thromboxane receptor antagonist and thromboxane synthase inhibitor, is a potent antithrombotic agent that does not affect bleeding time. Moreover, BM-573 lost the diuretic property of torasemide and has no impact on glycemia.

Animals↗

PubMed2004

Influence of zero flow pressure on fractional flow reserve.

Fractional flow reserve (FFR) is a commonly used index to assess the functional severity of a coronary artery stenosis. It is conventionally calculated as the ratio of the pressure distal (Pd) and proximal (Pa) to the stenosis (FFR= Pd/Pa). We hypothesize that the presence of a zero flow pressure (Pzf), requires a modification of this equation. Using a dynamic hydraulic bench model of the coronary circulation, which allows one to incorporate an adjustable Pzf, we studied the relation between pressure-derived FFR = Pdo/Pa, flow-derived true FFRQ = Qs/QN (= ratio of flow through a stenosed vessel to flow through a normal vessel), and the corrected pressure-derived FFRc = (Pd-Pzf)/(Pa-Pzf) under physiological aortic pressures (70 mmHg, 90 mmHg, and 110 mmHg). Imposed Pzf values varied between 0 mmHg and 30 mmHg. FFRc was in good agreement with FFRQ, whereas FFR consistently overestimated FFRQ. This overestimation increased when Pzf increased, or when Pa decreased, and could be as high as 56% (Pzf=30 mmHg and Pa =70 mmHg). According to our experimental study, calculating the corrected FFRC instead of FFR, if Pzf is known, provides a physiologically more accurate evaluation of the functional severity of a coronary artery stenosis.

Blood Pressure↗

PubMed2004

Functional analysis of the common carotid artery: relative distension differences over the vessel wall measured in vivo.

OBJECTIVES: Absolute (DeltaD) and relative (DeltaD/D) arterial diameter distension, parameters related to the elasticity of the vessel, can be measured in superficial arteries using ultrasound-based vessel "wall tracking" techniques. Currently available systems (e.g. the Wall Track System; WTS) measure the displacement of the media-adventitia transition (outer wall). We hypothesize that, given volume incompressibility of the vessel wall, DeltaD and DeltaD/D measured at the outer wall, significantly underestimate vessel distension at the lumen-intima interface (inner wall). METHODS: We measured DeltaD and DeltaD/D at both the inner and outer wall of the common carotid artery in 39 subjects (aged 18-83 years) using a new prototype "wall tracking" system based on the Vivid-7 scanner (GE Vingmed Ultrasound, Horten, Norway). In addition, DeltaD and DeltaD/D were also measured using WTS. RESULTS: As anticipated, tracking the inner wall yielded lower diastolic diameters than when tracking the outer wall (Ddia = 5.70 +/- 0.80 and 6.91+/- 0.98 mm, respectively, P < 0.0001). DeltaD (0.54+/- 0.16 versus 0.49 +/- 0.16 mm; P < 0.0001) and DeltaD/D (0.096+/- 0.030 versus 0.071+/- 0.026, P < 0.0001) were indeed larger at the inner than at the outer wall. For WTS, Ddia, DeltaD and DeltaD/D were 7.04 +/- 1.02 mm, 0.45 +/- 0.14 mm and 0.066 +/- 0.022, respectively. CONCLUSIONS: On average, DeltaD and DeltaD/D are 10 and 25% higher on the inner than on the outer wall, respectively. Follow-up studies in larger cohort trials are mandatory to assess whether tracking the inner wall yields arterial function parameters with a higher cardiovascular prognostic potential.

Adolescent↗

PubMed2004

Accuracy of commercially available processing algorithms for planar radionuclide ventriculography using data for a dynamic left ventricular phantom.

BACKGROUND: Automatic and semi-automatic algorithms to calculate ejection fraction (EF) from planar radionuclide ventriculography (PRV) have been used for many years in nuclear medicine. Validation of these algorithms is scarce and often performed on outdated versions of the software. Nevertheless, clinical trials where PRV is being used as the 'gold standard' for EF are numerous. Because of the importance attributed to the EF calculated by these programs, the accuracy of the resulting EF was assessed with a dynamic left ventricular physical phantom. METHODS: A dynamic left ventricular phantom was used to simulate 21 combinations of various ejection fractions (7-66%) and end diastolic volumes (27-290 ml). For each combination, a planar radionuclide ventriculograph was acquired, converted to an interfile format and transferred into processing stations with 10 different contemporaneously available commercial algorithms. The gold standard was the 'real' EF of the phantom, derived from the exact volume of the ventricle in end diastolic and end systolic position. Correlation and Bland-Altman analysis was performed between the real EF and the calculated EF. RESULTS: The correlation for all data was excellent (r=0.98), the mean difference was very acceptable (0.98%). Nevertheless, Bland-Altman analysis showed a significant trend in the difference between real and calculated EF, with a growing underestimation for higher ranges of EF, due to an overestimation of background in larger volumes compared to smaller ones. CONCLUSION: The determination of EF from PRV, calculated with commercially available algorithms, correlates closely to the real EF of a dynamic left ventricular phantom. This phantom can be used in the development and validation of algorithms for PRV studies, in software audits and in quality assurance procedures.

Algorithms↗

PubMed2004

Comparison between single-beat and multiple-beat methods for estimation of right ventricular contractility.

OBJECTIVE: It was investigated whether pharmacologically induced changes in right ventricular contractility can be detected by a so-called "single-beat" method that does not require preload reduction. DESIGN: Prospective animal research. SETTING: Laboratory at a large university medical center. SUBJECTS: Eight anesthetized pigs. INTERVENTIONS: End-systolic elastance values obtained by a recently proposed single-beat method (Eessb) were compared with those obtained using the reference multiple-beat method (Eesmb). MEASUREMENTS AND MAIN RESULTS: Administration of dobutamine increased Eesmb from 1.6 +/- 0.3 to 3.8 +/- 0.5 mm Hg/mL (p =.001), whereas there was only a trend toward an increase in Eessb from 1.5 +/- 0.2 to 1.7 +/- 0.4 mm Hg/mL. Esmolol decreased Eesmb from 1.7 +/- 0.3 to 1.1 +/- 0.2 mm Hg/mL (p =.006), whereas there was only a trend for a decrease in Eessb from 1.5 +/- 0.2 to 1.3 +/- 0.1. CONCLUSIONS: The present method using single-beat estimation to assess right ventricular contractility does not work as expected, since it failed to detect either increases or decreases in right ventricular contractility induced by pharmacologic interventions.

Animals↗

PubMed2004

Effect of a novel thromboxane A2 inhibitor on right ventricular-arterial coupling in endotoxic shock.

We investigated the effects of a dual thromboxane (TX)A2 synthase inhibitor and TXA2 receptor antagonist (BM-573) on right ventricular-arterial coupling in a porcine model of endotoxic shock. Thirty minutes before the onset of 0.5 mg/kg endotoxin infusion, six pigs (Endo group) received an infusion with a placebo solution, and six other pigs (Anta group) with BM-573. Right ventricular pressure-volume loops were obtained by the conductance catheter technique. The slope (Ees) of the end-systolic pressure-volume relationship and its volume intercept at 25 mmHg were calculated as measures of right ventricular systolic function. RV afterload was quantified by pulmonary arterial elastance (Ea), and Ees/Ea ratio represented right ventricular-arterial coupling. Mechanical efficiency was defined as the ratio of stroke work and pressure-volume area. In this model of endotoxic shock, BM-573 blunted the early phase of pulmonary hypertension, improved arterial oxygenation, and prevented a decrease in right ventricular myocardial efficiency and right ventricular dilatation. However, the drug could not prevent the loss of homeometric regulation and alterations in right ventricular-arterial coupling. In conclusion, dual TXA2 synthase inhibitor and receptor antagonists such as BM-573 have potential therapeutic applications, improving right ventricular efficiency and arterial oxygenation in endotoxic shock.

Animals↗

PubMed2004

The impact of pump speed and inlet cannulation site on left ventricular unloading with a rotary blood pump.

BACKGROUND: Ventricular assist devices are gaining ground in the therapeutic treatment of chronic heart failure. These devices are sometimes used as a bridge to recovery by unloading the left ventricle (LV) and restoring its function. It is therefore important to preserve the heart muscle and apply less invasive implantation methods. METHODS: In this study ventricular unloading was achieved in 7 healthy sheep with a rotary blood pump at different pump flow levels. Ventricular cannulation via the left atrium (LA) and through the mitral valve was compared to atrial cannulation. The unloading of the heart was assessed with LV pressure-volume loops, derived energetic parameters, and an estimate of LV wall stress. RESULTS: No significant difference between the cannulations was found for any flow or pressure. LA cannulation, however, resulted in significantly lower stroke volumes and stroke work for all pump flow levels. Irrespective of cannulation site, LV volumes and energetic parameters showed a significant decrease with increasing pump flow. CONCLUSION: LV assist with a rotary blood pump can provide sufficient unloading with atrial cannulation.

Animals↗

PubMed2004

In vitro assessment of the unloading and perfusion capacities of the PUCA II and the IABP.

The PUCA II pump is a minimally invasive intra-arterial left ventricular assist device that can be used as an alternative for the intra-aortic balloon pump (IABP). In this study, we assessed the cardiac unloading and organ perfusion capacities of both PUCA II and IABP in an in vitro set up, consisting of a heart simulator and a silicone arterial tree, mimicking anatomical geometry and flow distribution. The IABP was positioned in the descending aorta, while the PUCA II was tested both in 'trans-aortic' and 'abdominal' positions. All devices were driven by the same Arrow AutoCat IABP driver at different pump rates. Apart from flow, arterial pressure and pulse pressure, we also calculated haemodynamic indices for myocardial oxygen supply and demand. The 'abdominal' PUCA II assist and the IABP both provide mild unloading of the heart, and a limited improvement of arterial pressure and flow. The 'trans-aortic' PUCA II assist greatly enhances flow and pressure, but does not unload the heart properly in the tested configuration.

Animals↗

PubMed2003

Effects of endotoxic shock on right ventricular systolic function and mechanical efficiency.

OBJECTIVE: To investigate the effects of endotoxin infusion on right ventricular (RV) systolic function and mechanical efficiency. METHODS: Six anesthetized pigs (Endo group) received a 0.5 mg/kg endotoxin infusion over 30 min and were compared with six other anesthetized pigs (Control group) receiving placebo for 5 h. RV pressure-volume (PV) loops were obtained by the conductance catheter technique and pulmonary artery flow and pressure were measured with high-fidelity transducers. RESULTS: RV adaptation to increased afterload during the early phase of endotoxin-induced pulmonary hypertension (T30) was obtained by both homeometric and hetereometric regulations: the slope of the end-systolic PV relationship of the right ventricle increased from 1.4+/-0.2 mmHg/ml to 2.9+/-0.4 mmHg/ml (P<0.05) and RV end-diastolic volume increased from 56+/-6 ml to 64+/-11 ml (P<0.05). Consequently, right ventricular-vascular coupling was maintained at a maximum efficiency. Ninety minutes later (T120), facing the same increased afterload, the right ventricle failed to maintain its contractility to such an elevated level and, as a consequence, right ventricular-vascular uncoupling occurred. PV loop area, which is known to be highly correlated with oxygen myocardial consumption, increased from 1154+/-127 mmHg/ml (T0) to 1798+/-122 mmHg/ml (T180) (P<0.05) while RV mechanical efficiency decreased from 63+/-2% (T0) to 45+/-5% (T270) (P<0.05). CONCLUSIONS: In the very early phase of endotoxinic shock, right ventricular-vascular coupling is preserved by an increase in RV contractility. Later, myocardial oxygen consumption and energetic cost of RV contractility are increased, as evidenced by the decrease in RV efficiency, and right ventricular-vascular uncoupling occurs. Therefore, therapies aiming at restoring right ventricular-vascular coupling in endotoxic shock should attempt to increase RV contractility and to decrease RV afterload but also to preserve RV mechanical efficiency.

Animals↗

PubMed2003

Determinants of left ventricular preload-adjusted maximal power.

Maximal left ventricular (LV) hydraulic power output (PWR(max)), corrected for preload as PWR(max)/(V(ed))(beta) (where V(ed) is the end-diastolic volume and beta is a constant coefficient), is an index of LV contractility. Whereas preload-adjusted maximal power (PAMP) is usually calculated with beta = 2, there is uncertainty about the optimal value of beta (beta = 1 for the normal LV and 2 for the dilated LV). The aim of this work is to study the determining factors of beta. The data set consisted of 245 recordings (steady state and vena cava occlusion) in 10 animals in an ischemic heart pig model. The occlusion data yielded the slope (E(es); 2.01 +/- 0.77 mmHg/ml, range 0.71-4.16 mmHg/ml) and intercept (V(0); -11.9 +/- 22.6 ml; range -76 to 39 ml) of the end-systolic pressure-volume relation, and the optimal beta-factor (assessed by fitting an exponential curve through the V(ed)-PWR(max) relation) was 1.94 +/- 0.88 (range 0.29-4.73). The relation of beta with V(ed) was weak [beta = 0.60 + 0.02(V(ed)); r(2) = 0.20]. In contrast, we found an excellent exponential relation between V(0) and beta [beta = 2.16e(0.0189(V(0))), r(2) = 0.70]. PAMP, calculated from the steady-state data, was 0.64 +/- 0.40 mW/ml(2) (range 0.14-2.83 mW/ml(2)) with a poor correlation with E(es) (r = 0.30, P < 0.001). An alternative formulation of PAMP as PWR(max)/(V(ed) - V(0))(2), incorporating V(0), yielded 0.47 +/- 0.26 mW/ml(2) (range 0.09-1.42 mW/ml(2)) and was highly correlated with E(es) (r = 0.89, P < 0.001). In conclusion, correct preload adjustment of maximal LV power requires incorporation of V(0) and thus of data measured under altered loading conditions.

Animals↗

PubMed2003

Effects of levosimendan on right ventricular function and ventriculovascular coupling in open chest pigs.

OBJECTIVE: Levosimendan is a promising calcium sensitizer that potentially could be useful in settings of pulmonary vasoconstriction and right ventricular dysfunction. There is a shortage of information concerning its effects on right ventricular function and ventriculovascular coupling. The aim of the present study was to characterize the effects of levosimendan on right ventricular and pulmonary vascular function by means of pressure-volume and pulsatile flow analysis. DESIGN: Prospective laboratory investigation. SETTING: University hospital laboratory. SUBJECTS: Eight landrace pigs (mean weight, 37 kg). INTERVENTIONS: Following instrumentation with biventricular conductance catheters, pulmonary and right coronary artery flow probes, a high-fidelity pulmonary pressure catheter, and a right coronary venous catheter, hemodynamic measurements were performed in baseline conditions and during levosimendan infusion at three increasing plasma concentrations (mean values, 27.5, 67.6, and 142.5 ng/mL). MEASUREMENTS AND MAIN RESULTS: Levosimendan increased heart rate and cardiac output, reduced systemic vascular resistance, and had a positive inotropic effect on the left ventricle and increased left ventricular mechanical efficiency. Moreover, levosimendan increased right ventricular contractility and hydraulic power. However, total pulmonary vascular resistance and characteristic impedance did not change throughout the protocol, and right ventricular mechanical efficiency decreased slightly at the highest concentration of levosimendan. CONCLUSIONS: At clinical concentrations in the present model, levosimendan increases right ventricular contractility and performance without significantly influencing pulmonary vascular tone. Further studies are required in a model of pulmonary vasoconstriction to disclose possible pulmonary vasodilator effects of levosimendan.

Animals↗

PubMed2003

Unloading effect of a rotary blood pump assessed by mathematical modeling.

Due to the increased appeal of rotary blood pumps for long-term cardiac assist, we conducted a study of their capacity to unload the left ventricle (LV). We used a validated mathematical model of the cardiovascular system and implemented the pump characteristics of an investigational microdiagonal pump (Medos). The influence of the pump on systemic hemodynamics, LV energetic parameters, and wall stress was evaluated in continuous and synchronous pulsatile modes of operation. For the continuous mode simulations, the influence of heart rate, LV contractility, and pump speed was assessed in a parametric study. For the pulsatile mode, different onsets of a synchronous time-varying pump speed pattern were tested. Our data indicate that the effectiveness of unloading in continuous mode depends on the contractility of the native ventricle. Hypocontractile ventricles are most easily unloaded, while ventricles with moderate contractility require high continuous pump speeds to achieve notable unloading. In pulsatile mode, the pump timing is an important determinant of pump/cardiovascular system interaction, with a counterpulsation setting yielding the best unloading.

Biomechanical Phenomena↗

PubMed2003

Validation of gated blood-pool SPECT cardiac measurements tested using a biventricular dynamic physical phantom.

UNLABELLED: We have developed a biventricular dynamic physical cardiac phantom to test gated blood-pool (GBP) SPECT image-processing algorithms. Such phantoms provide absolute values against which to assess accuracy of both right and left computed ventricular volume and ejection fraction (EF) measurements. METHODS: Two silicon-rubber chambers driven by 2 piston pumps simulated crescent-shaped right ventricles wrapped partway around ellopsoid left ventricles. Twenty experiments were performed at Ghent University, for which right and left ventricular true volume and EF ranges were 65-275 mL and 55-165 mL and 7%-49% and 12%-69%, respectively. Resulting 64 x 64 simulated GBP SPECT images acquired at 16 frames per R-R interval were sent to Columbia University, where 2 observers analyzed images independently of each other, without knowledge of true values. Algorithms automatically segmented right ventricular activity volumetrically from left ventricular activity. Automated valve planes, midventricular planes, and segmentation regions were presented to observers, who accepted these choices or modified them as necessary. One observer repeated measurements >1 mo later without reference to previous determinations. RESULTS: Linear correlation coefficients (r) of the mean of the 3 GBP SPECT observations versus true values for right and left ventricles were 0.80 and 0.94 for EF and 0.94 and 0.95 for volumes, respectively. Correlations for right and left ventricles were 0.97 and 0.97 for EF and 0.96 and 0.89 for volumes, respectively, for interobserver agreement and 0.97 and 0.98 for EF and 0.96 and 0.90 for volumes, respectively, for intraobserver agreement. No trends were detected, though volumes and right ventricular EFs were significantly higher than true values. CONCLUSION: Overall, GBP SPECT measurements correlated strongly with true values. The phantom evaluated shows considerable promise for helping to guide algorithm developments for improved GBP SPECT accuracy.

Computer Simulation↗

PubMed2002

Preload-adjusted maximal power of right ventricle: contribution of end-systolic P-V relation intercept.

To assess whether preload-adjusted maximal power (PAMP), which is calculated as W(max)/V (where W(max) is maximal power and V(ed) is end-diastolic volume with beta = 2) is an index of right ventricular (RV) contractility, we measured RV pressure (P) and volume (V) and pulmonary artery pressure and flow in 10 dogs at baseline and after inotropic stimulation. PAMP was derived from steady-state data, whereas the slope (E(es)) and intercept (V(d)) of the end-systolic P-V relationship were derived from data obtained during vena caval occlusion. Inotropic stimulation increased E(es) (from 0.96 +/- 0.25 to 1.62 +/- 0.28 mmHg/ml; P < 0.001) and V(d) (from -3.0 +/- 17.2 to 12.4 +/- 10.8 ml; P < 0.05) but not PAMP (from 0.24 +/- 0.10 to 0.36 +/- 0.22 mW/ml(2); P = 0.09). We found a strong relationship between the optimal beta-factor for preload adjustment and V(d). A corrected PAMP, PAMP(c) = W(max)/(V(ed) - V(d))(2), which incorporated the V(d) dependency, was sensitive to the inotropic changes (from 0.23 +/- 0.12 to 0.54 +/- 0.17 mW/ml(2); P < 0.001) with a good correlation with E(es) (r = 0.88; P < 0.001).

Animals↗

PubMed2002

The role of whole blood viscosity in premature coronary artery disease in women.

BACKGROUND: Impaired hemorheology has been demonstrated in atherosclerotic disease and has shown a relationship with classical risk factors. Blood viscosity (eta), being the ratio of shear stress over shear rate, is an important parameter of hemorheology. In women with premature coronary artery disease (CAD), the underlying risk factors are a matter of debate and the role of whole blood viscosity in its pathogenesis has not been documented. AIM: To investigate the association of whole blood viscosity with premature CAD in women, with complaints suggestive of angina pectoris. METHODS: Eighty-eight women (mean age 53 years) were divided into two groups, those with a high likelihood of CAD (LIKELI+) and those with a low likelihood of CAD (LIKELI-), based on medical history and technical investigations. Assessment of risk factors comprised smoking, diabetes mellitus, arterial hypertension, left ventricular hypertrophy (LVH), systolic and diastolic blood pressures, total low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol, triglycerides, body mass index, menopause, hormone replacement therapy, uric acid and creatinine, and predicted 10-year cardiovascular risk according to the Framingham study was calculated. Whole blood viscosity was determined at 37 degrees C using a rotational cone-and-plate viscosimeter. RESULTS: Baseline characteristics did not differ significantly between the groups except for antiplatelet therapy (P=0.001), prevalence of diabetes mellitus (P=0.002), predicted 10-year cardiovascular risk (P=0.007), essential hypertension (P=0.02), LVH (P=0.03) and smoking habits (P=0.04). LIKELI+ women had a significantly higher whole blood viscosity at all shear rates compared with LIKELI- women (P<0.05). All blood viscosities measured from 25 to 125 s(-1) were highly significantly (P<0.0001) correlated with eta(250s(-1)). Univariate correlates with eta(250s(-1)) comprised triglycerides (P=0.006) and haematocrit (P=0.026). Binary logistic multivariate regression analysis for high likelihood of CAD revealed that only presence of arterial hypertension (P<0.0001) was predictive. Multiple regression analysis demonstrated that haematocrit (P=0.001) and likelihood of CAD (P=0.01) were the only significant determinants of eta(250s(-1)). CONCLUSION: In this study, blood viscosity did not appear as an independent risk factor for the prediction of premature CAD in women. Viscosity may act as a marker of CAD or of classical risk factors.

Adult↗