Biomedical subjects

C Corsi

Publications and source records attributed to C Corsi.

At least 19 recordsLinked to original sources

PubMed2006

Tracking of left ventricular long axis from real-time three-dimensional echocardiography using optical flow techniques.

Two-dimensional echocardiography (2DE) is routinely used in clinical practice to measure left ventricular (LV) mass, dimensions, and function. The reliability of these measurements is highly dependent on the ability to obtain nonforeshortened long axis (LA) images of the left ventricle from transthoracic apical acoustic windows. Real time three-dimensional echocardiography (RT3DE) is a novel imaging technique that allows the acquisition of dynamic pyramidal data structures encompassing the entire ventricle and could potentially overcome the effects of LA foreshortening. Accordingly, the aim of this paper was to develop a nearly automated method based on optical flow techniques for the measurement of the left ventricular (LV) LA throughout the cardiac cycle from RT3DE data. The LV LA measurements obtained with the automated technique has been compared with LA measurements derived from manual selection of the LA from a volumetric display of RT3DE data. High correlation (r = .99, SEE = 1.8%, y = .94x + 5.3), no significant bias (-0.18 mm), and narrow limits of agreement (SD: 1.91 mm) were found. The comparison between the LA length derived from 2DE and RT3DE data showed significant underestimation of the 2DE based measurements. In conclusion, this study proves that RT3DE data overcome the effects of foreshortening and indicates that the method we propose allows fast and accurate quantification of LA length throughout the cardiac cycle.

Algorithms↗

PubMed2005

Improved quantification of left ventricular mass based on endocardial and epicardial surface detection with real time three dimensional echocardiography.

OBJECTIVE: To develop a technique for volumetric analysis of real time three dimensional echocardiography (RT3DE) data aimed at quantifying left ventricular (LV) mass and to validate the technique against magnetic resonance (MR) assumed as the reference standard. DESIGN: RT3DE, which has recently become widely available, provides dynamic pyramidal data structures that encompass the entire heart and allows four dimensional assessment of cardiac anatomy and function. However, analysis techniques for the quantification of LV mass from RT3DE data are fundamentally two dimensional, rely on geometric modelling, and do not fully exploit the volumetric information contained in RT3DE datasets. Twenty one patients underwent two dimensional echocardiography (2DE), RT3DE, and cardiac MR. LV mass was measured from 2DE and MR images by conventional techniques. RT3DE data were analysed to semiautomatically detect endocardial and epicardial LV surfaces by the level set approach. From the detected surfaces, LV mass was computed directly in the three dimensional space as voxel counts. RESULTS: RT3DE measurement was feasible in 19 of 21 patients and resulted in higher correlation with MR (r = 0.96) than did 2DE (r = 0.79). RT3DE measurements also had a significantly smaller bias (-2.1 g) and tighter limits of agreement (2SD = +/-23 g) with MR than did the 2DE values (bias (2SD) -34.9 (50) g). Additionally, interobserver variability of RT3DE (12.5%) was significantly lower than that of 2DE (24.1%). CONCLUSIONS: Direct three dimensional model independent LV mass measurement from RT3DE images is feasible in the clinical setting and provides fast and accurate assessment of LV mass, superior to the two dimensional analysis techniques.

Echocardiography, Three-Dimensional↗

PubMed2004

Quantification of left ventricular modification in weightlessness conditions from the spatio-temporal analysis of 2D echocardiographic images.

Two-dimensional echocardiography (2DE) performed during flights with a parabolic trajectory to simulate weightlessness provides a unique means to study left ventricular (LV) modifications to prevent post-flight orthostatic intolerance in astronauts. However, conventional analysis of 2DE is based on manual tracings and depends on experience. Accordingly, the aim was objectively to quantify, from 2DE images, the LV modifications related to different gravity levels, by applying a semi-automated level-set border detection technique. The algorithm validation was performed by the comparison of manual tracing results, obtained by two independent observers with 20 images, with the semi-automated measurements. To quantify LV modifications, three consecutive cardiac cycles were analysed for each gravity phase (1 Gz, 1.8 Gz, 0 Gz). The level-set procedure was applied frame-by-frame to detect the LV endocardial contours and obtain LV area against time curves, from which end-diastolic (EDA) and end-systolic (ESA) areas were computed and averaged to compensate for respiratory variations. Linear regression (y = 0.91x + 1.47, r = 0.99, SEE:0.80cm2) and Bland-Altman analysis (bias = -0.58 cm2, 95% limits of agreement= +/- 2.14cm2) showed excellent correlation between the semi-automatic and manually traced values. Inter-observer variability was 5.4%, and the inter-technique variability was 4.1%. Modifications in LV dimensions during the parabola were found: compared with 1 Gz values, EDA and ESA were significantly reduced at 1.8 Gz by 8.8 +/- 5.5% and 12.1 +/- 10.1%, respectively, whereas, during 0 Gz, EDA and ESA increased by 13.3 +/- 7.3% and 11.6 +/- 5.1%, respectively, owing to abrupt changes in venous return. The proposed method resulted in fast and reliable estimations of LV dimensions, whose changes caused by different gravity conditions were objectively quantified.

Adult↗

PubMed2002

Fast interactive real-time volume rendering of real-time three-dimensional echocardiography: an implementation for low-end computers.

Real-time three-dimensional echocardiography (RT3DE) is an innovative cardiac imaging modality. However, partly due to lack of user-friendly software, RT3DE has not been widely accepted as a clinical tool. The object of this study was to develop and implement a fast and interactive volume renderer of RT3DE datasets designed for a clinical environment where speed and simplicity are not secondary to accuracy. Thirty-six patients (20 regurgitation, 8 normal, 8 cardiomyopathy) were imaged using RT3DE. Using our newly developed software, all 3D data sets were rendered in real-time throughout the cardiac cycle and assessment of cardiac function and pathology was performed for each case. The real-time interactive volume visualization system is user friendly and instantly provides consistent and reliable 3D images without expensive workstations or dedicated hardware. We believe that this novel tool can be used clinically for dynamic visualization of cardiac anatomy.

Artifacts↗

PubMed2002

Changes in left ventricular size during parabolic flights by two-dimensional echocardiography and level set method.

This study aims to evaluate changes on cardiac chambers size, induced by gravitational stresses. During parabolic flight, seven subjects underwent 2-D transthoracic echocardiography at three different gravity phases (1 Gz, 1.8 Gz, and 0 Gz). LV endocardial borders were detected applying a semi-automatic segmentation procedure based on level set methods. LV cavity area was computed frame-by-frame for a whole cardiac cycle during each gravity phase. Expected modifications in LV area with different gravity were found: at 1.8 Gz, end-diastolic (ED) and end-systolic (ES) areas were significantly (p<0.05) reduced of 10.7 +/- 5.4% and 21.6 +/- 11.1% respectively, compared to 1 Gz values, while they were increased of 11.2 +/- 5.4% and 11.1 +/- 6% during 0 Gz. Fractional area change was augmented of 20.9 +/- 29.1% at 1.8 Gz, while it remained unchanged at 0 Gz, compared with 1 Gz values. Furthermore, LV filling due to atrial contraction was increased at 0 Gz of 39 +/- 35.6%.

Adult↗

PubMed2001

Left ventricular endocardial surface detection based on real-time 3D echocardiographic data.

OBJECTIVE: A new computerized semi-automatic method for left ventricular (LV) chamber segmentation is presented. METHODS: The LV is imaged by real-time three-dimensional echocardiography (RT3DE). The surface detection model, based on level set techniques, is applied to RT3DE data for image analysis. The modified level set partial differential equation we use is solved by applying numerical methods for conservation laws. The initial conditions are manually established on some slices of the entire volume. The solution obtained for each slice is a contour line corresponding with the boundary between LV cavity and LV endocardium. RESULTS: The mathematical model has been applied to sequences of frames of human hearts (volume range: 34-109 ml) imaged by 2D and reconstructed off-line and RT3DE data. Volume estimation obtained by this new semi-automatic method shows an excellent correlation with those obtained by manual tracing (r = 0.992). Dynamic change of LV volume during the cardiac cycle is also obtained. CONCLUSION: The volume estimation method is accurate; edge based segmentation, image completion and volume reconstruction can be accomplished. The visualization technique also allows to navigate into the reconstructed volume and to display any section of the volume.

Echocardiography, Three-Dimensional↗

PubMed2001

Adenosine extracellular brain concentrations and role of A2A receptors in ischemia.

Various experimental approaches have been used to determine the concentration of adenosine in extracellular brain fluid. The cortical cup technique or the microdialysis technique, when adenosine concentrations are evaluated 24 hours after implantation of the microdialysis probe, are able to measure adenosine in the nM range under normoxic conditions and in the microM range under ischemia. In vitro estimation of adenosine show that it can reach 30 microM at the receptor level during ischemia, a concentration able to stimulate all adenosine receptor subtypes so far identified. Although the protective role of A1 receptors in ischemia seems consistent, the protective role of A2A receptors appears to be controversial. Both A2A agonists and antagonists have been shown to be neuroprotective in various in vivo ischemia models. Although A2A agonists may be protective, mainly through peripherally mediated effects, A2A antagonists may be protective through local brain mediated effects. It is possible that A2A receptors are tonically activated following a prolonged increase of adenosine concentration, such as occurs during ischemia. A2A receptor activation desensitizes A1 receptors and reduces A1 mediated effects. Under these conditions A2A receptor antagonists may be protective by potentiating all the neuroprotective A1 mediated effects, including decreased neurotoxicity due to reduced ischemia induced glutamate outflow.

Adenosine↗

PubMed2001

A semi-automatic method for left ventricle volume estimate: an in vivo validation study.

This study aims to the validation of the left ventricular (LV) volume estimates obtained by processing volumetric data utilizing a segmentation model based on level set technique. The validation has been performed by comparing real-time volumetric echo data (RT3DE) and magnetic resonance (MRI) data. A validation protocol has been defined. The validation protocol was applied to twenty-four estimates (range 61-467 ml) obtained from normal and pathologic subjects, which underwent both RT3DE and MRI. A statistical analysis was performed on each estimate and on clinical parameters as stroke volume (SV) and ejection fraction (EF). Assuming MRI estimates (x) as a reference, an excellent correlation was found with volume measured by utilizing the segmentation procedure (y) (y=0.89x + 13.78, r=0.98). The mean error on SV was 8 ml and the mean error on EF was 2%. This study demonstrated that the segmentation technique is reliably applicable on human hearts in clinical practice.

Echocardiography, Three-Dimensional↗

PubMed2000

Striatal A2A adenosine receptor antagonism differentially modifies striatal glutamate outflow in vivo in young and aged rats.

The effect of the adenosine A2A receptor antagonist SCH 58261 on glutamate release was investigated in the striatum of young and old rats by microdialysis experiments. SCH 58261 (50 nM) significantly decreased the spontaneous and K+-evoked glutamate outflow in young rats. In aged rats, spontaneous glutamate outflow was significantly reduced in comparison to young rats and SCH 58261 significantly increased spontaneous and K+-evoked glutamate outflow. It is suggested that the opposite effects of the A2A antagonist on glutamate outflow in young and aged rats can be respectively attributed to blockade of striatal A2A adenosine receptors located on glutamatergic terminals and on the striatal indirect output pathway.

Adenosine↗

PubMed2000

Real-time 3D echocardiographic data analysis for left ventricular volume estimation.

A new computerized semi-automatic method for left ventricular chamber segmentation is presented. The left ventricle is imaged by real-time three-dimensional echocardiography. This real-time data acquisition method allows accurate evaluation of chamber size and shape, even in case there are cavities with irregular geometry. The surface detection model is based on a partial differential equation that propagates interfaces with curvature dependent speeds. The equation is solved by applying numerical methods for conservation laws. The method consists of one step only. Initial conditions are manually established on a small subset of slices of the entire volume. The solution obtained is a surface corresponding to the surface between LV cavity and LV endocardium. This mathematical model is applied to sequences of frames of human hearts (volume range: 34-109 ml) imaged by real-time 3D echocardiography. Volume estimates show an excellent correlation with those obtained by manual tracing (r=0.99).

Cardiac Volume↗

PubMed1999

Effect of adenosine A2A receptor stimulation on GABA release from the striatum of young and aged rats in vivo.

The effect of the adenosine A2A receptor agonist CGS 21680 on GABA release from the striatum was investigated in vivo in young and old rats by microdialysis experiments. CGS 21680 at 10 microM significantly increased GABA spontaneous outflow in young but not in old rats. Conversely, CGS 21680 significantly increased potassium-evoked GABA release in old but not in young rats. The stimulating effect of CGS 21680 on spontaneous GABA release may be both secondary to an increased outflow of excitatory amino acids and to the removal, brought about by A2A receptor stimulation, of the inhibitory influence exerted by dopamine through D2 receptors on GABA-enkephalinergic neurones. The stimulating effect of CGS 21680 on potassium-evoked GABA release in old rats may be ascribed to an age-dependent imbalance in favour of adenosine vs. dopamine, recently described in the striatum of old rats.

Adenosine↗

PubMed1999

Effect of N-methyl-D-aspartate on motor activity and in vivo adenosine striatal outflow in the rat.

It has been previously found that the systemic administration of low doses of N-methyl-D-aspartate (NMDA) in mice induces motor depression. The effects of the systemic administration of different doses of NMDA (10, 30 and 60 mg/kg s.c.) on the motor activity and on the in vivo extracellular levels of adenosine in the striatum was studied in Sprague-Dawley rats. The adenosine concentration in samples of perfusate was determined 24 h after implantation of a transverse microdialysis probe. At 30 and 60 mg/kg, but not 10 mg/kg, NMDA induced both a significant motor depression (motility and rearing) and a significant increase in the striatal extracellular levels of adenosine. Both the motor depression and the changes in the extracellular levels of adenosine were only evident during the first 30 min after NMDA administration. The non-competitive NMDA receptor antagonist MK-801 (0.1 mg/kg s.c.) completely counteracted the effects of NMDA (30 mg/kg s.c.) on motor activity (motility) and on the striatal extracellular levels of adenosine. The correlation between the behavioural and the biochemical data strongly support the hypothesis that adenosine release in the striatum is a main mechanism responsible for the motor depressant effects produced by the systemic administration of NMDA.

Adenosine↗

PubMed1999

Striatal A2A adenosine receptors differentially regulate spontaneous and K+-evoked glutamate release in vivo in young and aged rats.

The effect of the adenosine A2A receptor agonist CGS 21680 on glutamate and aspartate release was investigated in the striatum of young and old rats by microdialysis experiments. CGS 21680 (10 microM) significantly increased glutamate and aspartate spontaneous outflow in young but not in old rats. On the contrary, CGS 21680 induced the same decrease in K+-evoked glutamate outflow in both young and aged rats. A lower dose of CGS 21680 (1 microM) failed to modify either spontaneous or K+-evoked outflow. It is suggested that the opposite effects of the A2A agonist on excitatory amino acid outflow may be respectively mediated by striatal A2A adenosine receptors located on glutamatergic terminals and on the striatal indirect output pathway.

Adenosine↗

PubMed1999

Striatal outflow of adenosine, excitatory amino acids, gamma-aminobutyric acid, and taurine in awake freely moving rats after middle cerebral artery occlusion: correlations with neurological deficit and histopathological damage.

BACKGROUND AND PURPOSE: While a number of studies have investigated transmitter outflow in anesthetized animals after middle cerebral artery occlusion (MCAO) performed by craniectomy, studies have never been performed after MCAO induced by intraluminal filament. In addition, it has been reported that after MCAO, infarct volume correlates with functional outcome and with transmitter outflow, although there are no studies that demonstrate a direct correlation between transmitter outflow and functional outcome. The purpose of the present study was to assess excitatory amino acids, gamma-aminobutyric acid, taurine, and adenosine outflow in awake rats after intraluminal MCAO and to determine whether, in the same animal, outflow was correlated with neurological outcome and histological damage. METHODS: Vertical microdialysis probes were placed in the striatum of male Wistar rats. After 24 hours, permanent MCAO was induced by the intraluminal suture technique. The transmitter concentrations in the dialysate were determined by high-performance liquid chromatography. Twenty-four hours after MCAO, neurological deficit and histological outcome were evaluated. RESULTS: All transmitters significantly increased after MCAO. Twenty-four hours after MCAO, the rats showed a severe sensorimotor deficit and massive ischemic damage in the striatum and in the cortex (9+/-2% and 25+/-6% of hemispheric volume, respectively). Significant correlations were found between the efflux of all transmitters, neurological score, and striatal infarct volume. CONCLUSIONS: In this study, for the first time, amino acid and adenosine extracellular concentrations during MCAO by the intraluminal suture technique were determined in awake and freely moving rats, and a significant correlation was found between transmitter outflow and neurological deficit. The evaluation of neurological deficit, histological damage, and transmitter outflow in the same animal may represent a useful approach for studying neuroprotective properties of new drugs/agents against focal ischemia.

Adenosine↗

PubMed1996

The source of brain adenosine outflow during ischemia and electrical stimulation.

Adenosine outflow and adenosine and adenine nucleotide content of hippocampal slices were evaluated under two different experimental conditions: ischemia-like conditions and electrical stimulation (10 Hz). Five minutes of ischemia-like conditions brought about an 8-fold increase in adenosine outflow in the following 5 min during reperfusion, and a 2-fold increase in adenosine content, a 43% decrease in ATP, a 72% increase in AMP and a 30% decrease in energy charge (E.C.) at the end of the ischemic period. After 10 min of reperfusion ATP, AMP and E.C. returned to control values, while the adenosine content was further increased. Five minutes of electrical stimulation brought about an 8-fold increase in adenosine outflow that peaked 5 min after the end of stimulation, a 4-fold increase in adenosine content and an 18% decrease in tissue E.C. at the end of stimulation. After 10 min of rest conditions the adenosine content and E.C. returned to basal values. The origin of extracellular adenosine from S-adenosylhomocysteine (SAH) was examined under the two different experimental conditions. The SAH hydrolase inhibitor, adenosine-2,3-dialdehyde (10 microM), does not significantly modify the adenosine outflow evoked by electrical stimulation or ischemia-like conditions. This finding excludes a significant contribution by the transmethylation pathway to adenosine extracellular accumulation evoked by an electrical or ischemic stimulus, and confirms that the most likely source of adenosine is from AMP dephosphorylation.

Adenine Nucleotides↗

PubMed1995

Regulation of extracellular adenosine levels in the striatum of aging rats.

Extracellular adenosine concentrations, evaluated by microdialysis in the striatum of young and aged rats, were 66.8 +/- 0.7 and 71.6 +/- 1.0 nM, respectively. The adenosine deaminase inhibitor EHNA (100 microM) increased the extracellular adenosine levels in young rats only. The adenosine kinase inhibitor iodotubercidin (10 microM) brought about the same increase in young and aged rats. In aged rats the resting adenosine outflow was reduced by the N-methyl-D-aspartate (NMDA) receptor antagonist D-(-)-2-amino-7-phophonoheptanoic acid (D-AP7) (1 mM). It is concluded that extracellular levels of adenosine in the striatum are not affected by age, irrespective of the differences in adenosine deaminase activity and that the release of excitatory amino acids is responsible for much of resting adenosine outflow in aged but not in young rats.

2-Amino-5-phosphonovalerate↗

PubMed1995

The source of brain adenosine outflow during ischemia and electrical stimulation.

Adenosine outflow and adenosine and adenine nucleotide content of hippocampal slices were evaluated under two different experimental conditions: ischemia-like conditions and electrical stimulation (10 Hz). Five minutes of ischemia-like conditions brought about an 8-fold increase in adenosine outflow in the following 5 min during reperfusion, and a 2-fold increase in adenosine content, a 43% decrease in ATP, a 72% increase in AMP and a 30% decrease in energy charge (EC) at the end of the ischemic period. After 10 min of reperfusion ATP, AMP and EC returned to control values, while the adenosine content was further increased. Five minutes of electrical stimulation brought about an 8-fold increase in adenosine outflow that peaked 5 min after the end of stimulation, a 4-fold increase in adenosine content and an 18% decrease in tissue EC at the end of stimulation. After 10 min of rest conditions the adenosine content and EC returned to basal values. The origin of extracellular adenosine from S-adenosylhomocysteine (SAH) was examined under the two different experimental conditions. The SAH hydrolase inhibitor, adenosine-2,3-dialdehyde (10 microM), does not significantly modify the adenosine outflow evoked by electrical stimulation or ischemia-like conditions. This finding excludes a significant contribution by the transmethylation pathway to adenosine extracellular accumulation evoked by an electrical or ischemic stimulus, and confirms that the most likely source of adenosine is from AMP dephosphorylation.

Adenine Nucleotides↗

PubMed1995

L-propionylcarnitine effect on postexercise and postischemic hyperemia in patients affected by peripheral vascular disease.

The hemodynamic effect of L-propionylcarnitine (LPC) administered intravenously was evaluated in a double-blind, randomized, three-period crossover study in 12 men (aged sixty to seventy-five years) with Leriche-Fontaine stage II peripheral arterial disease of lower limbs. At baseline, maximum working capacity of each patient was determined by a standardized ergometric test. This test was repeated at 80% of each patient's maximum working capacity before and after intravenous administration of LPC. Each patient received three single doses of 300 mg, 600 mg, and 1200 mg of LPC with a two-day rest period between them. Hemodynamic variables measured by strain-gauge plethysmography were: peak blood flow, peak flow time, and halftime and total time of hyperemia both after exercise and after induction of ischemia (with an occlusion cuff). LPC administration significantly shortened the halftime as well as the total time of hyperemia after exercise and after ischemia. With the two highest doses, LPC shortened the peak flow time after exercise. The peak blood flow after exercise and after ischemia increased, but this increase did not reach statistical significance. The results obtained indicate that LPC improves circulatory reserve of the ischemic limb and has no effect on heart rate and arterial blood pressure. No adverse events were reported. The effect of LPC on the hyperemic response to stress, mainly on halftime of hyperemia, is possibly due to a drug-induced increase of adenosine triphosphate utilization by the ischemic tissues.

Aged↗