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Biomedical subjects

P Besse

Publications and source records attributed to P Besse.

At least 37 records · Page 2Linked to original sources
PubMed1998

Primary cardiac lymphoma in an immunocompetent woman.

We report a fatal primary cardiac non-Hodgkin's lymphoma in a 62 years old immunocompetent woman presenting with tamponade and complete atrioventricular block. CT-scan, echocardiography and autopsy examination showed a tumor largely infiltrating the heart without extracardiac involvement. A surgical biopsy revealed high grade B-cell non-Hodgkin's lymphoma with a misleading myelomonocytic CD68 (KPI) expression. Polymerase Chain Reaction analysis revealed a clonal rearrangement of the immunoglobulin heavy chain gene and confirmed the B-cell origin of the lymphoma. Our report also emphasizes the role of immunohistochemical and molecular techniques in the diagnosis.

Antigens, CD↗
PubMed1997

Impact of restenosis after optimal directional coronary atherectomy on regional left ventricular function.

To assess the effect of optimal directional coronary atherectomy (DCA) on restenosis and left ventricular (LV) function, 95 patients who underwent DCA and adjunctive balloon angioplasty for de novo lesions were prospectively followed for 6 months. Absolute and relative coronary lumen measurements were analyzed with online quantitative coronary angiography. LV volumes, ejection fraction, and segmental wall motion were measured off-line according to the radial method for LV cineangiograms acquired in a right anterior oblique projection. Target vessels were the left anterior descending artery in 63 patients and right coronary artery in 32. Mean (+/- SD) reference diameter was 3.58 +/- 0.65 mm. Mean lumen diameter improved significantly after DCA from 1.19 +/- 0.44 to 3.03 +/- 0.45 mm, yielding a 14 +/- 10% residual stenosis. Overall angiographic restenosis rate (> 50% stenosis in diameter) at control was 23%. In patients without restenosis, there were no significant changes in LV volumes or in LV pressures. In this subgroup, ejection fraction improved significantly in the left anterior descending group (mean difference 3 +/- 10%, p < 0.04). Moreover, there was an increase in fractional shortening of all anterior segments (mean difference 11 +/- 16%, p < 0.005). Improvement in fractional shortening was less marked in the right coronary artery group even without restenosis. We conclude that: (1) optimal DCA can achieve a low restenosis rate in selected large vessels, (2) long-term beneficial effects on regional LV function are possible, particularly in patients with left anterior descending disease and in the absence of coronary restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1997

Reduced basal NO-mediated dilation and decreased endothelial NO-synthase expression in coronary vessels of spontaneously hypertensive rats.

Basal vasomotor tone in coronary vessels is, in part, maintained by nitric oxide (NO) production by endothelial constitutive NO synthase (ecNOS). Alteration of coronary circulation observed in left ventricular hypertrophy secondary to hypertension could be associated with a decrease in NO production. The aim of this study was to measure: (1) coronary flow in the Langendorff-perfused heart model at baseline, after maximum vasodilation in response to adenosine (10(-5) M), after endothelium-dependent vasodilation in response to bradykinin (10(-8) M) and after ecNOS inhibition by nitro-L-arginine methyl ester (L-NAME) (10(-4) M); (2) medial thickening of coronary microvessels and perivascular collagen on histological heart sections; and (3) ecNOS expression by immunohistochemical staining in these vessels using 20-week-old spontaneously hypertensive (SHR) and Wistar-Kyoto control rats (WKY). These measurements were determined by computer-directed color analysis. When SHR were compared with WKY rats, we found: (1) a decrease in basal flow (10.1+/-0.6 v 15.3+/-1.2 ml/min/g, n=10, P<0.0001), in maximum flow (15.4+/-0.7 v 24.3+/-1.3 ml/min/g, n=10, P<0.001), in bradykinin-induced flow increment (1.5+/-0.3 v 2.6+/-0.3 ml/min/g, n=5, P<0.05) and in L-NAME-sensitive flow (3.3+/-0.6 v 6.3+/-0.9 ml/min/g, n=7, P<0.05); (2) an increase in medial thickness (9.4+/-0.6 v 5.4+/-0.3 microm, n=8, P<0.001) and in perivascular collagen area (1509+/-311 v 462+/-120 microm2, n=8, P<0.01) of coronary arterioles; and (3) a decrease in ecNOS expression in the endothelium (ecNOS-stained cross-sectional area in arterioles: 40.0+/-9.1 v 84.6+/-9.0 microm2, n=7, P<O.005). These results suggest that in SHR the decrease in basal coronary flow can be related to a structural alteration of the microvessels with an increase of perivascular collagen but also to a decrease in ecNOS expression which might be associated with reduced NO production.

Animals↗
PubMed1997

[Predictive factors of coronary restenosis after optimal directional atherectomy. A multivariate analysis apropos of 102 patients].

The authors studied 102 patients prospectively who were undergoing coronary atherectomy optimised by balloon dilatation in order to assess the restenosis rate at 6 months. The coronary lesions were measured in a reproducible manner by quantitative angiography. The vessels dilated were the left anterior descending in 66 patients and the right coronary artery in 36 patients. The reference diameter was on average of 3.57 +/- 0.64 mm. Atherectomy increased the minimal diameter of the lesion of 1.20 +/- 0.44 to 3.01 +/- 0.44 mm giving a residual stenosis of 15 +/- 11%. At six months, 25% of patients had developed a restenosis (> 50% stenosis) with a residual lumen of 2.15 +/- 0.77 mm. The predictive factors of restenosis were the initial absolute gain, the length of the lesion, the reference diameter of the vessel and the presence of an endoluminal thrombus. In multivariate analysis, a small initial gain (p < 0.02) and length of stenosis (p < 0.02) were independently correlated with restenosis. The authors conclude: 1) that optimal atherectomy is associated with acceptable restenosis rates in selected vessels, 2) that short stenoses of large diameter arteries may be a privileged indication of the technique if the best results are obtained.

Adult↗
PubMed1997

[Restenosis after optimal coronary atherectomy and influence on left ventricular function].

The authors prospectively assessed 95 patients undergoing optimal guided atherectomy to assess the incidence of restenosis at 6 months. The coronary lesions were measured by a system of quantitative angiography to ensure reproducibility. Ventricular volumes, ejection fraction and segmental wall motion were assessed by ventriculography performed in the right anterior oblique projection. Sixty-three patients underwent atherectomy of the left anterior descending artery and 32 patients of the right coronary artery. The reference diameter was 3.58 +/- 0.65 mm. Atherectomy increased the minimal diameter of the lesion from 1.19 +/- 0.44 to 3.03 +/- 0.45 mm, with a residual stenosis of 14 +/- 10% of the diameter. At 6 months, 23% of patients had restenosed (> 50% stenosis) with a residual lumen at 1.16 +/- 0.39 mm. In the absence of restenosis, there was no significant change in left ventricular volumes or pressures and the global ejection fraction increased by +4 +/- 9% (p < 0.01), mainly in the group undergoing left anterior descending atherectomy. Moreover, fractional shortening increased in the anterior segments (+11 +/- 18%; p < 0.001). The authors conclude that optimal atherectomy is associated with acceptable rates of restenosis and that medium-term benefits of segmental wall motion are observed in patients without angiographic restenosis, mainly in those undergoing the procedure on the left anterior descending artery.

Adult↗
PubMed1997

[Local progression of atherosclerosis after optimal directional atherectomy. Endocoronary ultrasonography of 17 patients].

In vivo endovascular ultrasonography has confirmed the extension of atheroma to angiographically normal segments. The authors set out to determine by endocoronary ultrasonography if the introduction of the atherotome changed the intimal thickness 20 mm proximal and distal to the site treated. The area circumscribed by the external elastic layer (EEL) and the surface area of the lumen was measured in 17 patients: 1) before atherectomy; 2) after atherectomy; 3) at control 6 months later. Atherectomy immediately increased the luminal area at the site dilated from 1.9 + 0.9 to 8.1 +/- 2mm (p < 0.001). At the proximal segment, the surface area of the lumen was unchanged (mean + 0.6 +/- 1.5 mm2; p = 0.13). Similarly the procedure did not change the surface circumscribed by the EEL (mean + 0.8 +/- 3.2 mm2; p = 0.32) in this zone. The same results were observed at the distal site. At 6 months, the areas under the EEL and those of the lumen were unchanged at the unoperated sites. The mean of the differences (+/- 1 SD) for the area under the EEL was respectively -0.2 +/- 1.5 mm2 proximally and +0.7 +/- 2.5 mm2 distally. The means for the luminal area were 0.2 +/- 1 mm2 proximally and -0.01 +/- 1.1 mm2; distally. At the site of atherectomy, the luminal surface increased (+2.0 +/- 2.6 mm2; p < 0.01) as did the area under the EEL (+2.0 +/- 3.5 mm2; p < 0.05). This preliminary series shows no significant progression of atherosclerosis at the sites not affected by atherectomy.

Adult↗
PubMed1996

Development of the model of rat isolated perfused heart for the evaluation of anthracycline cardiotoxicity and its circumvention.

1. In order to develop a predictive model for the preclinical evaluation of anthracycline cardiotoxicity and the means of preventing it, we have studied the functional parameters of perfused hearts isolated from rats receiving repeated doses of several anthracyclines. 2. The anthracyclines studied were doxorubicin, epirubicin, pirarubicin and daunorubicin, and we also studied a liposomal formulation of daunorubicin (DaunoXome) and the co-administration of dexrazoxane (ICRF-187) and doxorubicin. 3. Anthracyclines were administered i.p. at equimolar doses corresponding to 3 mg kg-1 per injection of doxorubicin, every other day for a total of six doses. Dexrazoxane was used at the dose of 30 mg kg-1 per injection and was administered either 30 min before or 30 min after doxorubicin. We evaluated any general toxicity towards the animals as well as alterations of left ventricular contractility and relaxation ex vivo. 4. Epirubicin and daunorubicin were significantly less cardiotoxic than doxorubicin, and neither pirarubicin nor DaunoXome caused significant alterations in cardiac function. There was a direct relationship between the decrease in cardiac contractility or relaxation and anthracycline accumulation in the heart, evaluated after the same treatment schedule. 5. Dexrazoxane induced a significant protection against doxorubicin-induced cardiac toxicity when administered 30 min before doxorubicin, whereas this protection was ineffective when administered 30 min after doxorubicin. Direct perfusion of DaunoXome in isolated hearts of untreated animals resulted in a 12-fold reduction of the accumulation of daunorubicin in heart tissue as compared to the perfusion of free daunorubicin, and did not cause alterations in cardiac function at a dosage for which free daunorubicin induced major alterations. 6. The isolated perfused rat heart appears to be a valuable model for screening of new anthracyclines and of strategies for circumventing anthracycline cardiotoxicity.

Animals↗
PubMed1996

[A study of platelet activation following coronary angioplasty. Effect on acute occlusion and restenosis].

The development of monoclonal anti-platelet antibodies to activation-dependent epitopes has made possible the study of the appearance of activated platelets in the blood by cytometry. This was undertaken in 35 patients undergoing coronary angioplasty. Blood was sampled through the femoral venous catheter introducer before the procedure, at 3 minutes and 3, 24 and 48 hours after angioplasty. Systematic coronary angiography was performed at about 6 months and vessel diameters were quantified by a digitised technique. In general, platelet activation was not observed before angioplasty or in the first hours following the procedure. On the other hand, a significant number of activated platelets was observed secondarily : 7 +/- 7.3% at the 24th hour and 6.8 +/- 5.9% at the 48th hour. There was a significant correlation between the level of platelet activation before angioplasty and that at the 24th hour (r = 0.52, p = 0.01). There was a tendency to more activated circulating platelets before and 24 hours after angioplasty in patients with acute occlusion. The correlation coefficient between the level of activated platelets 24 hours after angioplasty and progression of stenosis at 6 months was not statistically significant (r = 0.29). Therefore, the authors demonstrated platelet activation, which was sometimes considerable, inconstantly in circulating venous blood of patients with angina 24 hours after coronary angioplasty despite treatment with aspirin. Activated platelets may play a role in constituting acute occlusion by thrombosis but their detection was not predictive of restenosis.

Adult↗
PubMed1996

PAICA: a method for characterizing platelet-associated antibodies--its application to the study of idiopathic thrombocytopenic purpura and to the detection of platelet-bound c7E3.

In idiopathic thrombocytopenic purpura (ITP), autoantibodies reacting with antigens on the platelet membrane bring about accelerated platelet destruction. We now report PAICA ("Platelet-Associated IgG Characterization Assay"), a method for detecting autoantibodies bound to specific membrane glycoproteins in total platelet lysates. This monoclonal antibody (MAb) capture assay takes into account the fact that antibodies on circulating platelets may be translocated to internal pools as well as being on the surface. A total of twenty ITP patients were examined by PAICA, and the results compared with those obtained by measuring (i) serum antibodies bound to paraformaldehyde-fixed control platelets by ELISA, (ii) IgG bound to the surface of the patient's own platelets by flow cytometry (PSIgG), (iii) total platelet-associated IgG (PAIgG) by ELISA and (iv) serum antibodies reacting with control platelets by MAIPA ("Monoclonal Antibody-specific Immobilization of Platelet Antigens"). Of twelve patients with elevated PAIgG, nine had increased PSIgG yet eleven reacted positively in PAICA. Of these, eight possessed antibodies directed against GP IIb-IIIa, two against GP Ib-IX and one patient possessed antibodies directed against GP IIb-IIIa and GP Ia-IIa respectively. Only seven of the patients possessed serum antibodies detectable by MAIPA. PAICA was also able to detect platelet-associated c7E3 (the chimeric form of Fab fragments of the MAb 7E3) following its infusion during antithrombotic therapy, when it proved more sensitive over a seven-day period than a MAIPA assay adapted for assessing surface-bound antibody. We propose that PAICA provides added sensitivity to the detection of platelet-associated antibodies in immune thrombocytopenias or following therapy with humanized MAbs.

Adult↗
PubMed1995

Evaluation of anthracycline cardiotoxicity with the model of isolated, perfused rat heart: comparison of new analogues versus doxorubicin.

We have compared the cardiotoxicity of 3 anthracyclines in a model of isolated perfused rat heart using the Langendorff technique. The contractile state and ventricular compliance were studied. Doxorubicin, epirubicin and pirarubicin were perfused at concentrations of 10(-6) and 10(-5) M during 70 min. The cardiac accumulation of the drugs was studied by HPLC. No significant alteration of cardiac functional parameters was observed at 10(-6) M. At 10(-5) M, epirubicin produced a significantly greater alteration of cardiac contractility than doxorubicin, whereas pirarubicin exerted first an inotropic effect followed by a recovery to initial values at the 60th min. Anthracycline accumulation in the heart was dose-dependent; epirubicin accumulated to a 30% greater extent than doxorubicin and pirarubicin heart concentrations were 4-5 times higher than those of doxorubicin at the end of the perfusion. These results suggest that doxorubicin and epirubicin have the same intrinsic cardiac toxicity, and that their distinct clinical cardiotoxicity must be explained by pharmacokinetic differences, whereas pirarubicin is much less cardiotoxic than the other anthracyclines because of different pharmacodynamic properties.

Animals↗
PubMed1995

Flow cytometry reveals activated GP IIb-IIIa complexes on platelets from patients undergoing thrombolytic therapy after acute myocardial infarction.

We report the detection of activated GP IIb-IIIa complexes on platelets of patients undergoing thrombolytic therapy after acute myocardial infarction. Protocols were established for the monoclonal antibodies (mAbs): VH10, anti-P-selectin, a marker of platelet secretion; 9F9 and F26, two anti-RIBS (receptor-induced binding sites) mAbs specific for fibrinogen (Fg) bound to the GP IIb-IIIa receptor. Of ten patients studied: two were treated with streptokinase, four with APSAC (anisoylated plasminogen-streptokinase activator complex), and three with rt-PA. Platelets were tested on at least five occasions in the week following therapy. The percentage of platelets positive with 9F9 was often high, and reached a maximum within three days. By this time, plasma Fg levels, which fell during fibrinolysis, had begun to return to normal. Levels of activated platelets had fallen to baseline after 7 days. PAC-1, a mAb which binds directly to the activated GP IIb-IIIa complex, confirmed the results with 9F9, but F26 was a less sensitive probe. Binding of the anti-P-selectin mAb (VH10) was low, showing that little secretion had occurred. A concentration-dependent inhibition of 9F9 binding by RGDW peptide, a competitive inhibitor for Fg on GP IIb-IIIa, confirmed that Fg (or epitope-containing degradation products) were being located by the antibody. The activation of GP IIb-IIIa occurred despite the patients receiving aspirin and heparin. Thus platelets of some fibrinolytic patients have an increased tendency for surface activation within the first 72 h after treatment, a finding which would be compatible with an increased thrombotic tendency.

Adult↗
PubMed1995

[Value of end diastolic pulmonary venous flow in the estimation of left ventricular diastolic pressure].

The aim of this study was to analyse the possible relationship between inversion of the end diastolic wave of pulmonary venous flow (Avp) recorded by transoesophageal echocardiography in the left superior pulmonary vein and left ventricular end-diastolic pressures (LVEDP) at cardiac catheterisation. In this series of patients, there was a poor correlation between the E/A ratio of transmitral blood flow and LVEDP. On the other hand, there was a better correlation between LVEDP and the difference of duration of the end diastolic Avp wave and the A wave of mitral flow. An even better correlation was found between LVEDP with respect to the contribution of atrial systole and the difference of duration Avp-A. When the pressure due to atrial contraction exceeds 15 mmHg, the difference between the durations of pulmonary and mitral A waves increases. Therefore, when the duration of the end diastolic Avp is greater than that of the mitral A wave, a LVEDP of over 15 mmHg may be predicted with a sensitivity of 88% and a specificity of 74%.

Adult↗
PubMed1994

Effect of angiotensin II on calcium release phenomena in normal and hypertrophied single cardiac myocytes.

The effects of angiotensin II (Ang II) (10(-9) M to 10(-7) M) on calcium releases were established in ventricular myocytes from normal and renal hypertensive adult rats. From each peak systolic indo-1 ratio (405 nm/480 nm), amplitude variation, duration (rise time and fall time), and frequency of spontaneous calcium releases were investigated on freshly isolated cardiomyocytes at rest or under electrical stimulation. The following changes were observed: (1) in spontaneous contracting myocytes, an increase in frequency of calcium transients at 10(-7) M in normal cells (+157%, P < 0.05) and at whatever angiotensin II concentration in hypertrophied cells (10(-9) M: +79% P < 0.05; 10(-8) M +82%, P < 0.01; 10(-7) M: +285%, P < 0.01) with a greater sensitivity of hypertrophied cells to Ang II (P < 0.05 at 10(-9) M, P < 0.01 at 10(-8) M). (2) In stimulated myocytes, a prolongation of the duration of calcium transients at 10(-7) M in normal cells (+68%, P < 0.01) and at 10(-9) M, 10(-8) M, 10(-7) M in hypertrophied cells: (+36%, P < 0.05; +39%, P < 0.01; +77%, P < 0.01) with a greater sensitivity of hypertrophied myocytes (P < 0.05 at 10(-9) M and 10(-8) M). An increase in duration may be explained by the occurrence of calcium releases during the fall time of calcium transients. Thus, both in normal and hypertrophied myocytes, Ang II induced the occurrence of calcium releases with increased sensitivity of hypertrophied cells to Ang II. Such calcium releases are known to be a possible cause of arrhythmias termed "triggered activity".

Angiotensin II↗
PubMed1994

Markers of platelet activation in coronary heart disease patients.

We have applied flow cytometry to the detection of activated platelets in patients with coronary heart disease. Paraformaldehyde-fixed platelets were incubated with one of the following monoclonal antibodies (MAbs): Bx-1 (anti-GP Ib), AP-2 (anti-GP IIb-IIIa complex), VH10 (anti-GMP-140, a glycoprotein of the alpha-granule membrane), or PAC-1 (directed against an activation-dependent determinant on GP IIb-IIIa complexes). Bound antibody was quantitated after the addition of FITC-conjugated anti-immunoglobulin. This report highlights studies on 16 unstable angina patients undergoing transluminal angioplasty. Blood samples were taken at different periods before and after the angioplasty. Levels of activated platelets were variable, remaining in the 2-4% range of control donors for some, but increasing to 10-30% post-angioplasty for others (despite all patients receiving heparin and aspirin). Maximum numbers of activated platelets were detected at 24 or 48 h. Nonetheless, the amount of antibody bound to individual platelets rarely reached the levels seen when control platelets were stimulated with thrombin in vitro. Results with VH10 and PAC-1 often, but not always, correlated suggesting different pathways of platelet activation.

Angina, Unstable↗
PubMed1994

[Effects of angiotensin II on spontaneous cytosolic calcium releases in ventricular myocytes of adult normal and hypertensive rats].

This study investigated the effects of angiotensin II (Ang II) (10(-9)M to 10(-7)M) on calcium releases in ventricular myocytes from normal and renal hypertensive adult rats (Goldblatt 2K-1C). Newly, isolated myocytes were loaded with fluorescent indo-1/AM and studied at rest or under electrical stimulation. The variation of the ratio of indo-1 emission (405 nm/480 nm) was taken as a measure of cytosolic calcium variations. Five parameters were investigated from each peak systolic indo-1 ratio before and after Ang II addition: amplitude variation, duration with analysis of a rise time and a fall time, and frequency of spontaneous calcium releases. Following changes were observed: in unstimulated myocytes exhibiting spontaneous contractile activity, increase in frequency of calcium transients, at 10(-7)M, in normal cells (+ 157 +/- 27%; p < 0.01) and whatever Ang II concentration in hypertrophied cells (+ 79 +/- 31%; p < 0.01; + 82 +/- 25%, p < 0.01; + 285 +/- 50%, p < 0.01 à 10(-9)M, 10(-8)M, 10(-7)M); in stimulated myocytes, prolongation of the duration of calcium transients explained by the occurrence of calcium releases during fall time. In addition, 50% of myocytes exhibited spontaneous releases of calcium in the interstimulus interval. Increase in calcium transients duration was statistically significant, whatever Ang II concentration in hypertrophied cells (+ 36 +/- 20%, p < 0.05; + 39 +/- 18%, p < 0.01; + 77 +/- 34%, p < 0.01 à 10(-9)M, 10(-8)M, 10(-7)M) and only at 10(-7)M in normal cells (+ 68 +/- 22% p < 0.01). Similar results were observed in fall time.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1994

[Continuous monitoring of cardiac output by analysis of the pulse contour].

One method of continuous cardiac output monitoring by analysis of the radial pulse contour (Qcp) relates left ventricular stroke volume and systolic blood pressure by calculating the impedence characteristic of the aorta (Zao). It was assessed during haemodynamic monitoring by comparing it with the thermodilation method in the pulmonary artery (Qtd) in 20 patients with cardiac failure due to dilated cardiomyopathy (6 cases) and ischaemic cardiomyopathy (14 cases) treated by inotropic agents or vasodilators. Over an average monitoring period of 35 hours 159 measurements of cardiac output were performed by the two methods. There was an excellent correlation between the two methods (r = 0.90; p < 0.001; Qcp = 0.97 Qtd). The systematic error (bias) between the two methods was about 2.5%. The accuracy of Qcp compared with Qtd was 12.5%. During infusion with a vasoactive agent (Piroximone), the method based on pulse contour analysis did not reflect sudden variations in cardiac output. The systematic error between the two methods rose to 19% of the value measured, reflecting the lack of adaptation of parameters of correction in this situation and which necessitated recalibration of Zao at least once after injection of the drug.

Cardiac Output↗